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Current Techniques in Treating Femoroacetabular Impingement: Capsular Repair and Plication
Take-Home Points
- Hip capsule provides static stabilization for the hip joint.
- Capsular management must weigh visualization to address underlying osseous deformity but also repair/plication of the capsule to maintain biomechanical characteristics.
- T-capsulotomy provides optimal visualization with a small interportal incision with a vertical incision along the femoral neck.
- Extensile interportal capsulotomy is the most widely used capsulotomy and size may vary depending on capsular and patient characteristics.
- Orthopedic surgeons should be equipped to employ either technique depending on the patients individual hip pathomorphology.
Hip arthroscopy has emerged as a common surgical treatment for a number of hip pathologies. Surgical treatment strategies, including management of the hip capsule, have evolved. Whereas earlier hip arthroscopies often involved capsulectomy or capsulotomy without repair, more recently capsular closure has been considered an important step in restoring the anatomy of the hip joint and preventing microinstability or gross macroinstability.
The anatomy of the hip joint includes both static and dynamic stabilizers designed to maintain a functioning articulation. The osseous articulation of the femoral head and acetabulum is the first static stabilizer, with variations in offset, version, and inclination of the acetabulum and the proximal femur. The joint capsule consists of 3 ligaments—iliofemoral, pubofemoral, and ischiofemoral—that converge to form the zona orbicularis. Other soft-tissue structures, such as the articular cartilage, the labrum, the transverse acetabular ligament, the pulvinar, and the ligamentum teres, also provide static constraint.1 The surrounding musculature provides the hip joint with dynamic stability, which contributes to overall maintenance of proper joint kinematics.
Management of the hip capsule has evolved as our understanding of hip pathology and biomechanics has matured. Initial articles on using hip arthroscopy to treat labral tears described improvement in clinical outcomes,2 but the cases involved limited focal capsulotomy. Not until the idea of femoroacetabular impingement (FAI) was introduced were extensive capsulotomies and capsulectomies performed to address the underlying osseous deformities and emulate open techniques. Soon after our ability to access osseous pathomorphology improved with enhanced visualization and comprehensive resection, cases of hip instability after hip arthroscopy surfaced.3-5 Although frank dislocation after hip arthroscopy is rare and largely underreported, it is a catastrophic complication. In addition, focal capsular defects were also described in cases of failed hip arthroscopy and thought to lead to microinstability of the hip.6 Iatrogenic microinstability is thought to be more common, but it is also underrecognized as a cause of failure of hip arthroscopy.7Microinstability is a pathologic condition that can affect hip function. In cases of recurrent pain and unimproved functional status after surgery, microinstability should be considered. In an imaging study of capsule integrity, McCormick and colleagues6 found that 78% of patients who underwent revision arthroscopic surgery after hip arthroscopic surgery for FAI showed evidence of capsular and iliofemoral defects on magnetic resonance angiography. Frank and colleagues8 reported that, though all patients showed preoperative-to-postoperative improvement on outcome measures, those who underwent complete repair of their T-capsulotomy (vs repair of only its longitudinal portion) had superior outcomes, particularly increased sport-specific activity.
For patients undergoing hip arthroscopy, several predisposing factors can increase the risk of postoperative instability. Patient-related hip instability factors include generalized ligamentous laxity, supraphysiologic athletics (eg, dance), and borderline or true hip dysplasia. Surgeon-related factors include overaggressive acetabular rim resection, excessive labral débridement, and lack of capsular repair.5,9 Although there are multiple techniques for accessing the hip joint and addressing capsular closure at the end of surgery,9-14 we think capsular closure is an important aspect of the case.
Surgical Technique
For a demonstration of this technique, click here to see the video that accompanies this article. The patient is moved to a traction table and placed in the supine position. Induction of general anesthesia with muscle relaxation allows for atraumatic axial traction. The anesthetized patient is assessed for passive motion and ligamentous laxity. Well-padded boots are applied, and a well-padded perineal post is used for positioning. Gentle traction is applied to the contralateral limb, and axial traction is applied through the surgical limb with the hip abducted and minimally flexed. The leg is then adducted and neutrally extended, inducing a transverse vector cantilever moment to the proximal femur. The foot is internally rotated to optimize femoral neck length on an anteroposterior radiograph. The circulating nursing staff notes the onset of hip distraction in order to ensure safe traction duration.
Bony landmarks are marked with a sterile marking pen. Under fluoroscopic guidance, an anterolateral (AL) portal is established 1 cm proximal and 1 cm anterior to the AL tip of the greater trochanter. Standard cannulation allows for intra-articular visualization with a 70° arthroscope. A needle is used to localize placement of a modified anterior portal. After cannulation, the arthroscope is placed in the modified anterior portal to confirm safe entry of the portal without labral violation. An arthroscopic scalpel (Samurai Blade; Stryker Sports Medicine) is used to make a transverse interportal capsulotomy 8 mm to 10 mm from the labrum and extending from 12 to 2 o’clock; length is 2 cm to 4 cm, depending on the extent of the intra-articular injury (Figure 1A).
The acetabular rim is trimmed with a 5.0-mm arthroscopic burr. Distal AL accessory (DALA) portal placement (4-6 cm distal to and in line with the AL portal) allows for suture anchor–based labral refixation. Generally, 2 to 4 anchors (1.4-mm NanoTack Anatomic Labrum Restoration System; Stryker Sports Medicine) are placed as near the articular cartilage as possible without penetration (Figure 1B). On completion of labral refixation, traction is released, and the hip is flexed to 20° to 30°.
T-Capsulotomy
Pericapsular fatty tissue is débrided with an arthroscopic shaver to visualize the interval between the iliocapsularis and gluteus minimus muscles. An arthroscopic scalpel is used, through a 5.0-mm cannula in the DALA portal, to extend the capsulotomy longitudinally and perpendicular to the interportal capsulotomy (Figure 1C). The T-capsulotomy is performed along the length of the femoral neck distally to the capsular reflection at the intertrochanteric line. The arthroscopic burr is used to perform a femoral osteochondroplasty between the lateral synovial folds (12 o’clock) and the medial synovial folds (6 o’clock). Dynamic examination and fluoroscopic imaging confirm that the entire cam deformity has been excised and that there is no evidence of impingement.
Although various suture-shuttling or tissue-penetrating/retrieving devices may be used, we recommend whichever device is appropriate for closing the capsule in its entirety. With the arthroscope in the modified anterior portal, an 8.25-mm × 90-mm cannula is placed in the AL portal, and an 8.25-mm × 110-mm cannula in the DALA portal. These portals will facilitate suture passage.
The vertical limb of the T-capsulotomy is closed with 2 to 4 side-to-side sutures, and the interportal capsulotomy limb with 2 or 3 sutures. Capsular closure begins with the distal portion of the longitudinal limb at the base of the iliofemoral ligament (IFL). A crescent tissue penetrating device (Slingshot; Stryker Sports Medicine) is loaded with high-strength No. 2 suture (Zipline; Stryker Sports Medicine) and placed through the AL portal to sharply pierce the lateral leaflet of the IFL (Figure 1D). The No. 2 suture is shuttled into the intra-articular side of the capsule (Figure 1E). Through the DALA portal, the penetrating device is used to pierce the medial leaflet to retrieve the free suture (Figure 1F). Next, the looped suture retriever is used to pull the suture from the AL portal to the DALA portal so the suture can be tied. We prefer to tie each suture individually after it is passed, but all of the sutures can be passed first, and then tied. As successive suture placement and knot tying inherently tighten the capsule, successive visualization requires more precision. Each subsequent suture is similarly passed, about 1 cm proximal to the previous stitch.
After closure of the vertical limb of the T-capsulotomy, we prefer to close the interportal capsulotomy with the InJector II Capsule Restoration System (Stryker Sports Medicine), a device that allows for closure through a single cannula lateral to medial. This device is passed through the AL cannula in order to bring the suture end through the proximal IFL attached to the acetabulum (Figure 1G). The device is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL (Figure 1H). The stitch is then tensioned and tied. Likewise, closure of the medial IFL involves passing the InJector through the DALA cannula and bringing the first suture end through the proximal IFL attached to the acetabulum. The Injector is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL. The stitch is then tensioned and tied with the hip in neutral extension. Generally, 2 or 3 stitches are used to close the interportal capsulotomy. Complete capsular closure is confirmed by the inability to visualize the underlying femoral head/neck and by probing the anterior capsule to ensure proper tension (Figure 1I).
Extensile Interportal Capsulotomy
An alternative to T-capsulotomy is interportal capsulotomy. Just as with T-capsulotomy closure, multiple different suture passing devices can be used. Good visualization for accessing the peripheral compartment generally is achieved by making the interportal capsulotomy 4 cm to 6 cm longer than the horizontal limb of the T-capsulotomy (Figures 2A, 2B). Capsular closure usually begins with the medial portion of the interportal capsulotomy. With the arthroscope in the AL portal, the 8.25-mm × 90-mm cannula is placed in the midanterior portal (MAP), and an 8.25-mm × 110-mm cannula is placed in the DALA portal.
Ligamentous laxity determines degree of capsular closure. The capsular leaflets can be closed end to end if there is little concern for laxity and instability. If there is more concern for capsular laxity, a larger bite of the capsular tissue can be taken to allow for a greater degree of plication. Further, the interportal capsule can be tightened by alternately advancing the location where sutures are passed through the capsule. Specifically, the sutures are passed such that larger bites of the distal capsule are taken, increasing the tightness of the capsule in external rotation.9
Rehabilitation
After surgery, hip extension and external rotation are limited to decrease stress on the capsular closure. The patient is placed into a hip orthosis with 0° to 90° of flexion and a night abduction pillow to limit hip external rotation. Crutch-assisted gait with 20 lb of foot-flat weight-bearing is maintained the first 3 weeks. Continuous passive motion and use of a stationary bicycle are recommended for the first 3 weeks, and then the patient slowly progresses to muscle strengthening, including core and proximal motor control. Closed-chain exercises are begun 6 weeks after surgery. Treadmill running may start at 12 weeks, with the goal of returning to sport at 4 to 6 months.
Discussion
Capsular closure during hip arthroscopy restores the normal anatomy of the IFL and therefore restores the biomechanical characteristics of the hip joint. Scientific studies have found that capsular repair or plication after hip arthroscopy restores normal hip translation, rotation, and strain. Clinical studies have also demonstrated a lower revision rate and more rapid return to athletic activity. Capsular closure, however, is technically challenging and increases operative time, but gross instability and microinstability can be avoided with meticulous closure/plication.
Am J Orthop. 2017;46(1):49-54. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Boykin RE, Anz AW, Bushnell BD, Kocher MS, Stubbs AJ, Philippon MJ. Hip instability. J Am Acad Orthop Surg. 2011;19(6):340-349.
2. Byrd JW, Jones KS. Hip arthroscopy for labral pathology: prospective analysis with 10-year follow-up. Arthroscopy. 2009;25(4):365-368.
3. Benali Y, Katthagen BD. Hip subluxation as a complication of arthroscopic debridement. Arthroscopy. 2009;25(4):405-407.
4. Matsuda DK. Acute iatrogenic dislocation following hip impingement arthroscopic surgery. Arthroscopy. 2009;25(4):400-404.
5. Ranawat AS, McClincy M, Sekiya JK. Anterior dislocation of the hip after arthroscopy in a patient with capsular laxity of the hip. A case report. J Bone Joint Surg Am. 2009;91(1):192-197.
6. McCormick F, Slikker W 3rd, Harris JD, et al. Evidence of capsular defect following hip arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):902-905.
7. Wylie JD, Beckmann JT, Maak TG, Aoki SK. Arthroscopic capsular repair for symptomatic hip instability after previous hip arthroscopic surgery. Am J Sports Med. 2016;44(1):39-45.
8. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
9. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
10. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
11. Camp CL, Reardon PJ, Levy BA, Krych AJ. A simple technique for capsular repair after hip arthroscopy. Arthrosc Tech. 2015;4(6):e737-e740.
12. Chow RM, Engasser WM, Krych AJ, Levy BA. Arthroscopic capsular repair in the treatment of femoroacetabular impingement. Arthrosc Tech. 2014;3(1):e27-e30.
13. Harris JD, Slikker W 3rd, Gupta AK, McCormick FM, Nho SJ. Routine complete capsular closure during hip arthroscopy. Arthrosc Tech. 2013;2(2):e89-e94.
14. Kuhns BD, Weber AE, Levy DM, et al. Capsular management in hip arthroscopy: an anatomic, biomechanical, and technical review. Front Surg. 2016;3:13.
Take-Home Points
- Hip capsule provides static stabilization for the hip joint.
- Capsular management must weigh visualization to address underlying osseous deformity but also repair/plication of the capsule to maintain biomechanical characteristics.
- T-capsulotomy provides optimal visualization with a small interportal incision with a vertical incision along the femoral neck.
- Extensile interportal capsulotomy is the most widely used capsulotomy and size may vary depending on capsular and patient characteristics.
- Orthopedic surgeons should be equipped to employ either technique depending on the patients individual hip pathomorphology.
Hip arthroscopy has emerged as a common surgical treatment for a number of hip pathologies. Surgical treatment strategies, including management of the hip capsule, have evolved. Whereas earlier hip arthroscopies often involved capsulectomy or capsulotomy without repair, more recently capsular closure has been considered an important step in restoring the anatomy of the hip joint and preventing microinstability or gross macroinstability.
The anatomy of the hip joint includes both static and dynamic stabilizers designed to maintain a functioning articulation. The osseous articulation of the femoral head and acetabulum is the first static stabilizer, with variations in offset, version, and inclination of the acetabulum and the proximal femur. The joint capsule consists of 3 ligaments—iliofemoral, pubofemoral, and ischiofemoral—that converge to form the zona orbicularis. Other soft-tissue structures, such as the articular cartilage, the labrum, the transverse acetabular ligament, the pulvinar, and the ligamentum teres, also provide static constraint.1 The surrounding musculature provides the hip joint with dynamic stability, which contributes to overall maintenance of proper joint kinematics.
Management of the hip capsule has evolved as our understanding of hip pathology and biomechanics has matured. Initial articles on using hip arthroscopy to treat labral tears described improvement in clinical outcomes,2 but the cases involved limited focal capsulotomy. Not until the idea of femoroacetabular impingement (FAI) was introduced were extensive capsulotomies and capsulectomies performed to address the underlying osseous deformities and emulate open techniques. Soon after our ability to access osseous pathomorphology improved with enhanced visualization and comprehensive resection, cases of hip instability after hip arthroscopy surfaced.3-5 Although frank dislocation after hip arthroscopy is rare and largely underreported, it is a catastrophic complication. In addition, focal capsular defects were also described in cases of failed hip arthroscopy and thought to lead to microinstability of the hip.6 Iatrogenic microinstability is thought to be more common, but it is also underrecognized as a cause of failure of hip arthroscopy.7Microinstability is a pathologic condition that can affect hip function. In cases of recurrent pain and unimproved functional status after surgery, microinstability should be considered. In an imaging study of capsule integrity, McCormick and colleagues6 found that 78% of patients who underwent revision arthroscopic surgery after hip arthroscopic surgery for FAI showed evidence of capsular and iliofemoral defects on magnetic resonance angiography. Frank and colleagues8 reported that, though all patients showed preoperative-to-postoperative improvement on outcome measures, those who underwent complete repair of their T-capsulotomy (vs repair of only its longitudinal portion) had superior outcomes, particularly increased sport-specific activity.
For patients undergoing hip arthroscopy, several predisposing factors can increase the risk of postoperative instability. Patient-related hip instability factors include generalized ligamentous laxity, supraphysiologic athletics (eg, dance), and borderline or true hip dysplasia. Surgeon-related factors include overaggressive acetabular rim resection, excessive labral débridement, and lack of capsular repair.5,9 Although there are multiple techniques for accessing the hip joint and addressing capsular closure at the end of surgery,9-14 we think capsular closure is an important aspect of the case.
Surgical Technique
For a demonstration of this technique, click here to see the video that accompanies this article. The patient is moved to a traction table and placed in the supine position. Induction of general anesthesia with muscle relaxation allows for atraumatic axial traction. The anesthetized patient is assessed for passive motion and ligamentous laxity. Well-padded boots are applied, and a well-padded perineal post is used for positioning. Gentle traction is applied to the contralateral limb, and axial traction is applied through the surgical limb with the hip abducted and minimally flexed. The leg is then adducted and neutrally extended, inducing a transverse vector cantilever moment to the proximal femur. The foot is internally rotated to optimize femoral neck length on an anteroposterior radiograph. The circulating nursing staff notes the onset of hip distraction in order to ensure safe traction duration.
Bony landmarks are marked with a sterile marking pen. Under fluoroscopic guidance, an anterolateral (AL) portal is established 1 cm proximal and 1 cm anterior to the AL tip of the greater trochanter. Standard cannulation allows for intra-articular visualization with a 70° arthroscope. A needle is used to localize placement of a modified anterior portal. After cannulation, the arthroscope is placed in the modified anterior portal to confirm safe entry of the portal without labral violation. An arthroscopic scalpel (Samurai Blade; Stryker Sports Medicine) is used to make a transverse interportal capsulotomy 8 mm to 10 mm from the labrum and extending from 12 to 2 o’clock; length is 2 cm to 4 cm, depending on the extent of the intra-articular injury (Figure 1A).
The acetabular rim is trimmed with a 5.0-mm arthroscopic burr. Distal AL accessory (DALA) portal placement (4-6 cm distal to and in line with the AL portal) allows for suture anchor–based labral refixation. Generally, 2 to 4 anchors (1.4-mm NanoTack Anatomic Labrum Restoration System; Stryker Sports Medicine) are placed as near the articular cartilage as possible without penetration (Figure 1B). On completion of labral refixation, traction is released, and the hip is flexed to 20° to 30°.
T-Capsulotomy
Pericapsular fatty tissue is débrided with an arthroscopic shaver to visualize the interval between the iliocapsularis and gluteus minimus muscles. An arthroscopic scalpel is used, through a 5.0-mm cannula in the DALA portal, to extend the capsulotomy longitudinally and perpendicular to the interportal capsulotomy (Figure 1C). The T-capsulotomy is performed along the length of the femoral neck distally to the capsular reflection at the intertrochanteric line. The arthroscopic burr is used to perform a femoral osteochondroplasty between the lateral synovial folds (12 o’clock) and the medial synovial folds (6 o’clock). Dynamic examination and fluoroscopic imaging confirm that the entire cam deformity has been excised and that there is no evidence of impingement.
Although various suture-shuttling or tissue-penetrating/retrieving devices may be used, we recommend whichever device is appropriate for closing the capsule in its entirety. With the arthroscope in the modified anterior portal, an 8.25-mm × 90-mm cannula is placed in the AL portal, and an 8.25-mm × 110-mm cannula in the DALA portal. These portals will facilitate suture passage.
The vertical limb of the T-capsulotomy is closed with 2 to 4 side-to-side sutures, and the interportal capsulotomy limb with 2 or 3 sutures. Capsular closure begins with the distal portion of the longitudinal limb at the base of the iliofemoral ligament (IFL). A crescent tissue penetrating device (Slingshot; Stryker Sports Medicine) is loaded with high-strength No. 2 suture (Zipline; Stryker Sports Medicine) and placed through the AL portal to sharply pierce the lateral leaflet of the IFL (Figure 1D). The No. 2 suture is shuttled into the intra-articular side of the capsule (Figure 1E). Through the DALA portal, the penetrating device is used to pierce the medial leaflet to retrieve the free suture (Figure 1F). Next, the looped suture retriever is used to pull the suture from the AL portal to the DALA portal so the suture can be tied. We prefer to tie each suture individually after it is passed, but all of the sutures can be passed first, and then tied. As successive suture placement and knot tying inherently tighten the capsule, successive visualization requires more precision. Each subsequent suture is similarly passed, about 1 cm proximal to the previous stitch.
After closure of the vertical limb of the T-capsulotomy, we prefer to close the interportal capsulotomy with the InJector II Capsule Restoration System (Stryker Sports Medicine), a device that allows for closure through a single cannula lateral to medial. This device is passed through the AL cannula in order to bring the suture end through the proximal IFL attached to the acetabulum (Figure 1G). The device is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL (Figure 1H). The stitch is then tensioned and tied. Likewise, closure of the medial IFL involves passing the InJector through the DALA cannula and bringing the first suture end through the proximal IFL attached to the acetabulum. The Injector is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL. The stitch is then tensioned and tied with the hip in neutral extension. Generally, 2 or 3 stitches are used to close the interportal capsulotomy. Complete capsular closure is confirmed by the inability to visualize the underlying femoral head/neck and by probing the anterior capsule to ensure proper tension (Figure 1I).
Extensile Interportal Capsulotomy
An alternative to T-capsulotomy is interportal capsulotomy. Just as with T-capsulotomy closure, multiple different suture passing devices can be used. Good visualization for accessing the peripheral compartment generally is achieved by making the interportal capsulotomy 4 cm to 6 cm longer than the horizontal limb of the T-capsulotomy (Figures 2A, 2B). Capsular closure usually begins with the medial portion of the interportal capsulotomy. With the arthroscope in the AL portal, the 8.25-mm × 90-mm cannula is placed in the midanterior portal (MAP), and an 8.25-mm × 110-mm cannula is placed in the DALA portal.
Ligamentous laxity determines degree of capsular closure. The capsular leaflets can be closed end to end if there is little concern for laxity and instability. If there is more concern for capsular laxity, a larger bite of the capsular tissue can be taken to allow for a greater degree of plication. Further, the interportal capsule can be tightened by alternately advancing the location where sutures are passed through the capsule. Specifically, the sutures are passed such that larger bites of the distal capsule are taken, increasing the tightness of the capsule in external rotation.9
Rehabilitation
After surgery, hip extension and external rotation are limited to decrease stress on the capsular closure. The patient is placed into a hip orthosis with 0° to 90° of flexion and a night abduction pillow to limit hip external rotation. Crutch-assisted gait with 20 lb of foot-flat weight-bearing is maintained the first 3 weeks. Continuous passive motion and use of a stationary bicycle are recommended for the first 3 weeks, and then the patient slowly progresses to muscle strengthening, including core and proximal motor control. Closed-chain exercises are begun 6 weeks after surgery. Treadmill running may start at 12 weeks, with the goal of returning to sport at 4 to 6 months.
Discussion
Capsular closure during hip arthroscopy restores the normal anatomy of the IFL and therefore restores the biomechanical characteristics of the hip joint. Scientific studies have found that capsular repair or plication after hip arthroscopy restores normal hip translation, rotation, and strain. Clinical studies have also demonstrated a lower revision rate and more rapid return to athletic activity. Capsular closure, however, is technically challenging and increases operative time, but gross instability and microinstability can be avoided with meticulous closure/plication.
Am J Orthop. 2017;46(1):49-54. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Hip capsule provides static stabilization for the hip joint.
- Capsular management must weigh visualization to address underlying osseous deformity but also repair/plication of the capsule to maintain biomechanical characteristics.
- T-capsulotomy provides optimal visualization with a small interportal incision with a vertical incision along the femoral neck.
- Extensile interportal capsulotomy is the most widely used capsulotomy and size may vary depending on capsular and patient characteristics.
- Orthopedic surgeons should be equipped to employ either technique depending on the patients individual hip pathomorphology.
Hip arthroscopy has emerged as a common surgical treatment for a number of hip pathologies. Surgical treatment strategies, including management of the hip capsule, have evolved. Whereas earlier hip arthroscopies often involved capsulectomy or capsulotomy without repair, more recently capsular closure has been considered an important step in restoring the anatomy of the hip joint and preventing microinstability or gross macroinstability.
The anatomy of the hip joint includes both static and dynamic stabilizers designed to maintain a functioning articulation. The osseous articulation of the femoral head and acetabulum is the first static stabilizer, with variations in offset, version, and inclination of the acetabulum and the proximal femur. The joint capsule consists of 3 ligaments—iliofemoral, pubofemoral, and ischiofemoral—that converge to form the zona orbicularis. Other soft-tissue structures, such as the articular cartilage, the labrum, the transverse acetabular ligament, the pulvinar, and the ligamentum teres, also provide static constraint.1 The surrounding musculature provides the hip joint with dynamic stability, which contributes to overall maintenance of proper joint kinematics.
Management of the hip capsule has evolved as our understanding of hip pathology and biomechanics has matured. Initial articles on using hip arthroscopy to treat labral tears described improvement in clinical outcomes,2 but the cases involved limited focal capsulotomy. Not until the idea of femoroacetabular impingement (FAI) was introduced were extensive capsulotomies and capsulectomies performed to address the underlying osseous deformities and emulate open techniques. Soon after our ability to access osseous pathomorphology improved with enhanced visualization and comprehensive resection, cases of hip instability after hip arthroscopy surfaced.3-5 Although frank dislocation after hip arthroscopy is rare and largely underreported, it is a catastrophic complication. In addition, focal capsular defects were also described in cases of failed hip arthroscopy and thought to lead to microinstability of the hip.6 Iatrogenic microinstability is thought to be more common, but it is also underrecognized as a cause of failure of hip arthroscopy.7Microinstability is a pathologic condition that can affect hip function. In cases of recurrent pain and unimproved functional status after surgery, microinstability should be considered. In an imaging study of capsule integrity, McCormick and colleagues6 found that 78% of patients who underwent revision arthroscopic surgery after hip arthroscopic surgery for FAI showed evidence of capsular and iliofemoral defects on magnetic resonance angiography. Frank and colleagues8 reported that, though all patients showed preoperative-to-postoperative improvement on outcome measures, those who underwent complete repair of their T-capsulotomy (vs repair of only its longitudinal portion) had superior outcomes, particularly increased sport-specific activity.
For patients undergoing hip arthroscopy, several predisposing factors can increase the risk of postoperative instability. Patient-related hip instability factors include generalized ligamentous laxity, supraphysiologic athletics (eg, dance), and borderline or true hip dysplasia. Surgeon-related factors include overaggressive acetabular rim resection, excessive labral débridement, and lack of capsular repair.5,9 Although there are multiple techniques for accessing the hip joint and addressing capsular closure at the end of surgery,9-14 we think capsular closure is an important aspect of the case.
Surgical Technique
For a demonstration of this technique, click here to see the video that accompanies this article. The patient is moved to a traction table and placed in the supine position. Induction of general anesthesia with muscle relaxation allows for atraumatic axial traction. The anesthetized patient is assessed for passive motion and ligamentous laxity. Well-padded boots are applied, and a well-padded perineal post is used for positioning. Gentle traction is applied to the contralateral limb, and axial traction is applied through the surgical limb with the hip abducted and minimally flexed. The leg is then adducted and neutrally extended, inducing a transverse vector cantilever moment to the proximal femur. The foot is internally rotated to optimize femoral neck length on an anteroposterior radiograph. The circulating nursing staff notes the onset of hip distraction in order to ensure safe traction duration.
Bony landmarks are marked with a sterile marking pen. Under fluoroscopic guidance, an anterolateral (AL) portal is established 1 cm proximal and 1 cm anterior to the AL tip of the greater trochanter. Standard cannulation allows for intra-articular visualization with a 70° arthroscope. A needle is used to localize placement of a modified anterior portal. After cannulation, the arthroscope is placed in the modified anterior portal to confirm safe entry of the portal without labral violation. An arthroscopic scalpel (Samurai Blade; Stryker Sports Medicine) is used to make a transverse interportal capsulotomy 8 mm to 10 mm from the labrum and extending from 12 to 2 o’clock; length is 2 cm to 4 cm, depending on the extent of the intra-articular injury (Figure 1A).
The acetabular rim is trimmed with a 5.0-mm arthroscopic burr. Distal AL accessory (DALA) portal placement (4-6 cm distal to and in line with the AL portal) allows for suture anchor–based labral refixation. Generally, 2 to 4 anchors (1.4-mm NanoTack Anatomic Labrum Restoration System; Stryker Sports Medicine) are placed as near the articular cartilage as possible without penetration (Figure 1B). On completion of labral refixation, traction is released, and the hip is flexed to 20° to 30°.
T-Capsulotomy
Pericapsular fatty tissue is débrided with an arthroscopic shaver to visualize the interval between the iliocapsularis and gluteus minimus muscles. An arthroscopic scalpel is used, through a 5.0-mm cannula in the DALA portal, to extend the capsulotomy longitudinally and perpendicular to the interportal capsulotomy (Figure 1C). The T-capsulotomy is performed along the length of the femoral neck distally to the capsular reflection at the intertrochanteric line. The arthroscopic burr is used to perform a femoral osteochondroplasty between the lateral synovial folds (12 o’clock) and the medial synovial folds (6 o’clock). Dynamic examination and fluoroscopic imaging confirm that the entire cam deformity has been excised and that there is no evidence of impingement.
Although various suture-shuttling or tissue-penetrating/retrieving devices may be used, we recommend whichever device is appropriate for closing the capsule in its entirety. With the arthroscope in the modified anterior portal, an 8.25-mm × 90-mm cannula is placed in the AL portal, and an 8.25-mm × 110-mm cannula in the DALA portal. These portals will facilitate suture passage.
The vertical limb of the T-capsulotomy is closed with 2 to 4 side-to-side sutures, and the interportal capsulotomy limb with 2 or 3 sutures. Capsular closure begins with the distal portion of the longitudinal limb at the base of the iliofemoral ligament (IFL). A crescent tissue penetrating device (Slingshot; Stryker Sports Medicine) is loaded with high-strength No. 2 suture (Zipline; Stryker Sports Medicine) and placed through the AL portal to sharply pierce the lateral leaflet of the IFL (Figure 1D). The No. 2 suture is shuttled into the intra-articular side of the capsule (Figure 1E). Through the DALA portal, the penetrating device is used to pierce the medial leaflet to retrieve the free suture (Figure 1F). Next, the looped suture retriever is used to pull the suture from the AL portal to the DALA portal so the suture can be tied. We prefer to tie each suture individually after it is passed, but all of the sutures can be passed first, and then tied. As successive suture placement and knot tying inherently tighten the capsule, successive visualization requires more precision. Each subsequent suture is similarly passed, about 1 cm proximal to the previous stitch.
After closure of the vertical limb of the T-capsulotomy, we prefer to close the interportal capsulotomy with the InJector II Capsule Restoration System (Stryker Sports Medicine), a device that allows for closure through a single cannula lateral to medial. This device is passed through the AL cannula in order to bring the suture end through the proximal IFL attached to the acetabulum (Figure 1G). The device is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL (Figure 1H). The stitch is then tensioned and tied. Likewise, closure of the medial IFL involves passing the InJector through the DALA cannula and bringing the first suture end through the proximal IFL attached to the acetabulum. The Injector is removed from the cannula, and the other suture end is placed in the device and passed through the distal IFL. The stitch is then tensioned and tied with the hip in neutral extension. Generally, 2 or 3 stitches are used to close the interportal capsulotomy. Complete capsular closure is confirmed by the inability to visualize the underlying femoral head/neck and by probing the anterior capsule to ensure proper tension (Figure 1I).
Extensile Interportal Capsulotomy
An alternative to T-capsulotomy is interportal capsulotomy. Just as with T-capsulotomy closure, multiple different suture passing devices can be used. Good visualization for accessing the peripheral compartment generally is achieved by making the interportal capsulotomy 4 cm to 6 cm longer than the horizontal limb of the T-capsulotomy (Figures 2A, 2B). Capsular closure usually begins with the medial portion of the interportal capsulotomy. With the arthroscope in the AL portal, the 8.25-mm × 90-mm cannula is placed in the midanterior portal (MAP), and an 8.25-mm × 110-mm cannula is placed in the DALA portal.
Ligamentous laxity determines degree of capsular closure. The capsular leaflets can be closed end to end if there is little concern for laxity and instability. If there is more concern for capsular laxity, a larger bite of the capsular tissue can be taken to allow for a greater degree of plication. Further, the interportal capsule can be tightened by alternately advancing the location where sutures are passed through the capsule. Specifically, the sutures are passed such that larger bites of the distal capsule are taken, increasing the tightness of the capsule in external rotation.9
Rehabilitation
After surgery, hip extension and external rotation are limited to decrease stress on the capsular closure. The patient is placed into a hip orthosis with 0° to 90° of flexion and a night abduction pillow to limit hip external rotation. Crutch-assisted gait with 20 lb of foot-flat weight-bearing is maintained the first 3 weeks. Continuous passive motion and use of a stationary bicycle are recommended for the first 3 weeks, and then the patient slowly progresses to muscle strengthening, including core and proximal motor control. Closed-chain exercises are begun 6 weeks after surgery. Treadmill running may start at 12 weeks, with the goal of returning to sport at 4 to 6 months.
Discussion
Capsular closure during hip arthroscopy restores the normal anatomy of the IFL and therefore restores the biomechanical characteristics of the hip joint. Scientific studies have found that capsular repair or plication after hip arthroscopy restores normal hip translation, rotation, and strain. Clinical studies have also demonstrated a lower revision rate and more rapid return to athletic activity. Capsular closure, however, is technically challenging and increases operative time, but gross instability and microinstability can be avoided with meticulous closure/plication.
Am J Orthop. 2017;46(1):49-54. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Boykin RE, Anz AW, Bushnell BD, Kocher MS, Stubbs AJ, Philippon MJ. Hip instability. J Am Acad Orthop Surg. 2011;19(6):340-349.
2. Byrd JW, Jones KS. Hip arthroscopy for labral pathology: prospective analysis with 10-year follow-up. Arthroscopy. 2009;25(4):365-368.
3. Benali Y, Katthagen BD. Hip subluxation as a complication of arthroscopic debridement. Arthroscopy. 2009;25(4):405-407.
4. Matsuda DK. Acute iatrogenic dislocation following hip impingement arthroscopic surgery. Arthroscopy. 2009;25(4):400-404.
5. Ranawat AS, McClincy M, Sekiya JK. Anterior dislocation of the hip after arthroscopy in a patient with capsular laxity of the hip. A case report. J Bone Joint Surg Am. 2009;91(1):192-197.
6. McCormick F, Slikker W 3rd, Harris JD, et al. Evidence of capsular defect following hip arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):902-905.
7. Wylie JD, Beckmann JT, Maak TG, Aoki SK. Arthroscopic capsular repair for symptomatic hip instability after previous hip arthroscopic surgery. Am J Sports Med. 2016;44(1):39-45.
8. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
9. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
10. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
11. Camp CL, Reardon PJ, Levy BA, Krych AJ. A simple technique for capsular repair after hip arthroscopy. Arthrosc Tech. 2015;4(6):e737-e740.
12. Chow RM, Engasser WM, Krych AJ, Levy BA. Arthroscopic capsular repair in the treatment of femoroacetabular impingement. Arthrosc Tech. 2014;3(1):e27-e30.
13. Harris JD, Slikker W 3rd, Gupta AK, McCormick FM, Nho SJ. Routine complete capsular closure during hip arthroscopy. Arthrosc Tech. 2013;2(2):e89-e94.
14. Kuhns BD, Weber AE, Levy DM, et al. Capsular management in hip arthroscopy: an anatomic, biomechanical, and technical review. Front Surg. 2016;3:13.
1. Boykin RE, Anz AW, Bushnell BD, Kocher MS, Stubbs AJ, Philippon MJ. Hip instability. J Am Acad Orthop Surg. 2011;19(6):340-349.
2. Byrd JW, Jones KS. Hip arthroscopy for labral pathology: prospective analysis with 10-year follow-up. Arthroscopy. 2009;25(4):365-368.
3. Benali Y, Katthagen BD. Hip subluxation as a complication of arthroscopic debridement. Arthroscopy. 2009;25(4):405-407.
4. Matsuda DK. Acute iatrogenic dislocation following hip impingement arthroscopic surgery. Arthroscopy. 2009;25(4):400-404.
5. Ranawat AS, McClincy M, Sekiya JK. Anterior dislocation of the hip after arthroscopy in a patient with capsular laxity of the hip. A case report. J Bone Joint Surg Am. 2009;91(1):192-197.
6. McCormick F, Slikker W 3rd, Harris JD, et al. Evidence of capsular defect following hip arthroscopy. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):902-905.
7. Wylie JD, Beckmann JT, Maak TG, Aoki SK. Arthroscopic capsular repair for symptomatic hip instability after previous hip arthroscopic surgery. Am J Sports Med. 2016;44(1):39-45.
8. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
9. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
10. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
11. Camp CL, Reardon PJ, Levy BA, Krych AJ. A simple technique for capsular repair after hip arthroscopy. Arthrosc Tech. 2015;4(6):e737-e740.
12. Chow RM, Engasser WM, Krych AJ, Levy BA. Arthroscopic capsular repair in the treatment of femoroacetabular impingement. Arthrosc Tech. 2014;3(1):e27-e30.
13. Harris JD, Slikker W 3rd, Gupta AK, McCormick FM, Nho SJ. Routine complete capsular closure during hip arthroscopy. Arthrosc Tech. 2013;2(2):e89-e94.
14. Kuhns BD, Weber AE, Levy DM, et al. Capsular management in hip arthroscopy: an anatomic, biomechanical, and technical review. Front Surg. 2016;3:13.
Shoulder Dislocations
IN THIS ARTICLE
- Types of shoulder dislocations
- Schematics of the shoulder with three types of dislocations
- Association with seizures
CASE A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.
An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).
The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations).
The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.1 While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.1 For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.2
The three types of shoulder dislocations include anterior, posterior, and inferior.
ANTERIOR
Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.3 They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).
A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed.
Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.4 The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.5 The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.4
Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.6 Both can be seen on plain films, although Bankart lesions are best seen on CT.4
The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.7
POSTERIOR
Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.2 They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures).
Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).8 This position is sometimes misdiagnosed as a “frozen shoulder.”2
INFERIOR
Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall.
Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction: a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.9
ASSOCIATION WITH SEIZURES
Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.10
Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.11
Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.12
In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).10
The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.8
After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon.
CONCLUSION
This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.
1. Omoumi P, Teixeira P, Lecouvet F, Chung CB. Glenohumeral joint instability. J Magn Reson Imaging. 2010;33(1):2-16.
2. Rouleau DM, Hebert-Davies J. Incidence of associated injury in posterior shoulder dislocation: systematic review of the literature. J Orthop Trauma. 2012;26(4):246-251.
3. Sachit M, Shekhar A, Shekhar S, Joban SH. Acute spontaneous atraumatic bilateral anterior dislocation of the shoulder joint with Hill-Sach’s lesions: a rare case. J Orthop Case Rep. 2015;5(1):55-57.
4. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl. 2009;91(1):2-7.
5. Magee DJ. Orthopedic Physical Assessment. 5th ed. St. Louis, MO. Saunders Elsevier; 2008.
6. Greenspan A. Orthopedic Imaging: A Practical Approach. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
7. Karimi-Nasab MH, Shayesteh-Azar M, Sajjadi-Saravi M, Mehdi Daneshpoor SM. Anterior shoulder dislocation and ipsilateral humeral shaft fracture. Iran J Med Sci. 2012; 37(3):202-204.
8. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am. 2005; 87(3):639-650.
9. Cacioppo E, Waymack JR. Bilateral inferior shoulder dislocation. West J Emerg Med. 2015;16(1):157.
10. Tiamkao S, Shorvon SD. Seizure-related injury in an adult tertiary epilepsy clinic. Hong Kong Med J. 2006;12(4):260-263.
11. Shaw JL. Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures. J Bone Joint Surg Am. 1971;53(7):1437-1440.
12. Lawn ND, Bamlet WR, Radhakirshnan K, et al. Injuries due to seizures in persons with epilepsy: a population-based study. Neurology. 2004;63(9):1565-1570.
IN THIS ARTICLE
- Types of shoulder dislocations
- Schematics of the shoulder with three types of dislocations
- Association with seizures
CASE A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.
An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).
The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations).
The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.1 While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.1 For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.2
The three types of shoulder dislocations include anterior, posterior, and inferior.
ANTERIOR
Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.3 They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).
A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed.
Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.4 The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.5 The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.4
Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.6 Both can be seen on plain films, although Bankart lesions are best seen on CT.4
The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.7
POSTERIOR
Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.2 They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures).
Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).8 This position is sometimes misdiagnosed as a “frozen shoulder.”2
INFERIOR
Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall.
Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction: a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.9
ASSOCIATION WITH SEIZURES
Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.10
Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.11
Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.12
In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).10
The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.8
After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon.
CONCLUSION
This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.
IN THIS ARTICLE
- Types of shoulder dislocations
- Schematics of the shoulder with three types of dislocations
- Association with seizures
CASE A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.
An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).
The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations).
The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.1 While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.1 For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.2
The three types of shoulder dislocations include anterior, posterior, and inferior.
ANTERIOR
Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.3 They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).
A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed.
Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.4 The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.5 The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.4
Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.6 Both can be seen on plain films, although Bankart lesions are best seen on CT.4
The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.7
POSTERIOR
Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.2 They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures).
Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).8 This position is sometimes misdiagnosed as a “frozen shoulder.”2
INFERIOR
Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall.
Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction: a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.9
ASSOCIATION WITH SEIZURES
Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.10
Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.11
Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.12
In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).10
The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.8
After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon.
CONCLUSION
This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.
1. Omoumi P, Teixeira P, Lecouvet F, Chung CB. Glenohumeral joint instability. J Magn Reson Imaging. 2010;33(1):2-16.
2. Rouleau DM, Hebert-Davies J. Incidence of associated injury in posterior shoulder dislocation: systematic review of the literature. J Orthop Trauma. 2012;26(4):246-251.
3. Sachit M, Shekhar A, Shekhar S, Joban SH. Acute spontaneous atraumatic bilateral anterior dislocation of the shoulder joint with Hill-Sach’s lesions: a rare case. J Orthop Case Rep. 2015;5(1):55-57.
4. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl. 2009;91(1):2-7.
5. Magee DJ. Orthopedic Physical Assessment. 5th ed. St. Louis, MO. Saunders Elsevier; 2008.
6. Greenspan A. Orthopedic Imaging: A Practical Approach. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
7. Karimi-Nasab MH, Shayesteh-Azar M, Sajjadi-Saravi M, Mehdi Daneshpoor SM. Anterior shoulder dislocation and ipsilateral humeral shaft fracture. Iran J Med Sci. 2012; 37(3):202-204.
8. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am. 2005; 87(3):639-650.
9. Cacioppo E, Waymack JR. Bilateral inferior shoulder dislocation. West J Emerg Med. 2015;16(1):157.
10. Tiamkao S, Shorvon SD. Seizure-related injury in an adult tertiary epilepsy clinic. Hong Kong Med J. 2006;12(4):260-263.
11. Shaw JL. Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures. J Bone Joint Surg Am. 1971;53(7):1437-1440.
12. Lawn ND, Bamlet WR, Radhakirshnan K, et al. Injuries due to seizures in persons with epilepsy: a population-based study. Neurology. 2004;63(9):1565-1570.
1. Omoumi P, Teixeira P, Lecouvet F, Chung CB. Glenohumeral joint instability. J Magn Reson Imaging. 2010;33(1):2-16.
2. Rouleau DM, Hebert-Davies J. Incidence of associated injury in posterior shoulder dislocation: systematic review of the literature. J Orthop Trauma. 2012;26(4):246-251.
3. Sachit M, Shekhar A, Shekhar S, Joban SH. Acute spontaneous atraumatic bilateral anterior dislocation of the shoulder joint with Hill-Sach’s lesions: a rare case. J Orthop Case Rep. 2015;5(1):55-57.
4. Cutts S, Prempeh M, Drew S. Anterior shoulder dislocation. Ann R Coll Surg Engl. 2009;91(1):2-7.
5. Magee DJ. Orthopedic Physical Assessment. 5th ed. St. Louis, MO. Saunders Elsevier; 2008.
6. Greenspan A. Orthopedic Imaging: A Practical Approach. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
7. Karimi-Nasab MH, Shayesteh-Azar M, Sajjadi-Saravi M, Mehdi Daneshpoor SM. Anterior shoulder dislocation and ipsilateral humeral shaft fracture. Iran J Med Sci. 2012; 37(3):202-204.
8. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am. 2005; 87(3):639-650.
9. Cacioppo E, Waymack JR. Bilateral inferior shoulder dislocation. West J Emerg Med. 2015;16(1):157.
10. Tiamkao S, Shorvon SD. Seizure-related injury in an adult tertiary epilepsy clinic. Hong Kong Med J. 2006;12(4):260-263.
11. Shaw JL. Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures. J Bone Joint Surg Am. 1971;53(7):1437-1440.
12. Lawn ND, Bamlet WR, Radhakirshnan K, et al. Injuries due to seizures in persons with epilepsy: a population-based study. Neurology. 2004;63(9):1565-1570.
Bariatric surgery or total joint replacement: which first?
NEW ORLEANS – Performing bariatric surgery prior to total knee or hip replacement instead of vice versa resulted in significantly shorter orthopedic surgical operating time and length of stay in an observational study, Emanuel E. Nearing II, MD, reported at Obesity Week 2016.
“We propose that strong consideration be given to bariatric surgery as a means of weight loss and BMI [body mass index] reduction in patients with obesity prior to total joint replacement,” he said at the meeting presented by the Obesity Society of America and the American Society for Metabolic and Bariatric Surgery.
“A common complaint of patients presenting with obesity is that their osteoarthritis has limited their mobility and that their weight gain is secondary to that reduced mobility. They believe that a new joint will help them regain their mobility and then lose weight. Interestingly, this does not appear to be the case. In fact, the majority of patients in our study actually gained weight following joint replacement. Given that, these patients need to be weight-optimized prior to total joint replacement. Bariatric surgery is a durable way to facilitate this,” he continued.
Dr. Nearing presented a retrospective observational study of 102 patients who underwent either laparoscopic Roux-en-Y gastric bypass or laparoscopic sleeve gastrectomy plus a total knee or hip replacement in the Gundersen system. Sixty-six patients had their bariatric surgery first, by a mean of 4.3 years, while the other 36 had arthroplasty a mean of 4.9 years before their bariatric surgery. The two groups were similar in terms of demographics and baseline comorbid conditions.
Patients who had their total joint replacement first had a mean preoperative BMI of 43.7 kg/m2 and a mean pre–bariatric surgery BMI of 46.3 kg/m2. The patients who had bariatric surgery first had a preoperative BMI of 49.6 kg/m2 and a mean pre–orthopedic surgery BMI of 37.6 kgm2. One year after joint replacement surgery, patients who had that operation first had a mean BMI of 43.9 kg/m2, compared with 37.8 kg/m2 for those who waited until after they underwent bariatric surgery.
Mean operative time for total joint replacement when it was the first operation was 113.5 minutes and substantially less at 71 minutes when it was done after bariatric surgery. Mean hospital length of stay for total joint replacement when it followed bariatric surgery was 2.9 days, a full day less than when joint replacement came first.
Rates of complications including skin or soft tissue infection, venous thromboembolism, hematoma, need for transfusion, and periprosthetic infection at 30 and 90 days didn’t differ between the two groups. Neither did the need for late reinterventions.
Dr. Nearing noted that a working group of the American Association of Hip and Knee Surgeons has conducted a review of the orthopedic surgery literature and concluded that all patients with a BMI of 30 kg/m2 or more undergoing total knee or hip arthroplasty are at increased risk for perioperative respiratory complications, thromboembolic events, delayed wound healing, infection, and need for joint revision surgery (J Arthroplasty. 2013 May;28[5]:714-21).
He observed that a retrospective study such as his cannot shed light on the optimal time interval for total joint replacement following bariatric surgery. That key question is being addressed by the ongoing prospective SWIFT (Surgical Weight-Loss to Improve Functional Status Trajectories Following Total Knee Arthroplasty) trial. The study hypothesis is that bariatric surgery prior to the knee replacement surgery will reduce risk and improve long-term outcomes and physical function.
Several audience member commented that, based upon their experience, they would have anticipated that complication rates would have been significantly lower in total joint replacement patients when that operation followed bariatric surgery.
“We were surprised, too,” Dr. Nearing replied. “I think the explanation is that at Gundersen we have three bariatric surgeons and only a handful of orthopedic surgeons, and we use protocols and pathways. We just routinely do our operations the same way each and every time.”
John M. Morton, MD, a former American Society for Metabolic and Bariatric Surgery president, commented that the Gundersen study findings sound a call for more cross-specialty collaboration in steering obese patients with severe knee or hip osteoarthritis to bariatric surgery first in order to maximize the results of the joint replacement surgery.
“I think we’re all seeing weight loss as another form of prehabilitation for other specialties. Our orthopedic colleagues are kind of like us – surgeons – so this seems to be a great place for us to partner with them,” said Dr. Morton, chief of bariatric and minimally invasive surgery at Stanford (Calif.) University.
Dr. Nearing reported having no financial interests relevant to his study.
NEW ORLEANS – Performing bariatric surgery prior to total knee or hip replacement instead of vice versa resulted in significantly shorter orthopedic surgical operating time and length of stay in an observational study, Emanuel E. Nearing II, MD, reported at Obesity Week 2016.
“We propose that strong consideration be given to bariatric surgery as a means of weight loss and BMI [body mass index] reduction in patients with obesity prior to total joint replacement,” he said at the meeting presented by the Obesity Society of America and the American Society for Metabolic and Bariatric Surgery.
“A common complaint of patients presenting with obesity is that their osteoarthritis has limited their mobility and that their weight gain is secondary to that reduced mobility. They believe that a new joint will help them regain their mobility and then lose weight. Interestingly, this does not appear to be the case. In fact, the majority of patients in our study actually gained weight following joint replacement. Given that, these patients need to be weight-optimized prior to total joint replacement. Bariatric surgery is a durable way to facilitate this,” he continued.
Dr. Nearing presented a retrospective observational study of 102 patients who underwent either laparoscopic Roux-en-Y gastric bypass or laparoscopic sleeve gastrectomy plus a total knee or hip replacement in the Gundersen system. Sixty-six patients had their bariatric surgery first, by a mean of 4.3 years, while the other 36 had arthroplasty a mean of 4.9 years before their bariatric surgery. The two groups were similar in terms of demographics and baseline comorbid conditions.
Patients who had their total joint replacement first had a mean preoperative BMI of 43.7 kg/m2 and a mean pre–bariatric surgery BMI of 46.3 kg/m2. The patients who had bariatric surgery first had a preoperative BMI of 49.6 kg/m2 and a mean pre–orthopedic surgery BMI of 37.6 kgm2. One year after joint replacement surgery, patients who had that operation first had a mean BMI of 43.9 kg/m2, compared with 37.8 kg/m2 for those who waited until after they underwent bariatric surgery.
Mean operative time for total joint replacement when it was the first operation was 113.5 minutes and substantially less at 71 minutes when it was done after bariatric surgery. Mean hospital length of stay for total joint replacement when it followed bariatric surgery was 2.9 days, a full day less than when joint replacement came first.
Rates of complications including skin or soft tissue infection, venous thromboembolism, hematoma, need for transfusion, and periprosthetic infection at 30 and 90 days didn’t differ between the two groups. Neither did the need for late reinterventions.
Dr. Nearing noted that a working group of the American Association of Hip and Knee Surgeons has conducted a review of the orthopedic surgery literature and concluded that all patients with a BMI of 30 kg/m2 or more undergoing total knee or hip arthroplasty are at increased risk for perioperative respiratory complications, thromboembolic events, delayed wound healing, infection, and need for joint revision surgery (J Arthroplasty. 2013 May;28[5]:714-21).
He observed that a retrospective study such as his cannot shed light on the optimal time interval for total joint replacement following bariatric surgery. That key question is being addressed by the ongoing prospective SWIFT (Surgical Weight-Loss to Improve Functional Status Trajectories Following Total Knee Arthroplasty) trial. The study hypothesis is that bariatric surgery prior to the knee replacement surgery will reduce risk and improve long-term outcomes and physical function.
Several audience member commented that, based upon their experience, they would have anticipated that complication rates would have been significantly lower in total joint replacement patients when that operation followed bariatric surgery.
“We were surprised, too,” Dr. Nearing replied. “I think the explanation is that at Gundersen we have three bariatric surgeons and only a handful of orthopedic surgeons, and we use protocols and pathways. We just routinely do our operations the same way each and every time.”
John M. Morton, MD, a former American Society for Metabolic and Bariatric Surgery president, commented that the Gundersen study findings sound a call for more cross-specialty collaboration in steering obese patients with severe knee or hip osteoarthritis to bariatric surgery first in order to maximize the results of the joint replacement surgery.
“I think we’re all seeing weight loss as another form of prehabilitation for other specialties. Our orthopedic colleagues are kind of like us – surgeons – so this seems to be a great place for us to partner with them,” said Dr. Morton, chief of bariatric and minimally invasive surgery at Stanford (Calif.) University.
Dr. Nearing reported having no financial interests relevant to his study.
NEW ORLEANS – Performing bariatric surgery prior to total knee or hip replacement instead of vice versa resulted in significantly shorter orthopedic surgical operating time and length of stay in an observational study, Emanuel E. Nearing II, MD, reported at Obesity Week 2016.
“We propose that strong consideration be given to bariatric surgery as a means of weight loss and BMI [body mass index] reduction in patients with obesity prior to total joint replacement,” he said at the meeting presented by the Obesity Society of America and the American Society for Metabolic and Bariatric Surgery.
“A common complaint of patients presenting with obesity is that their osteoarthritis has limited their mobility and that their weight gain is secondary to that reduced mobility. They believe that a new joint will help them regain their mobility and then lose weight. Interestingly, this does not appear to be the case. In fact, the majority of patients in our study actually gained weight following joint replacement. Given that, these patients need to be weight-optimized prior to total joint replacement. Bariatric surgery is a durable way to facilitate this,” he continued.
Dr. Nearing presented a retrospective observational study of 102 patients who underwent either laparoscopic Roux-en-Y gastric bypass or laparoscopic sleeve gastrectomy plus a total knee or hip replacement in the Gundersen system. Sixty-six patients had their bariatric surgery first, by a mean of 4.3 years, while the other 36 had arthroplasty a mean of 4.9 years before their bariatric surgery. The two groups were similar in terms of demographics and baseline comorbid conditions.
Patients who had their total joint replacement first had a mean preoperative BMI of 43.7 kg/m2 and a mean pre–bariatric surgery BMI of 46.3 kg/m2. The patients who had bariatric surgery first had a preoperative BMI of 49.6 kg/m2 and a mean pre–orthopedic surgery BMI of 37.6 kgm2. One year after joint replacement surgery, patients who had that operation first had a mean BMI of 43.9 kg/m2, compared with 37.8 kg/m2 for those who waited until after they underwent bariatric surgery.
Mean operative time for total joint replacement when it was the first operation was 113.5 minutes and substantially less at 71 minutes when it was done after bariatric surgery. Mean hospital length of stay for total joint replacement when it followed bariatric surgery was 2.9 days, a full day less than when joint replacement came first.
Rates of complications including skin or soft tissue infection, venous thromboembolism, hematoma, need for transfusion, and periprosthetic infection at 30 and 90 days didn’t differ between the two groups. Neither did the need for late reinterventions.
Dr. Nearing noted that a working group of the American Association of Hip and Knee Surgeons has conducted a review of the orthopedic surgery literature and concluded that all patients with a BMI of 30 kg/m2 or more undergoing total knee or hip arthroplasty are at increased risk for perioperative respiratory complications, thromboembolic events, delayed wound healing, infection, and need for joint revision surgery (J Arthroplasty. 2013 May;28[5]:714-21).
He observed that a retrospective study such as his cannot shed light on the optimal time interval for total joint replacement following bariatric surgery. That key question is being addressed by the ongoing prospective SWIFT (Surgical Weight-Loss to Improve Functional Status Trajectories Following Total Knee Arthroplasty) trial. The study hypothesis is that bariatric surgery prior to the knee replacement surgery will reduce risk and improve long-term outcomes and physical function.
Several audience member commented that, based upon their experience, they would have anticipated that complication rates would have been significantly lower in total joint replacement patients when that operation followed bariatric surgery.
“We were surprised, too,” Dr. Nearing replied. “I think the explanation is that at Gundersen we have three bariatric surgeons and only a handful of orthopedic surgeons, and we use protocols and pathways. We just routinely do our operations the same way each and every time.”
John M. Morton, MD, a former American Society for Metabolic and Bariatric Surgery president, commented that the Gundersen study findings sound a call for more cross-specialty collaboration in steering obese patients with severe knee or hip osteoarthritis to bariatric surgery first in order to maximize the results of the joint replacement surgery.
“I think we’re all seeing weight loss as another form of prehabilitation for other specialties. Our orthopedic colleagues are kind of like us – surgeons – so this seems to be a great place for us to partner with them,” said Dr. Morton, chief of bariatric and minimally invasive surgery at Stanford (Calif.) University.
Dr. Nearing reported having no financial interests relevant to his study.
AT OBESITY WEEK 2016
Key clinical point:
Major finding: When total joint replacement in obese patients was performed after bariatric surgery, mean hospital length of stay was a full day less than when the orthopedic surgery preceded the bariatric surgery.
Data source: This retrospective observational study included 102 obese patients who underwent bariatric surgery and total knee or hip replacement.
Disclosures: The study presenter reported having no financial conflicts of interest.
A Multimodal Strategy to Manage Pain in an In-Patient and Out-Patient Total Joint Program: What Do You Need to Know?
Contents
Opioid-Sparing Pain Control in Outpatient Total Joint Arthroplasty
John W. Barrington, MD
Addressing the Opioid Epidemic With Multimodal Pain Management
Michael A. Kelly, MD
Comprehensive Care for Joint Replacement (CJR) Bundle Expense in Perioperative Pain Management
Susan D. Bear, PharmD, BCPS
The Role of Liposomal Bupivacaine in Value-Based Care
Richard Iorio, MD
Contents
Opioid-Sparing Pain Control in Outpatient Total Joint Arthroplasty
John W. Barrington, MD
Addressing the Opioid Epidemic With Multimodal Pain Management
Michael A. Kelly, MD
Comprehensive Care for Joint Replacement (CJR) Bundle Expense in Perioperative Pain Management
Susan D. Bear, PharmD, BCPS
The Role of Liposomal Bupivacaine in Value-Based Care
Richard Iorio, MD
Contents
Opioid-Sparing Pain Control in Outpatient Total Joint Arthroplasty
John W. Barrington, MD
Addressing the Opioid Epidemic With Multimodal Pain Management
Michael A. Kelly, MD
Comprehensive Care for Joint Replacement (CJR) Bundle Expense in Perioperative Pain Management
Susan D. Bear, PharmD, BCPS
The Role of Liposomal Bupivacaine in Value-Based Care
Richard Iorio, MD
Ulnar Collateral Ligament Reconstruction: Current Philosophy in 2016
The ulnar collateral ligament (UCL) is the primary restraint to valgus stress between 20° and 125° of motion.1-5 Overhead athletes, most commonly baseball pitchers, are at risk of developing UCL insufficiency, and dysfunction presents as pain with loss of velocity and control. Some injuries may present acutely while throwing, but many patients, when questioned, report a preceding period of either pain or loss of velocity and control.
Authors have documented a significant rise in elbow injuries in young athletes, especially pitchers.6 Extended seasons, higher pitch counts, year-round pitching, pitching while fatigued, and pitching for multiple teams are risk factors for elbow injuries.7 Pitchers in the southern United States are more likely to undergo UCL reconstruction than those from the northern states.8 Pitchers who also play catcher are at a higher risk due to more total throws than those who pitch and play other positions or pitch only. Throwers with higher velocity are more likely to pitch in showcases, pitch for multiple teams, and pitch with pain and fatigue, and these are all risk factors.6 Also, in one study of youth baseball injuries, individuals in the injured group were found to be taller and heavier than those in the uninjured group.6 Pitch counts, rest from pitching during the off-season, adequate rest, and ensuring pain-free pitching can lessen the risk of injury.6 As expected with the rise in throwing injuries, the rise in medial elbow procedures has risen.9
While throwing, stress across the medial elbow has been measured to be nearly 300 N. A maximum varus force during pitching was measured to be 64 N-m at 95° ± 14°.10 Morrey and An4 determined that the UCL generated 54% of the varus force at 90° of flexion. During active pitching, this value is likely reduced due to simultaneous muscle contraction, but if one assumes the UCL bears 54% of the maximal load, the UCL must be able to withstand 34 N-m. The UCL can withstand a maximum valgus torque between 22.7 and 34 N-m11-13; therefore, during pitching, the UCL is at or above its failure load. After thousands of cycles over many years, one can imagine how the UCL might be injured.
Multiple techniques have been proposed in the surgical treatment of UCL injuries. Jobe14 pioneered UCL reconstruction in 1974 in Tommy John, a Major League Baseball pitcher. John returned to pitch successfully, and both the UCL and the reconstruction are commonly called by his name. Jobe14 reported his technique in 1986, and it has remained, with a few modifications, the primary method for reconstruction of the UCL (Figure 1).
Evaluation
A standard evaluation with physical examination and imaging is completed in all throwers with elbow pain. In our prior study,16 we found that 100% of patients experienced pain during athletic activity and that 96% of throwers complained of pain during late cocking and acceleration phases of the throwing motion. Nearly half reported an acute onset of pain, while 53% were unable to identify a single inciting event. Seventy-five percent of the acute injuries were during competition. Delayed diagnosis was very common, with an average time to diagnosis after onset of symptoms of 6.4 months. Neurologic symptoms were seen in 23% of athletes, most of which were ulnar nerve paresthesias during throwing.16
Physical examination includes inspection for swelling, hand intrinsic atrophy, neurovascular examination, range of motion, shoulder examination, and elbow stress examination. Range of motion at presentation averaged 5° to 135° with 85° of supination and pronation.16 All patients need neurologic evaluation for ulnar nerve dysfunction. Tinel test of the cubital tunnel was positive in 21%.16 Significant ulnar nerve dysfunction, including hand weakness, is much less common but must be well examined and documented. The shoulder must also be evaluated for loss of rotation, which can lead to increased stress on the elbow. An evaluation of mechanics may point out flaws in technique, which may be contributing to elbow stress. The UCL stress examination includes static stress at 30° of flexion, the milking test at 90°, and the moving valgus stress test. The presence of pain directly over the UCL or laxity compared to the uninvolved side is suggestive of UCL injury.
Radiographic evaluation is completed in all patients with concern for UCL injury. Standard x-rays of the elbow, including anteroposterior, medial, and lateral obliques, axial olecranon, and lateral views, are obtained to evaluate bony abnormalities. Fifty-seven percent of our series showed some abnormality, most commonly olecranon osteophyte formation or ectopic calcification within the UCL substance. Stress radiography rarely changed the treatment course and is somewhat difficult to interpret because of the reports documenting normal increased medial elbow opening in the dominant arm of throwing athletes.21 Magnetic resonance imaging (MRI) is obtained very commonly in this patient population, and intra-articular contrast is crucial. Partial, undersurface tears are common, and a contrasted study better demonstrates undersurface tears or avulsions. The T-sign as described by Timmerman and colleagues22 using computed tomography (CT) arthrography shows partial undersurface detachment, which can be difficult to see without intra-articular contrast.22 This finding is very well visualized on MRI arthrogram as well (Figure 3).
Nonoperative Management
Nonoperative treatment is recommended for 3 months prior to performing reconstruction. Patients are given complete rest from throwing, but rehabilitation is initiated immediately. Rehabilitation exercises and nonsteroidal anti-inflammatory medications are prescribed, and activities that place valgus stress across the elbow are avoided. After resolution of symptoms, an interval throwing program is initiated, and the athlete is gradually returned to sport. Unfortunately, due to season-specific schedules and time-sensitive demands in high-level throwers, operative treatment is often chosen without an extended period of conservative treatment.
Platelet-rich plasma (PRP) therapy has recently been shown to improve healing rates and promote healing in partial UCL tears,23 and as orthobiologics are advanced, they will likely play a larger role in the treatment of UCL injuries.
Surgical Technique
At our institution, UCL reconstruction is performed with the modified Jobe technique as described by Azar and colleagues.17 Arthroscopy prior to reconstruction was routinely performed at our institution until we recognized that arthroscopy rarely changed the preoperative plan.16 Currently, the presence of anterior pathology such as loose bodies or osteochondral defect is our only indication for arthroscopy before reconstruction.
Ipsilateral palmaris autograft is our current graft of choice. This must be examined preoperatively because 16% of patients have unilateral absence and 9% have bilateral absence.24 In revision cases or in patients with insufficient or absent palmaris, contralateral palmaris followed by contralateral gracilis tendon is used. The contralateral gracilis is chosen because of ease of setup and position of the surgeon during the harvest. Gracilis tendon is also used in cases with bony involvement of the ligament based on the results from Dugas and colleagues.25 Toe extensors, plantaris, and patellar tendon grafts have also been used. One recent study showed that neither graft choice nor diameter affected resistance to valgus stress, and that all reconstruction types restored strength at 60° to 120° of flexion.26
Ulnar nerve transposition is performed in all cases regardless of the presence of preoperative nerve symptoms. A complete decompression is completed proximally to the Arcade of Struthers and distally to the deep portion of the flexor carpi ulnaris. A single fascial sling of medial intermuscular septum originating from the epicondylar attachment is used to stabilize the nerve without compression. At wound closure, the deep fascia on the posterior skin flap is also sewn into the cubital tunnel to prevent the nerve from subluxating back into the groove. A single suture is placed distally closing the muscle fascia to prevent propagation of the fascial incision, which can lead to herniation. Transposition is necessary because of the ulnar nerve exposure required in the modified Jobe technique to allow elevation of the deep flexor muscle mass for ligament exposure.
The reconstruction is completed as described by Jobe14 but with a few modifications as described by Azar and colleagues17 and slight adaptations implemented since that time. The flexor-pronator mass is retracted laterally instead of detachment or splitting as described by Thompson and colleagues.27 A subcutaneous rather than a submuscular ulnar nerve transposition is used.
The patient is positioned supine using an arm board. If gracilis tendon is chosen, the contralateral leg is prepped and draped simultaneously. A tourniquet is inflated after exsanguination. A medial approach is performed, and the medial antebrachial nerve is located and protected. The ulnar nerve is then located in the cubital tunnel and mobilized. The neurolysis extends to the deep portion of the flexor carpi ulnaris distally and proximally to the Arcade of Struthers, and the nerve is retracted with a vessel loop. The flexor muscle mass is not elevated from the medial epicondyle; rather, it is retracted anteriorly by small Hohmann retractors. The dissection is carried down to the UCL and found at its attachments to the medial epicondyle and sublime tubercle. If no tear is seen on the superficial surface of the ligament, a longitudinal incision is made through the ligament. Undersurface tears, partial tears, and avulsions can then be identified (Figure 4).
The autologous graft of choice is then harvested. Our technique for palmaris harvest is performed with three 1-cm transverse incisions. The palmaris is palpated and marked with the first incision made near the distal wrist crease, and the second incision is made 3 to 4 cm proximal to the first. The tendon is found in both distal incisions and cut distally with the wrist flexed to maximize tendon length. The tendon is then pulled through the second incision and tensioned to identify the most proximal location the tendon can be palpated. A third incision is made directly over this point and carried down to cut the tendon. This usually provides a graft length of 15 to 20 cm; 13 cm is the minimum graft length to ensure good graft fixation. Muscle is removed from the tendon and each end is secured with a No. 1 nonabsorbable suture in a locking fashion.
If posterior osteophytes are present, they are removed through a posterior, vertical arthrotomy. Over-resection of the olecranon must be avoided, as this can further destabilize the elbow and place increased stress on the reconstruction. Posterior loose bodies can also be removed through this arthrotomy. The arthrotomy is then closed with absorbable suture.
Tunnel placement is critical to success. A 3.2-mm drill bit is used with palmaris grafts and a 4-mm drill bit is used with gracilis grafts. Two convergent tunnels are drilled in the medial epicondyle in a Y fashion and 2 convergent tunnels are drilled at the sublime tubercle in a U or V fashion. After drilling the first tunnel on each side, a hemostat is placed in the tunnel as an aiming point to ensure a complete tunnel is made. The junction is smoothed with a curette, leaving a 5-mm bone bridge between the articular surface and the tunnels. A bent Hewson suture passer is used to pass one end of the graft through the ulna. The 2 limbs of the tendon graft are then passed through the humeral tunnels, creating a figure-of-eight. A varus stress is applied with the elbow at roughly 30° and the 2 limbs are tied together with a No. 1 nonabsorbable suture. If enough graft remains, one or both limbs are passed back through the tunnels and secured again with No. 1 nonabsorbable suture. The 2 limbs are then tied side-to-side, incorporating the native ligament to further secure and tighten the reconstruction.
The ulnar nerve is then secured using a strip of medial intermuscular septum left intact to its insertion at the medial epicondyle. This is attached to the flexor-pronator muscle fascia with a 3-0 nonabsorbable suture. Enough length should be harvested from the septum to ensure there is no compression on the nerve. The deep posterior fascial tissue is then sewn to the periosteum of the medial epicondyle to further prevent subluxation of the nerve back into the groove. The skin is then closed in layered fashion over a superficial drain. The patient is placed in a well-padded posterior splint for 1 week, then the rehabilitation protocol is initiated as discussed below.
Postoperative Rehabilitation
A standardized postoperative 4-phase rehabilitation program for ulnar collateral reconstruction is followed as described by Wilk and colleagues.28-30 The first phase begins immediately after surgery and continues for 4 weeks. During surgery, the patient’s elbow is placed in a compression dressing with a posterior splint to immobilize the elbow in 90° of flexion with wrist motion for 1 week to allow initial healing. Full range of motion of the elbow joint is restored by the end of the fifth to sixth week after surgery.
During phase II (weeks 4-10), a progressive isotonic strengthening program is initiated. Exercises are focused on scapular, rotator cuff, deltoid, and arm musculature. Shoulder range of motion and stretching exercises are performed during this phase and the Thrower’s Ten exercise program is initiated. Any adaptations or strength deficits are addressed during this phase.
During the advanced strengthening phase (phase III), from weeks 10 to 16, a sport-specific exercise/rehabilitation program is initiated. During this phase, stretching and flexibility exercises are performed to enhance strength, power, and endurance. During this phase the patient is placed on the advanced Thrower’s Ten program. Isotonic strengthening exercises are progressed, and at week 12, the athlete is allowed to begin an isotonic lifting program, including bench press, seated rowing, latissimus dorsi pull downs, triceps push downs, and biceps curls. In addition, the athlete performs specific exercises to emphasize sport-specific movements. At week 12, overhead athletes begin a 2-hand plyometric throwing program, and at 14 weeks, a 1
Discussion
Results after ulnar collateral reconstruction have been good. In our series of 743 patients, 83% returned to the same or higher level at an average of 11.6 months.16 There was a 4% major complication rate and 16% minor complication rate. Major complications included medial epicondyle fracture (0.5%), significant ulnar nerve dysfunction (1 patient), rupture of graft (1%), and graft site infection. Sixteen percent of patients had ulnar nerve dysfunction, and 82% of these resolved within 6 weeks. All but 1 patient’s paresthesias resolved within 1 year.16 The 10-year follow-up of this group of patients included 256 patients and was reported by Osbahr and colleagues31 in 2014. Retirement from baseball was due to reasons other than the elbow in 86%, and 98% were still able to throw on at least a recreational level. The overall longevity was 3.6 years, with 2.9 years at pre-injury level or higher. Statistically, pitchers performed at a higher level after reconstruction.31
A recent review by Erickson and colleagues9 showed an overall 82% excellent and 8% good result when evaluating different techniques, including the American Sports Medicine Institute (ASMI) modification of Jobe’s technique, docking technique, and Jobe’s technique. With an overall complication rate of 10% (75% of which was transient ulnar neuritis), the procedure was deemed overall a safe surgical option. Collegiate athletes had the highest return to sport (95%) compared with high school athletes (89%) and professional athletes (86%). The docking technique had the highest rate of return to play (97%) compared with ASMI technique (93%) and Jobe technique (66%).9 Results after repair have not been as good as reconstruction, as reported in 2 studies.16,32 Savoie and colleagues,15 however, reported 93% good/excellent results after primary UCL repair alone.
Another recent review of outcomes showed an overall return to same or higher level was best with docking or modified docking techniques (90.4% and 91.3%, respectively).19 Overall return with modified Jobe technique was 77%.19 O’Brien and colleagues20 performed a review of 33 patients with either modified Jobe or docking technique that showed 81% return to same or higher level with modified Jobe vs 92% with docking technique. The Kerlan-Jobe Orthopaedic Clinic scores were higher in the modified Jobe group (79 vs 74) and the docking technique group returned to play nearly 1 month sooner (12.4 months vs 11.8 months).20 However, comparing different techniques in a heterogenous patient population over 40 years is difficult. Many of the modified Jobe technique cases were performed in the early evolution of the rehabilitation and return-to-play programs. We believe that the current modified Jobe technique has results equal to any other variation.
Despite good results with reconstructions, the recovery is lengthy and most pitchers cannot fully return to competition level for 12 to 18 months. Extensive research has been performed in exploring alternatives to the traditional reconstruction. Advancements in orthobiologics and development of new surgical options seem to provide an alternative to reconstruction, and may allow faster return to competition with less morbidity.
PRP has been at the forefront of orthopedic research for the last 2 decades, mostly focused in tendon and bone healing. Due to the release of many inflammatory mediators, PRP is theorized to initiate a healing response with growth factors that can direct healing towards normal tissue.33 Two main types of PRP are reported based on the presence or absence of leukocytes. PRP has been studied in many applications, but only one clinical study on the UCL has been published to date. Podesta and colleagues23 injected PRP into the elbow of 34 baseball players with MRI-confirmed partial UCL tear. The athletes then underwent a rehabilitation program, which limited stress across the UCL. Type 1A PRP was used (leukocyte-rich, unactivated, 5x or greater platelet concentration33). Athletes were allowed to return to sport based on symptoms and examination findings. Eighty-eight percent returned to same level of play without complaints at average 70 week follow-up, and average return to play ranged from 10 to 15 weeks.23 No specific data were given on the 16 pitchers in the group, but with such a high rate of return, PRP needs to be further evaluated in the treatment of UCL injuries.
Another recent study from Dugas and colleagues18 presented primary UCL repair using a tape augment (InternalBrace, Arthrex). Nine matched cadaver elbows underwent UCL sectioning and then either modified Jobe reconstruction or primary repair of the UCL with placement of the InternalBrace. The biomechanical data showed the repair with internal brace to have slightly less gap, more stiffness, and higher failure strength, although these findings were not statistically significant.18 This bone-preserving technique with less exposure and healing of the native ligament may be another step towards good results with a quicker return to throwing.
Conclusion
UCL injuries can be disabling in throwers. Reconstruction has afforded throwers a high rate of return to preinjury function or better, and several techniques have been presented that produce acceptable results. Overall complication rates range from 10% to 15%, and the majority of complications are transient ulnar neuropraxias. Orthobiologics and repair with augmentation have more recently offered additional options that may improve success of nonoperative treatment or allow less-invasive surgical treatment. Increased involvement in youth sports and early specialization is driving injury rates in young athletes. The orthopedic community must continue to look for better ways to prevent these injuries and investigate better methods to return athletes to high-level competition.
Am J Orthop. 2016;45(7):E534-E540. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Fuss FK. The ulnar collateral ligament of the human elbow joint. Anatomy, function and biomechanics. J Anat. 1991;175:203-212.
2. Hotchkiss RN, Weiland AJ. Valgus stability of the elbow. J Orthop Res. 1987;5(3):372-377.
3. Morrey BF. Applied anatomy and biomechanics of the elbow joint. Instr Course Lect. 1986;35:59-68.
4. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med. 1983;11(5):315-319.
5. Morrey BF, An KN. Functional anatomy of the ligaments of the elbow. Clin Orthop. 1985;(201):84-90.
6. Olsen SJ 2nd, Fleisig GS, Dun S, Loftice J, Andrews JR. Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med. 2006;34(6):905-912.
7. Fleisig GS, Andrews JR. Prevention of elbow injuries in youth baseball pitchers. Sports Health. 2012;4(5):419-424.
8. Zaremski JL, Horodyski M, Donlan RM, Brisbane ST, Farmer KW. Does geographic location matter on the prevalence of ulnar collateral ligament reconstruction in collegiate baseball pitchers? Orthop J Sports Med. 2015;3(11):2325967115616582.
9. Erickson BJ, Nwachukwu BU, Rosas S, et al. Trends in medial ulnar collateral ligament reconstruction in the United States: A retrospective review of a large private-payer database from 2007 to 2011. Am J Sports Med. 2015;43(7):1770-1774.
10. Fleisig GS, Andrews JR, Dillman CJ. Kinetics of baseball pitching with implications about injury mechanism. Am J Sports Med. 1995;23(2):233-239.
11. Dillman CJ, Smutz P, Werner S. Valgus extension overload in baseball pitching. Med Sci Sports Exerc. 1991;23(suppl 4):S135.
12. Hechtman KS, Tjin-A-Tsoi EW, Zvijac JE, Uribe JW, Latta LL. Biomechanics of a less invasive procedure for reconstruction of the ulnar collateral ligament of the elbow. Am J Sports Med. 1998;26(5):620-624.
13. Ahmad CS, Lee TQ, ElAttrache NS. Biomechanical evaluation of a new ulnar collateral ligament reconstruction technique with interference screw fixation. Am J Sports Med. 2003;31(3):332-337.
14. Jobe FW, Stark HE, Lombardo SJ. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am. 1986;68(8):1158-1163.
15. Savoie FH 3rd, Trenhaile SW, Roberts J, Field LD, Ramsey JR. Primary repair of ulnar collateral ligament injuries of the elbow in young athletes: a case series of injuries to the proximal and distal ends of the ligament. Am J Sports Med. 2008;36(6):1066-1072.
16. Cain EL, Andrews JR, Dugas JR, et al. Outcome of ulnar collateral ligament reconstruction of the elbow in 1281 athletes results in 743 athletes with minimum 2-year follow-up. Am J Sports Med. 2010;38(12):2426-2434.
17. Azar FM, Andrews JR, Wilk KE, Groh D. Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am J Sports Med. 2000;28(1):16-23.
18. Dugas JR, Walters BL, Beason DP, Fleisig GS, Chronister JE. Biomechanical comparison of ulnar collateral ligament repair with internal bracing versus modified Jobe reconstruction. Am J Sports Med. 2016;44(3):735-741.
19. Watson JN, McQueen P, Hutchinson MR. A systematic review of ulnar collateral ligament reconstruction techniques. Am J Sports Med. 2014;42(10):2510-2516.
20. O’Brien DF, O’Hagan T, Stewart R, et al. Outcomes for ulnar collateral ligament reconstruction: A retrospective review using the KJOC assessment score with two-year follow-up in an overhead throwing population. J Shoulder Elbow Surg. 2015;24(6):934-940.
21. Ellenbecker TS, Mattalino AJ, Elam EA, Caplinger RA. Medial elbow joint laxity in professional baseball pitchers a bilateral comparison using stress radiography. Am J Sports Med. 1998;26(3):420-424.
22. Timmerman LA, Schwartz ML, Andrews JR. Preoperative evaluation of the ulnar collateral ligament by magnetic resonance imaging and computed tomography arthrography evaluation in 25 baseball players with surgical confirmation. Am J Sports Med. 1994;22(1):26-32.
23. Podesta L, Crow SA, Volkmer D, Bert T, Yocum LA. Treatment of partial ulnar collateral ligament tears in the elbow with platelet-rich plasma. Am J Sports Med. 2013;41(7):1689-1694.
24. Thompson NW, Mockford BJ, Cran GW. Absence of the palmaris longus muscle: a population study. Ulster Med J. 2001;70(1):22-24.
25. Dugas JR, Bilotta J, Watts CD, et al. Ulnar collateral ligament reconstruction with gracilis tendon in athletes with intraligamentous bony excision technique and results. Am J Sports Med. 2012;40(7):1578-1582.
26. Dargel J, Küpper F, Wegmann K, Oppermann J, Eysel P, Müller LP. Graft diameter does not influence primary stability of ulnar collateral ligament reconstruction of the elbow. J Orthop Sci. 2015;20(2):307-313.
27. Thompson WH, Jobe FW, Yocum LA, Pink MM. Ulnar collateral ligament reconstruction in athletes: muscle-splitting approach without transposition of the ulnar nerve. J Shoulder Elbow Surg. 2001;10(2):152-157.
28. Wilk KE, Arrigo CA, Andrews JR. Rehabilitation of the elbow in the throwing athlete. J Orthop Sports Phys Ther. 1993;17(6):305-317.
29. Wilk KE, Arrigo CA, Andrews JR, et al. Rehabilitation following elbow surgery in the throwing athlete. Oper Tech Sports Med. 1996;4:114-132.
30. Wilk KE, Arrigo CA, Andrews JR, et al. Preventative and Rehabilitation Exercises for the Shoulder and Elbow. 4th ed. Birmingham, AL: American Sports Medicine Institute; 1996.
31. Osbahr DC, Cain EL, Raines BT, Fortenbaugh D, Dugas JR, Andrews JR. Long-term outcomes after ulnar collateral ligament reconstruction in competitive baseball players minimum 10-year follow-up. Am J Sports Med. 2014;42(6):1333-1342.
32. 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.
33. Mishra A, Harmon K, Woodall J, Vieira A. Sports medicine applications of platelet rich plasma. Curr Pharm Biotechnol. 2012;13(7):1185-1195.
The ulnar collateral ligament (UCL) is the primary restraint to valgus stress between 20° and 125° of motion.1-5 Overhead athletes, most commonly baseball pitchers, are at risk of developing UCL insufficiency, and dysfunction presents as pain with loss of velocity and control. Some injuries may present acutely while throwing, but many patients, when questioned, report a preceding period of either pain or loss of velocity and control.
Authors have documented a significant rise in elbow injuries in young athletes, especially pitchers.6 Extended seasons, higher pitch counts, year-round pitching, pitching while fatigued, and pitching for multiple teams are risk factors for elbow injuries.7 Pitchers in the southern United States are more likely to undergo UCL reconstruction than those from the northern states.8 Pitchers who also play catcher are at a higher risk due to more total throws than those who pitch and play other positions or pitch only. Throwers with higher velocity are more likely to pitch in showcases, pitch for multiple teams, and pitch with pain and fatigue, and these are all risk factors.6 Also, in one study of youth baseball injuries, individuals in the injured group were found to be taller and heavier than those in the uninjured group.6 Pitch counts, rest from pitching during the off-season, adequate rest, and ensuring pain-free pitching can lessen the risk of injury.6 As expected with the rise in throwing injuries, the rise in medial elbow procedures has risen.9
While throwing, stress across the medial elbow has been measured to be nearly 300 N. A maximum varus force during pitching was measured to be 64 N-m at 95° ± 14°.10 Morrey and An4 determined that the UCL generated 54% of the varus force at 90° of flexion. During active pitching, this value is likely reduced due to simultaneous muscle contraction, but if one assumes the UCL bears 54% of the maximal load, the UCL must be able to withstand 34 N-m. The UCL can withstand a maximum valgus torque between 22.7 and 34 N-m11-13; therefore, during pitching, the UCL is at or above its failure load. After thousands of cycles over many years, one can imagine how the UCL might be injured.
Multiple techniques have been proposed in the surgical treatment of UCL injuries. Jobe14 pioneered UCL reconstruction in 1974 in Tommy John, a Major League Baseball pitcher. John returned to pitch successfully, and both the UCL and the reconstruction are commonly called by his name. Jobe14 reported his technique in 1986, and it has remained, with a few modifications, the primary method for reconstruction of the UCL (Figure 1).
Evaluation
A standard evaluation with physical examination and imaging is completed in all throwers with elbow pain. In our prior study,16 we found that 100% of patients experienced pain during athletic activity and that 96% of throwers complained of pain during late cocking and acceleration phases of the throwing motion. Nearly half reported an acute onset of pain, while 53% were unable to identify a single inciting event. Seventy-five percent of the acute injuries were during competition. Delayed diagnosis was very common, with an average time to diagnosis after onset of symptoms of 6.4 months. Neurologic symptoms were seen in 23% of athletes, most of which were ulnar nerve paresthesias during throwing.16
Physical examination includes inspection for swelling, hand intrinsic atrophy, neurovascular examination, range of motion, shoulder examination, and elbow stress examination. Range of motion at presentation averaged 5° to 135° with 85° of supination and pronation.16 All patients need neurologic evaluation for ulnar nerve dysfunction. Tinel test of the cubital tunnel was positive in 21%.16 Significant ulnar nerve dysfunction, including hand weakness, is much less common but must be well examined and documented. The shoulder must also be evaluated for loss of rotation, which can lead to increased stress on the elbow. An evaluation of mechanics may point out flaws in technique, which may be contributing to elbow stress. The UCL stress examination includes static stress at 30° of flexion, the milking test at 90°, and the moving valgus stress test. The presence of pain directly over the UCL or laxity compared to the uninvolved side is suggestive of UCL injury.
Radiographic evaluation is completed in all patients with concern for UCL injury. Standard x-rays of the elbow, including anteroposterior, medial, and lateral obliques, axial olecranon, and lateral views, are obtained to evaluate bony abnormalities. Fifty-seven percent of our series showed some abnormality, most commonly olecranon osteophyte formation or ectopic calcification within the UCL substance. Stress radiography rarely changed the treatment course and is somewhat difficult to interpret because of the reports documenting normal increased medial elbow opening in the dominant arm of throwing athletes.21 Magnetic resonance imaging (MRI) is obtained very commonly in this patient population, and intra-articular contrast is crucial. Partial, undersurface tears are common, and a contrasted study better demonstrates undersurface tears or avulsions. The T-sign as described by Timmerman and colleagues22 using computed tomography (CT) arthrography shows partial undersurface detachment, which can be difficult to see without intra-articular contrast.22 This finding is very well visualized on MRI arthrogram as well (Figure 3).
Nonoperative Management
Nonoperative treatment is recommended for 3 months prior to performing reconstruction. Patients are given complete rest from throwing, but rehabilitation is initiated immediately. Rehabilitation exercises and nonsteroidal anti-inflammatory medications are prescribed, and activities that place valgus stress across the elbow are avoided. After resolution of symptoms, an interval throwing program is initiated, and the athlete is gradually returned to sport. Unfortunately, due to season-specific schedules and time-sensitive demands in high-level throwers, operative treatment is often chosen without an extended period of conservative treatment.
Platelet-rich plasma (PRP) therapy has recently been shown to improve healing rates and promote healing in partial UCL tears,23 and as orthobiologics are advanced, they will likely play a larger role in the treatment of UCL injuries.
Surgical Technique
At our institution, UCL reconstruction is performed with the modified Jobe technique as described by Azar and colleagues.17 Arthroscopy prior to reconstruction was routinely performed at our institution until we recognized that arthroscopy rarely changed the preoperative plan.16 Currently, the presence of anterior pathology such as loose bodies or osteochondral defect is our only indication for arthroscopy before reconstruction.
Ipsilateral palmaris autograft is our current graft of choice. This must be examined preoperatively because 16% of patients have unilateral absence and 9% have bilateral absence.24 In revision cases or in patients with insufficient or absent palmaris, contralateral palmaris followed by contralateral gracilis tendon is used. The contralateral gracilis is chosen because of ease of setup and position of the surgeon during the harvest. Gracilis tendon is also used in cases with bony involvement of the ligament based on the results from Dugas and colleagues.25 Toe extensors, plantaris, and patellar tendon grafts have also been used. One recent study showed that neither graft choice nor diameter affected resistance to valgus stress, and that all reconstruction types restored strength at 60° to 120° of flexion.26
Ulnar nerve transposition is performed in all cases regardless of the presence of preoperative nerve symptoms. A complete decompression is completed proximally to the Arcade of Struthers and distally to the deep portion of the flexor carpi ulnaris. A single fascial sling of medial intermuscular septum originating from the epicondylar attachment is used to stabilize the nerve without compression. At wound closure, the deep fascia on the posterior skin flap is also sewn into the cubital tunnel to prevent the nerve from subluxating back into the groove. A single suture is placed distally closing the muscle fascia to prevent propagation of the fascial incision, which can lead to herniation. Transposition is necessary because of the ulnar nerve exposure required in the modified Jobe technique to allow elevation of the deep flexor muscle mass for ligament exposure.
The reconstruction is completed as described by Jobe14 but with a few modifications as described by Azar and colleagues17 and slight adaptations implemented since that time. The flexor-pronator mass is retracted laterally instead of detachment or splitting as described by Thompson and colleagues.27 A subcutaneous rather than a submuscular ulnar nerve transposition is used.
The patient is positioned supine using an arm board. If gracilis tendon is chosen, the contralateral leg is prepped and draped simultaneously. A tourniquet is inflated after exsanguination. A medial approach is performed, and the medial antebrachial nerve is located and protected. The ulnar nerve is then located in the cubital tunnel and mobilized. The neurolysis extends to the deep portion of the flexor carpi ulnaris distally and proximally to the Arcade of Struthers, and the nerve is retracted with a vessel loop. The flexor muscle mass is not elevated from the medial epicondyle; rather, it is retracted anteriorly by small Hohmann retractors. The dissection is carried down to the UCL and found at its attachments to the medial epicondyle and sublime tubercle. If no tear is seen on the superficial surface of the ligament, a longitudinal incision is made through the ligament. Undersurface tears, partial tears, and avulsions can then be identified (Figure 4).
The autologous graft of choice is then harvested. Our technique for palmaris harvest is performed with three 1-cm transverse incisions. The palmaris is palpated and marked with the first incision made near the distal wrist crease, and the second incision is made 3 to 4 cm proximal to the first. The tendon is found in both distal incisions and cut distally with the wrist flexed to maximize tendon length. The tendon is then pulled through the second incision and tensioned to identify the most proximal location the tendon can be palpated. A third incision is made directly over this point and carried down to cut the tendon. This usually provides a graft length of 15 to 20 cm; 13 cm is the minimum graft length to ensure good graft fixation. Muscle is removed from the tendon and each end is secured with a No. 1 nonabsorbable suture in a locking fashion.
If posterior osteophytes are present, they are removed through a posterior, vertical arthrotomy. Over-resection of the olecranon must be avoided, as this can further destabilize the elbow and place increased stress on the reconstruction. Posterior loose bodies can also be removed through this arthrotomy. The arthrotomy is then closed with absorbable suture.
Tunnel placement is critical to success. A 3.2-mm drill bit is used with palmaris grafts and a 4-mm drill bit is used with gracilis grafts. Two convergent tunnels are drilled in the medial epicondyle in a Y fashion and 2 convergent tunnels are drilled at the sublime tubercle in a U or V fashion. After drilling the first tunnel on each side, a hemostat is placed in the tunnel as an aiming point to ensure a complete tunnel is made. The junction is smoothed with a curette, leaving a 5-mm bone bridge between the articular surface and the tunnels. A bent Hewson suture passer is used to pass one end of the graft through the ulna. The 2 limbs of the tendon graft are then passed through the humeral tunnels, creating a figure-of-eight. A varus stress is applied with the elbow at roughly 30° and the 2 limbs are tied together with a No. 1 nonabsorbable suture. If enough graft remains, one or both limbs are passed back through the tunnels and secured again with No. 1 nonabsorbable suture. The 2 limbs are then tied side-to-side, incorporating the native ligament to further secure and tighten the reconstruction.
The ulnar nerve is then secured using a strip of medial intermuscular septum left intact to its insertion at the medial epicondyle. This is attached to the flexor-pronator muscle fascia with a 3-0 nonabsorbable suture. Enough length should be harvested from the septum to ensure there is no compression on the nerve. The deep posterior fascial tissue is then sewn to the periosteum of the medial epicondyle to further prevent subluxation of the nerve back into the groove. The skin is then closed in layered fashion over a superficial drain. The patient is placed in a well-padded posterior splint for 1 week, then the rehabilitation protocol is initiated as discussed below.
Postoperative Rehabilitation
A standardized postoperative 4-phase rehabilitation program for ulnar collateral reconstruction is followed as described by Wilk and colleagues.28-30 The first phase begins immediately after surgery and continues for 4 weeks. During surgery, the patient’s elbow is placed in a compression dressing with a posterior splint to immobilize the elbow in 90° of flexion with wrist motion for 1 week to allow initial healing. Full range of motion of the elbow joint is restored by the end of the fifth to sixth week after surgery.
During phase II (weeks 4-10), a progressive isotonic strengthening program is initiated. Exercises are focused on scapular, rotator cuff, deltoid, and arm musculature. Shoulder range of motion and stretching exercises are performed during this phase and the Thrower’s Ten exercise program is initiated. Any adaptations or strength deficits are addressed during this phase.
During the advanced strengthening phase (phase III), from weeks 10 to 16, a sport-specific exercise/rehabilitation program is initiated. During this phase, stretching and flexibility exercises are performed to enhance strength, power, and endurance. During this phase the patient is placed on the advanced Thrower’s Ten program. Isotonic strengthening exercises are progressed, and at week 12, the athlete is allowed to begin an isotonic lifting program, including bench press, seated rowing, latissimus dorsi pull downs, triceps push downs, and biceps curls. In addition, the athlete performs specific exercises to emphasize sport-specific movements. At week 12, overhead athletes begin a 2-hand plyometric throwing program, and at 14 weeks, a 1
Discussion
Results after ulnar collateral reconstruction have been good. In our series of 743 patients, 83% returned to the same or higher level at an average of 11.6 months.16 There was a 4% major complication rate and 16% minor complication rate. Major complications included medial epicondyle fracture (0.5%), significant ulnar nerve dysfunction (1 patient), rupture of graft (1%), and graft site infection. Sixteen percent of patients had ulnar nerve dysfunction, and 82% of these resolved within 6 weeks. All but 1 patient’s paresthesias resolved within 1 year.16 The 10-year follow-up of this group of patients included 256 patients and was reported by Osbahr and colleagues31 in 2014. Retirement from baseball was due to reasons other than the elbow in 86%, and 98% were still able to throw on at least a recreational level. The overall longevity was 3.6 years, with 2.9 years at pre-injury level or higher. Statistically, pitchers performed at a higher level after reconstruction.31
A recent review by Erickson and colleagues9 showed an overall 82% excellent and 8% good result when evaluating different techniques, including the American Sports Medicine Institute (ASMI) modification of Jobe’s technique, docking technique, and Jobe’s technique. With an overall complication rate of 10% (75% of which was transient ulnar neuritis), the procedure was deemed overall a safe surgical option. Collegiate athletes had the highest return to sport (95%) compared with high school athletes (89%) and professional athletes (86%). The docking technique had the highest rate of return to play (97%) compared with ASMI technique (93%) and Jobe technique (66%).9 Results after repair have not been as good as reconstruction, as reported in 2 studies.16,32 Savoie and colleagues,15 however, reported 93% good/excellent results after primary UCL repair alone.
Another recent review of outcomes showed an overall return to same or higher level was best with docking or modified docking techniques (90.4% and 91.3%, respectively).19 Overall return with modified Jobe technique was 77%.19 O’Brien and colleagues20 performed a review of 33 patients with either modified Jobe or docking technique that showed 81% return to same or higher level with modified Jobe vs 92% with docking technique. The Kerlan-Jobe Orthopaedic Clinic scores were higher in the modified Jobe group (79 vs 74) and the docking technique group returned to play nearly 1 month sooner (12.4 months vs 11.8 months).20 However, comparing different techniques in a heterogenous patient population over 40 years is difficult. Many of the modified Jobe technique cases were performed in the early evolution of the rehabilitation and return-to-play programs. We believe that the current modified Jobe technique has results equal to any other variation.
Despite good results with reconstructions, the recovery is lengthy and most pitchers cannot fully return to competition level for 12 to 18 months. Extensive research has been performed in exploring alternatives to the traditional reconstruction. Advancements in orthobiologics and development of new surgical options seem to provide an alternative to reconstruction, and may allow faster return to competition with less morbidity.
PRP has been at the forefront of orthopedic research for the last 2 decades, mostly focused in tendon and bone healing. Due to the release of many inflammatory mediators, PRP is theorized to initiate a healing response with growth factors that can direct healing towards normal tissue.33 Two main types of PRP are reported based on the presence or absence of leukocytes. PRP has been studied in many applications, but only one clinical study on the UCL has been published to date. Podesta and colleagues23 injected PRP into the elbow of 34 baseball players with MRI-confirmed partial UCL tear. The athletes then underwent a rehabilitation program, which limited stress across the UCL. Type 1A PRP was used (leukocyte-rich, unactivated, 5x or greater platelet concentration33). Athletes were allowed to return to sport based on symptoms and examination findings. Eighty-eight percent returned to same level of play without complaints at average 70 week follow-up, and average return to play ranged from 10 to 15 weeks.23 No specific data were given on the 16 pitchers in the group, but with such a high rate of return, PRP needs to be further evaluated in the treatment of UCL injuries.
Another recent study from Dugas and colleagues18 presented primary UCL repair using a tape augment (InternalBrace, Arthrex). Nine matched cadaver elbows underwent UCL sectioning and then either modified Jobe reconstruction or primary repair of the UCL with placement of the InternalBrace. The biomechanical data showed the repair with internal brace to have slightly less gap, more stiffness, and higher failure strength, although these findings were not statistically significant.18 This bone-preserving technique with less exposure and healing of the native ligament may be another step towards good results with a quicker return to throwing.
Conclusion
UCL injuries can be disabling in throwers. Reconstruction has afforded throwers a high rate of return to preinjury function or better, and several techniques have been presented that produce acceptable results. Overall complication rates range from 10% to 15%, and the majority of complications are transient ulnar neuropraxias. Orthobiologics and repair with augmentation have more recently offered additional options that may improve success of nonoperative treatment or allow less-invasive surgical treatment. Increased involvement in youth sports and early specialization is driving injury rates in young athletes. The orthopedic community must continue to look for better ways to prevent these injuries and investigate better methods to return athletes to high-level competition.
Am J Orthop. 2016;45(7):E534-E540. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
The ulnar collateral ligament (UCL) is the primary restraint to valgus stress between 20° and 125° of motion.1-5 Overhead athletes, most commonly baseball pitchers, are at risk of developing UCL insufficiency, and dysfunction presents as pain with loss of velocity and control. Some injuries may present acutely while throwing, but many patients, when questioned, report a preceding period of either pain or loss of velocity and control.
Authors have documented a significant rise in elbow injuries in young athletes, especially pitchers.6 Extended seasons, higher pitch counts, year-round pitching, pitching while fatigued, and pitching for multiple teams are risk factors for elbow injuries.7 Pitchers in the southern United States are more likely to undergo UCL reconstruction than those from the northern states.8 Pitchers who also play catcher are at a higher risk due to more total throws than those who pitch and play other positions or pitch only. Throwers with higher velocity are more likely to pitch in showcases, pitch for multiple teams, and pitch with pain and fatigue, and these are all risk factors.6 Also, in one study of youth baseball injuries, individuals in the injured group were found to be taller and heavier than those in the uninjured group.6 Pitch counts, rest from pitching during the off-season, adequate rest, and ensuring pain-free pitching can lessen the risk of injury.6 As expected with the rise in throwing injuries, the rise in medial elbow procedures has risen.9
While throwing, stress across the medial elbow has been measured to be nearly 300 N. A maximum varus force during pitching was measured to be 64 N-m at 95° ± 14°.10 Morrey and An4 determined that the UCL generated 54% of the varus force at 90° of flexion. During active pitching, this value is likely reduced due to simultaneous muscle contraction, but if one assumes the UCL bears 54% of the maximal load, the UCL must be able to withstand 34 N-m. The UCL can withstand a maximum valgus torque between 22.7 and 34 N-m11-13; therefore, during pitching, the UCL is at or above its failure load. After thousands of cycles over many years, one can imagine how the UCL might be injured.
Multiple techniques have been proposed in the surgical treatment of UCL injuries. Jobe14 pioneered UCL reconstruction in 1974 in Tommy John, a Major League Baseball pitcher. John returned to pitch successfully, and both the UCL and the reconstruction are commonly called by his name. Jobe14 reported his technique in 1986, and it has remained, with a few modifications, the primary method for reconstruction of the UCL (Figure 1).
Evaluation
A standard evaluation with physical examination and imaging is completed in all throwers with elbow pain. In our prior study,16 we found that 100% of patients experienced pain during athletic activity and that 96% of throwers complained of pain during late cocking and acceleration phases of the throwing motion. Nearly half reported an acute onset of pain, while 53% were unable to identify a single inciting event. Seventy-five percent of the acute injuries were during competition. Delayed diagnosis was very common, with an average time to diagnosis after onset of symptoms of 6.4 months. Neurologic symptoms were seen in 23% of athletes, most of which were ulnar nerve paresthesias during throwing.16
Physical examination includes inspection for swelling, hand intrinsic atrophy, neurovascular examination, range of motion, shoulder examination, and elbow stress examination. Range of motion at presentation averaged 5° to 135° with 85° of supination and pronation.16 All patients need neurologic evaluation for ulnar nerve dysfunction. Tinel test of the cubital tunnel was positive in 21%.16 Significant ulnar nerve dysfunction, including hand weakness, is much less common but must be well examined and documented. The shoulder must also be evaluated for loss of rotation, which can lead to increased stress on the elbow. An evaluation of mechanics may point out flaws in technique, which may be contributing to elbow stress. The UCL stress examination includes static stress at 30° of flexion, the milking test at 90°, and the moving valgus stress test. The presence of pain directly over the UCL or laxity compared to the uninvolved side is suggestive of UCL injury.
Radiographic evaluation is completed in all patients with concern for UCL injury. Standard x-rays of the elbow, including anteroposterior, medial, and lateral obliques, axial olecranon, and lateral views, are obtained to evaluate bony abnormalities. Fifty-seven percent of our series showed some abnormality, most commonly olecranon osteophyte formation or ectopic calcification within the UCL substance. Stress radiography rarely changed the treatment course and is somewhat difficult to interpret because of the reports documenting normal increased medial elbow opening in the dominant arm of throwing athletes.21 Magnetic resonance imaging (MRI) is obtained very commonly in this patient population, and intra-articular contrast is crucial. Partial, undersurface tears are common, and a contrasted study better demonstrates undersurface tears or avulsions. The T-sign as described by Timmerman and colleagues22 using computed tomography (CT) arthrography shows partial undersurface detachment, which can be difficult to see without intra-articular contrast.22 This finding is very well visualized on MRI arthrogram as well (Figure 3).
Nonoperative Management
Nonoperative treatment is recommended for 3 months prior to performing reconstruction. Patients are given complete rest from throwing, but rehabilitation is initiated immediately. Rehabilitation exercises and nonsteroidal anti-inflammatory medications are prescribed, and activities that place valgus stress across the elbow are avoided. After resolution of symptoms, an interval throwing program is initiated, and the athlete is gradually returned to sport. Unfortunately, due to season-specific schedules and time-sensitive demands in high-level throwers, operative treatment is often chosen without an extended period of conservative treatment.
Platelet-rich plasma (PRP) therapy has recently been shown to improve healing rates and promote healing in partial UCL tears,23 and as orthobiologics are advanced, they will likely play a larger role in the treatment of UCL injuries.
Surgical Technique
At our institution, UCL reconstruction is performed with the modified Jobe technique as described by Azar and colleagues.17 Arthroscopy prior to reconstruction was routinely performed at our institution until we recognized that arthroscopy rarely changed the preoperative plan.16 Currently, the presence of anterior pathology such as loose bodies or osteochondral defect is our only indication for arthroscopy before reconstruction.
Ipsilateral palmaris autograft is our current graft of choice. This must be examined preoperatively because 16% of patients have unilateral absence and 9% have bilateral absence.24 In revision cases or in patients with insufficient or absent palmaris, contralateral palmaris followed by contralateral gracilis tendon is used. The contralateral gracilis is chosen because of ease of setup and position of the surgeon during the harvest. Gracilis tendon is also used in cases with bony involvement of the ligament based on the results from Dugas and colleagues.25 Toe extensors, plantaris, and patellar tendon grafts have also been used. One recent study showed that neither graft choice nor diameter affected resistance to valgus stress, and that all reconstruction types restored strength at 60° to 120° of flexion.26
Ulnar nerve transposition is performed in all cases regardless of the presence of preoperative nerve symptoms. A complete decompression is completed proximally to the Arcade of Struthers and distally to the deep portion of the flexor carpi ulnaris. A single fascial sling of medial intermuscular septum originating from the epicondylar attachment is used to stabilize the nerve without compression. At wound closure, the deep fascia on the posterior skin flap is also sewn into the cubital tunnel to prevent the nerve from subluxating back into the groove. A single suture is placed distally closing the muscle fascia to prevent propagation of the fascial incision, which can lead to herniation. Transposition is necessary because of the ulnar nerve exposure required in the modified Jobe technique to allow elevation of the deep flexor muscle mass for ligament exposure.
The reconstruction is completed as described by Jobe14 but with a few modifications as described by Azar and colleagues17 and slight adaptations implemented since that time. The flexor-pronator mass is retracted laterally instead of detachment or splitting as described by Thompson and colleagues.27 A subcutaneous rather than a submuscular ulnar nerve transposition is used.
The patient is positioned supine using an arm board. If gracilis tendon is chosen, the contralateral leg is prepped and draped simultaneously. A tourniquet is inflated after exsanguination. A medial approach is performed, and the medial antebrachial nerve is located and protected. The ulnar nerve is then located in the cubital tunnel and mobilized. The neurolysis extends to the deep portion of the flexor carpi ulnaris distally and proximally to the Arcade of Struthers, and the nerve is retracted with a vessel loop. The flexor muscle mass is not elevated from the medial epicondyle; rather, it is retracted anteriorly by small Hohmann retractors. The dissection is carried down to the UCL and found at its attachments to the medial epicondyle and sublime tubercle. If no tear is seen on the superficial surface of the ligament, a longitudinal incision is made through the ligament. Undersurface tears, partial tears, and avulsions can then be identified (Figure 4).
The autologous graft of choice is then harvested. Our technique for palmaris harvest is performed with three 1-cm transverse incisions. The palmaris is palpated and marked with the first incision made near the distal wrist crease, and the second incision is made 3 to 4 cm proximal to the first. The tendon is found in both distal incisions and cut distally with the wrist flexed to maximize tendon length. The tendon is then pulled through the second incision and tensioned to identify the most proximal location the tendon can be palpated. A third incision is made directly over this point and carried down to cut the tendon. This usually provides a graft length of 15 to 20 cm; 13 cm is the minimum graft length to ensure good graft fixation. Muscle is removed from the tendon and each end is secured with a No. 1 nonabsorbable suture in a locking fashion.
If posterior osteophytes are present, they are removed through a posterior, vertical arthrotomy. Over-resection of the olecranon must be avoided, as this can further destabilize the elbow and place increased stress on the reconstruction. Posterior loose bodies can also be removed through this arthrotomy. The arthrotomy is then closed with absorbable suture.
Tunnel placement is critical to success. A 3.2-mm drill bit is used with palmaris grafts and a 4-mm drill bit is used with gracilis grafts. Two convergent tunnels are drilled in the medial epicondyle in a Y fashion and 2 convergent tunnels are drilled at the sublime tubercle in a U or V fashion. After drilling the first tunnel on each side, a hemostat is placed in the tunnel as an aiming point to ensure a complete tunnel is made. The junction is smoothed with a curette, leaving a 5-mm bone bridge between the articular surface and the tunnels. A bent Hewson suture passer is used to pass one end of the graft through the ulna. The 2 limbs of the tendon graft are then passed through the humeral tunnels, creating a figure-of-eight. A varus stress is applied with the elbow at roughly 30° and the 2 limbs are tied together with a No. 1 nonabsorbable suture. If enough graft remains, one or both limbs are passed back through the tunnels and secured again with No. 1 nonabsorbable suture. The 2 limbs are then tied side-to-side, incorporating the native ligament to further secure and tighten the reconstruction.
The ulnar nerve is then secured using a strip of medial intermuscular septum left intact to its insertion at the medial epicondyle. This is attached to the flexor-pronator muscle fascia with a 3-0 nonabsorbable suture. Enough length should be harvested from the septum to ensure there is no compression on the nerve. The deep posterior fascial tissue is then sewn to the periosteum of the medial epicondyle to further prevent subluxation of the nerve back into the groove. The skin is then closed in layered fashion over a superficial drain. The patient is placed in a well-padded posterior splint for 1 week, then the rehabilitation protocol is initiated as discussed below.
Postoperative Rehabilitation
A standardized postoperative 4-phase rehabilitation program for ulnar collateral reconstruction is followed as described by Wilk and colleagues.28-30 The first phase begins immediately after surgery and continues for 4 weeks. During surgery, the patient’s elbow is placed in a compression dressing with a posterior splint to immobilize the elbow in 90° of flexion with wrist motion for 1 week to allow initial healing. Full range of motion of the elbow joint is restored by the end of the fifth to sixth week after surgery.
During phase II (weeks 4-10), a progressive isotonic strengthening program is initiated. Exercises are focused on scapular, rotator cuff, deltoid, and arm musculature. Shoulder range of motion and stretching exercises are performed during this phase and the Thrower’s Ten exercise program is initiated. Any adaptations or strength deficits are addressed during this phase.
During the advanced strengthening phase (phase III), from weeks 10 to 16, a sport-specific exercise/rehabilitation program is initiated. During this phase, stretching and flexibility exercises are performed to enhance strength, power, and endurance. During this phase the patient is placed on the advanced Thrower’s Ten program. Isotonic strengthening exercises are progressed, and at week 12, the athlete is allowed to begin an isotonic lifting program, including bench press, seated rowing, latissimus dorsi pull downs, triceps push downs, and biceps curls. In addition, the athlete performs specific exercises to emphasize sport-specific movements. At week 12, overhead athletes begin a 2-hand plyometric throwing program, and at 14 weeks, a 1
Discussion
Results after ulnar collateral reconstruction have been good. In our series of 743 patients, 83% returned to the same or higher level at an average of 11.6 months.16 There was a 4% major complication rate and 16% minor complication rate. Major complications included medial epicondyle fracture (0.5%), significant ulnar nerve dysfunction (1 patient), rupture of graft (1%), and graft site infection. Sixteen percent of patients had ulnar nerve dysfunction, and 82% of these resolved within 6 weeks. All but 1 patient’s paresthesias resolved within 1 year.16 The 10-year follow-up of this group of patients included 256 patients and was reported by Osbahr and colleagues31 in 2014. Retirement from baseball was due to reasons other than the elbow in 86%, and 98% were still able to throw on at least a recreational level. The overall longevity was 3.6 years, with 2.9 years at pre-injury level or higher. Statistically, pitchers performed at a higher level after reconstruction.31
A recent review by Erickson and colleagues9 showed an overall 82% excellent and 8% good result when evaluating different techniques, including the American Sports Medicine Institute (ASMI) modification of Jobe’s technique, docking technique, and Jobe’s technique. With an overall complication rate of 10% (75% of which was transient ulnar neuritis), the procedure was deemed overall a safe surgical option. Collegiate athletes had the highest return to sport (95%) compared with high school athletes (89%) and professional athletes (86%). The docking technique had the highest rate of return to play (97%) compared with ASMI technique (93%) and Jobe technique (66%).9 Results after repair have not been as good as reconstruction, as reported in 2 studies.16,32 Savoie and colleagues,15 however, reported 93% good/excellent results after primary UCL repair alone.
Another recent review of outcomes showed an overall return to same or higher level was best with docking or modified docking techniques (90.4% and 91.3%, respectively).19 Overall return with modified Jobe technique was 77%.19 O’Brien and colleagues20 performed a review of 33 patients with either modified Jobe or docking technique that showed 81% return to same or higher level with modified Jobe vs 92% with docking technique. The Kerlan-Jobe Orthopaedic Clinic scores were higher in the modified Jobe group (79 vs 74) and the docking technique group returned to play nearly 1 month sooner (12.4 months vs 11.8 months).20 However, comparing different techniques in a heterogenous patient population over 40 years is difficult. Many of the modified Jobe technique cases were performed in the early evolution of the rehabilitation and return-to-play programs. We believe that the current modified Jobe technique has results equal to any other variation.
Despite good results with reconstructions, the recovery is lengthy and most pitchers cannot fully return to competition level for 12 to 18 months. Extensive research has been performed in exploring alternatives to the traditional reconstruction. Advancements in orthobiologics and development of new surgical options seem to provide an alternative to reconstruction, and may allow faster return to competition with less morbidity.
PRP has been at the forefront of orthopedic research for the last 2 decades, mostly focused in tendon and bone healing. Due to the release of many inflammatory mediators, PRP is theorized to initiate a healing response with growth factors that can direct healing towards normal tissue.33 Two main types of PRP are reported based on the presence or absence of leukocytes. PRP has been studied in many applications, but only one clinical study on the UCL has been published to date. Podesta and colleagues23 injected PRP into the elbow of 34 baseball players with MRI-confirmed partial UCL tear. The athletes then underwent a rehabilitation program, which limited stress across the UCL. Type 1A PRP was used (leukocyte-rich, unactivated, 5x or greater platelet concentration33). Athletes were allowed to return to sport based on symptoms and examination findings. Eighty-eight percent returned to same level of play without complaints at average 70 week follow-up, and average return to play ranged from 10 to 15 weeks.23 No specific data were given on the 16 pitchers in the group, but with such a high rate of return, PRP needs to be further evaluated in the treatment of UCL injuries.
Another recent study from Dugas and colleagues18 presented primary UCL repair using a tape augment (InternalBrace, Arthrex). Nine matched cadaver elbows underwent UCL sectioning and then either modified Jobe reconstruction or primary repair of the UCL with placement of the InternalBrace. The biomechanical data showed the repair with internal brace to have slightly less gap, more stiffness, and higher failure strength, although these findings were not statistically significant.18 This bone-preserving technique with less exposure and healing of the native ligament may be another step towards good results with a quicker return to throwing.
Conclusion
UCL injuries can be disabling in throwers. Reconstruction has afforded throwers a high rate of return to preinjury function or better, and several techniques have been presented that produce acceptable results. Overall complication rates range from 10% to 15%, and the majority of complications are transient ulnar neuropraxias. Orthobiologics and repair with augmentation have more recently offered additional options that may improve success of nonoperative treatment or allow less-invasive surgical treatment. Increased involvement in youth sports and early specialization is driving injury rates in young athletes. The orthopedic community must continue to look for better ways to prevent these injuries and investigate better methods to return athletes to high-level competition.
Am J Orthop. 2016;45(7):E534-E540. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Fuss FK. The ulnar collateral ligament of the human elbow joint. Anatomy, function and biomechanics. J Anat. 1991;175:203-212.
2. Hotchkiss RN, Weiland AJ. Valgus stability of the elbow. J Orthop Res. 1987;5(3):372-377.
3. Morrey BF. Applied anatomy and biomechanics of the elbow joint. Instr Course Lect. 1986;35:59-68.
4. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med. 1983;11(5):315-319.
5. Morrey BF, An KN. Functional anatomy of the ligaments of the elbow. Clin Orthop. 1985;(201):84-90.
6. Olsen SJ 2nd, Fleisig GS, Dun S, Loftice J, Andrews JR. Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med. 2006;34(6):905-912.
7. Fleisig GS, Andrews JR. Prevention of elbow injuries in youth baseball pitchers. Sports Health. 2012;4(5):419-424.
8. Zaremski JL, Horodyski M, Donlan RM, Brisbane ST, Farmer KW. Does geographic location matter on the prevalence of ulnar collateral ligament reconstruction in collegiate baseball pitchers? Orthop J Sports Med. 2015;3(11):2325967115616582.
9. Erickson BJ, Nwachukwu BU, Rosas S, et al. Trends in medial ulnar collateral ligament reconstruction in the United States: A retrospective review of a large private-payer database from 2007 to 2011. Am J Sports Med. 2015;43(7):1770-1774.
10. Fleisig GS, Andrews JR, Dillman CJ. Kinetics of baseball pitching with implications about injury mechanism. Am J Sports Med. 1995;23(2):233-239.
11. Dillman CJ, Smutz P, Werner S. Valgus extension overload in baseball pitching. Med Sci Sports Exerc. 1991;23(suppl 4):S135.
12. Hechtman KS, Tjin-A-Tsoi EW, Zvijac JE, Uribe JW, Latta LL. Biomechanics of a less invasive procedure for reconstruction of the ulnar collateral ligament of the elbow. Am J Sports Med. 1998;26(5):620-624.
13. Ahmad CS, Lee TQ, ElAttrache NS. Biomechanical evaluation of a new ulnar collateral ligament reconstruction technique with interference screw fixation. Am J Sports Med. 2003;31(3):332-337.
14. Jobe FW, Stark HE, Lombardo SJ. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am. 1986;68(8):1158-1163.
15. Savoie FH 3rd, Trenhaile SW, Roberts J, Field LD, Ramsey JR. Primary repair of ulnar collateral ligament injuries of the elbow in young athletes: a case series of injuries to the proximal and distal ends of the ligament. Am J Sports Med. 2008;36(6):1066-1072.
16. Cain EL, Andrews JR, Dugas JR, et al. Outcome of ulnar collateral ligament reconstruction of the elbow in 1281 athletes results in 743 athletes with minimum 2-year follow-up. Am J Sports Med. 2010;38(12):2426-2434.
17. Azar FM, Andrews JR, Wilk KE, Groh D. Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am J Sports Med. 2000;28(1):16-23.
18. Dugas JR, Walters BL, Beason DP, Fleisig GS, Chronister JE. Biomechanical comparison of ulnar collateral ligament repair with internal bracing versus modified Jobe reconstruction. Am J Sports Med. 2016;44(3):735-741.
19. Watson JN, McQueen P, Hutchinson MR. A systematic review of ulnar collateral ligament reconstruction techniques. Am J Sports Med. 2014;42(10):2510-2516.
20. O’Brien DF, O’Hagan T, Stewart R, et al. Outcomes for ulnar collateral ligament reconstruction: A retrospective review using the KJOC assessment score with two-year follow-up in an overhead throwing population. J Shoulder Elbow Surg. 2015;24(6):934-940.
21. Ellenbecker TS, Mattalino AJ, Elam EA, Caplinger RA. Medial elbow joint laxity in professional baseball pitchers a bilateral comparison using stress radiography. Am J Sports Med. 1998;26(3):420-424.
22. Timmerman LA, Schwartz ML, Andrews JR. Preoperative evaluation of the ulnar collateral ligament by magnetic resonance imaging and computed tomography arthrography evaluation in 25 baseball players with surgical confirmation. Am J Sports Med. 1994;22(1):26-32.
23. Podesta L, Crow SA, Volkmer D, Bert T, Yocum LA. Treatment of partial ulnar collateral ligament tears in the elbow with platelet-rich plasma. Am J Sports Med. 2013;41(7):1689-1694.
24. Thompson NW, Mockford BJ, Cran GW. Absence of the palmaris longus muscle: a population study. Ulster Med J. 2001;70(1):22-24.
25. Dugas JR, Bilotta J, Watts CD, et al. Ulnar collateral ligament reconstruction with gracilis tendon in athletes with intraligamentous bony excision technique and results. Am J Sports Med. 2012;40(7):1578-1582.
26. Dargel J, Küpper F, Wegmann K, Oppermann J, Eysel P, Müller LP. Graft diameter does not influence primary stability of ulnar collateral ligament reconstruction of the elbow. J Orthop Sci. 2015;20(2):307-313.
27. Thompson WH, Jobe FW, Yocum LA, Pink MM. Ulnar collateral ligament reconstruction in athletes: muscle-splitting approach without transposition of the ulnar nerve. J Shoulder Elbow Surg. 2001;10(2):152-157.
28. Wilk KE, Arrigo CA, Andrews JR. Rehabilitation of the elbow in the throwing athlete. J Orthop Sports Phys Ther. 1993;17(6):305-317.
29. Wilk KE, Arrigo CA, Andrews JR, et al. Rehabilitation following elbow surgery in the throwing athlete. Oper Tech Sports Med. 1996;4:114-132.
30. Wilk KE, Arrigo CA, Andrews JR, et al. Preventative and Rehabilitation Exercises for the Shoulder and Elbow. 4th ed. Birmingham, AL: American Sports Medicine Institute; 1996.
31. Osbahr DC, Cain EL, Raines BT, Fortenbaugh D, Dugas JR, Andrews JR. Long-term outcomes after ulnar collateral ligament reconstruction in competitive baseball players minimum 10-year follow-up. Am J Sports Med. 2014;42(6):1333-1342.
32. 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.
33. Mishra A, Harmon K, Woodall J, Vieira A. Sports medicine applications of platelet rich plasma. Curr Pharm Biotechnol. 2012;13(7):1185-1195.
1. Fuss FK. The ulnar collateral ligament of the human elbow joint. Anatomy, function and biomechanics. J Anat. 1991;175:203-212.
2. Hotchkiss RN, Weiland AJ. Valgus stability of the elbow. J Orthop Res. 1987;5(3):372-377.
3. Morrey BF. Applied anatomy and biomechanics of the elbow joint. Instr Course Lect. 1986;35:59-68.
4. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med. 1983;11(5):315-319.
5. Morrey BF, An KN. Functional anatomy of the ligaments of the elbow. Clin Orthop. 1985;(201):84-90.
6. Olsen SJ 2nd, Fleisig GS, Dun S, Loftice J, Andrews JR. Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med. 2006;34(6):905-912.
7. Fleisig GS, Andrews JR. Prevention of elbow injuries in youth baseball pitchers. Sports Health. 2012;4(5):419-424.
8. Zaremski JL, Horodyski M, Donlan RM, Brisbane ST, Farmer KW. Does geographic location matter on the prevalence of ulnar collateral ligament reconstruction in collegiate baseball pitchers? Orthop J Sports Med. 2015;3(11):2325967115616582.
9. Erickson BJ, Nwachukwu BU, Rosas S, et al. Trends in medial ulnar collateral ligament reconstruction in the United States: A retrospective review of a large private-payer database from 2007 to 2011. Am J Sports Med. 2015;43(7):1770-1774.
10. Fleisig GS, Andrews JR, Dillman CJ. Kinetics of baseball pitching with implications about injury mechanism. Am J Sports Med. 1995;23(2):233-239.
11. Dillman CJ, Smutz P, Werner S. Valgus extension overload in baseball pitching. Med Sci Sports Exerc. 1991;23(suppl 4):S135.
12. Hechtman KS, Tjin-A-Tsoi EW, Zvijac JE, Uribe JW, Latta LL. Biomechanics of a less invasive procedure for reconstruction of the ulnar collateral ligament of the elbow. Am J Sports Med. 1998;26(5):620-624.
13. Ahmad CS, Lee TQ, ElAttrache NS. Biomechanical evaluation of a new ulnar collateral ligament reconstruction technique with interference screw fixation. Am J Sports Med. 2003;31(3):332-337.
14. Jobe FW, Stark HE, Lombardo SJ. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am. 1986;68(8):1158-1163.
15. Savoie FH 3rd, Trenhaile SW, Roberts J, Field LD, Ramsey JR. Primary repair of ulnar collateral ligament injuries of the elbow in young athletes: a case series of injuries to the proximal and distal ends of the ligament. Am J Sports Med. 2008;36(6):1066-1072.
16. Cain EL, Andrews JR, Dugas JR, et al. Outcome of ulnar collateral ligament reconstruction of the elbow in 1281 athletes results in 743 athletes with minimum 2-year follow-up. Am J Sports Med. 2010;38(12):2426-2434.
17. Azar FM, Andrews JR, Wilk KE, Groh D. Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am J Sports Med. 2000;28(1):16-23.
18. Dugas JR, Walters BL, Beason DP, Fleisig GS, Chronister JE. Biomechanical comparison of ulnar collateral ligament repair with internal bracing versus modified Jobe reconstruction. Am J Sports Med. 2016;44(3):735-741.
19. Watson JN, McQueen P, Hutchinson MR. A systematic review of ulnar collateral ligament reconstruction techniques. Am J Sports Med. 2014;42(10):2510-2516.
20. O’Brien DF, O’Hagan T, Stewart R, et al. Outcomes for ulnar collateral ligament reconstruction: A retrospective review using the KJOC assessment score with two-year follow-up in an overhead throwing population. J Shoulder Elbow Surg. 2015;24(6):934-940.
21. Ellenbecker TS, Mattalino AJ, Elam EA, Caplinger RA. Medial elbow joint laxity in professional baseball pitchers a bilateral comparison using stress radiography. Am J Sports Med. 1998;26(3):420-424.
22. Timmerman LA, Schwartz ML, Andrews JR. Preoperative evaluation of the ulnar collateral ligament by magnetic resonance imaging and computed tomography arthrography evaluation in 25 baseball players with surgical confirmation. Am J Sports Med. 1994;22(1):26-32.
23. Podesta L, Crow SA, Volkmer D, Bert T, Yocum LA. Treatment of partial ulnar collateral ligament tears in the elbow with platelet-rich plasma. Am J Sports Med. 2013;41(7):1689-1694.
24. Thompson NW, Mockford BJ, Cran GW. Absence of the palmaris longus muscle: a population study. Ulster Med J. 2001;70(1):22-24.
25. Dugas JR, Bilotta J, Watts CD, et al. Ulnar collateral ligament reconstruction with gracilis tendon in athletes with intraligamentous bony excision technique and results. Am J Sports Med. 2012;40(7):1578-1582.
26. Dargel J, Küpper F, Wegmann K, Oppermann J, Eysel P, Müller LP. Graft diameter does not influence primary stability of ulnar collateral ligament reconstruction of the elbow. J Orthop Sci. 2015;20(2):307-313.
27. Thompson WH, Jobe FW, Yocum LA, Pink MM. Ulnar collateral ligament reconstruction in athletes: muscle-splitting approach without transposition of the ulnar nerve. J Shoulder Elbow Surg. 2001;10(2):152-157.
28. Wilk KE, Arrigo CA, Andrews JR. Rehabilitation of the elbow in the throwing athlete. J Orthop Sports Phys Ther. 1993;17(6):305-317.
29. Wilk KE, Arrigo CA, Andrews JR, et al. Rehabilitation following elbow surgery in the throwing athlete. Oper Tech Sports Med. 1996;4:114-132.
30. Wilk KE, Arrigo CA, Andrews JR, et al. Preventative and Rehabilitation Exercises for the Shoulder and Elbow. 4th ed. Birmingham, AL: American Sports Medicine Institute; 1996.
31. Osbahr DC, Cain EL, Raines BT, Fortenbaugh D, Dugas JR, Andrews JR. Long-term outcomes after ulnar collateral ligament reconstruction in competitive baseball players minimum 10-year follow-up. Am J Sports Med. 2014;42(6):1333-1342.
32. 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.
33. Mishra A, Harmon K, Woodall J, Vieira A. Sports medicine applications of platelet rich plasma. Curr Pharm Biotechnol. 2012;13(7):1185-1195.
Potential Operating Room Fire Hazard of Bone Cement
Approximately 600 cases of operating room (OR) fires are reported annually.1 The incidence of OR fires in the United States equals that of wrong-site surgeries, and 20% of cases have associated morbidity.1,2 The estimated mortality rate is 1 to 2 cases per year.3-5 The most commonly involved anatomical regions are the airway (33%) and the face (28%).4 Most surgical fires are reported in anesthetized patients with open oxygen delivery systems during head, neck, and upper chest surgeries; electrosurgical instruments are the ignition source in 90% of these cases.6 Despite extensive fire safety education and training, complete elimination of OR fires still has not been achieved.
Each fire requires an ignition source, a fuel source, and an oxidizer.7 In the OR, the 2 most common oxidizers are oxygen and nitrous oxide. Head and neck surgeries have a high concentration of these gases near the working field and therefore a higher risk and incidence of fires. Furthermore, surgical drapes and equipment (eg, closed or semi-closed breathing systems, masks) may potentiate this risk by reducing ventilation in areas where gases can accumulate and ignite. Ignition sources provide the energy that starts fires; common sources are electrocautery, lasers, fiber-optic light cords, drills/burrs, and defibrillator paddles. Fires are propagated by fuel sources, which encompass any flammable material, including tracheal tubes, sponges, alcohol-based solutions, hair, gastrointestinal tract gases, gloves, and packaging materials.8 Of note, alcohol-based skin-preparation agents emit flammable vapors that can ignite.9-14 Before draping or exposure to an ignition source, chlorhexidine gluconate-based preparations must be allowed to dry for at least 3 minutes after application to hairless skin and up to 1 hour after application to hair.15 Inadequate drying poses a risk of fire.10We present the case of an OR fire ignited by electrocautery near freshly applied bone cement. No patient information is disclosed in this report.
Case Report
Our patient was evaluated in clinic and scheduled for total knee arthroplasty (TKA). All preoperative safety checklists and time-out procedures were followed and documented at the start of surgery. The TKA was performed with a standard medial patellar arthrotomy. Tourniquet control was used after Esmarch exsanguination. The surgery proceeded uneventfully until just after the bone cement was applied to the tibial surface. The surgeon was using a Bovie to resect residual lateral meniscus tissue when a fire instantaneously erupted within the joint space. Fortunately, the surgeon quickly suffocated the fire with a dry towel. The ignited bone cement was removed, and the patient was examined. There was no injury to surrounding tissue or joint space. Surgery was resumed with application of new bone cement to the tibial surface. The artificial joint was then successfully implanted and the case completed without further incident. The patient was discharged from the hospital and followed up as an outpatient without any postoperative complications.
Discussion
Bone cement, which is commonly used in artificial joint anchoring, craniofacial reconstruction, and vertebroplasty, has liquid and powder components. The liquid monomer methyl methacrylate (MMA) is colorless and flammable and has a distinct odor.16 Exposure to heat or light can prematurely polymerize MMA, requiring the addition of hydroquinone to inhibit the reaction.16 The powder polymethylmethacrylate affords excellent structural support, radiopacity, and facility of use.17 Dibenzoyl peroxide and N,N-dimethyl-p-toluidine are added to the powder to facilitate the polymerization reaction at room temperature (ie, cold curing of cement). Premature application of unpolymerized cement increases the risk of fire from the volatile liquid component.
In the OR, bone cement is prepared by mixing together its powder and liquid components.18 The reaction is exothermic polymerization. The liquid is highly volatile and flammable in both liquid and vapor states.16,19 The vapors are denser than air and can concentrate in poorly ventilated areas. The OR and the application site must be adequately ventilated to eliminate any pockets of vapor accumulation.16 A vacuum mixer can be used to minimize fume exposure, enhance cement strength, and reduce fire risk while combining the 2 components.
MMA’s flash point, the temperature at which the fumes could ignite in the presence of an ignition source, is 10.5ºC. The auto-ignition point, the temperature at which MMA spontaneously combusts, is 421ºC.20 The OR is usually warmer than the flash point temperature, but the electrocautery tip can generate up to 1200ºC of heat.21 Therefore, bone cement is a potential fire hazard, and use of Bovies or other ignition sources in its vicinity must be avoided.
The Table lists the recommended times for preparing various bone cement products.22,23Mix time is the time needed to combine the liquid and powder into a homogenous putty.
For OR fires, the standard guidelines for rapid containment and safety apply. These guidelines are detailed by the American Society of Anesthesiologists.8 Briefly, delivery of all airway gases to the patient is discontinued. Any burning material is removed and extinguished by the OR staff.1 Carbon dioxide fire extinguishers are used to put out any patient fires and minimize the risk of thermal injury. (Water-mist fire extinguishers can contaminate surgical wounds and present an electric shock hazard with surgical devices and should be avoided.24) If a fire occurs in a patient’s airway, the tracheal tube is removed, and airway patency is maintained with use of other invasive or noninvasive techniques. Often, noninvasive positive pressure ventilation without supplemental oxygen is used until the fire is controlled and the patient is safe. Once the patient fire is controlled, ventilation is restarted, and the patient is evacuated from the OR and away from any other hazards, as required. Last, the patient is physically examined for any injuries and treated.24 Specific to TKA, the procedure is resumed after removal of all bone cement, inspection of the operative site, and treatment of any fire-related injuries.
We have reported the case of an OR fire during TKA. Appropriate selection and use of bone cement products, proper assessment of set time, and avoidance of electrocautery near cement application sites may dramatically reduce associated fire risks.
Am J Orthop. 2016;45(7):E512-E514. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Hart SR, Yajnik A, Ashford J, Springer R, Harvey S. Operating room fire safety. Ochsner J. 2011;11(1):37-42.
2. American Society of Anesthesiologists Task Force on Operating Room Fires; Caplan RA, Barker SJ, Connis RT, et al. Practice advisory for the prevention and management of operating room fires. Anesthesiology. 2008;108(5):786-801.
3. Bruley M. Surgical fires: perioperative communication is essential to prevent this rare but devastating complication. Qual Saf HealthCare. 2004;13(6):467-471.
4. Daane SP, Toth BA. Fire in the operating room: principles and prevention. Plast Reconstr Surg. 2005;115(5):73e-75e.
5. Rinder CS. Fire safety in the operating room. Curr Opin Anaesthesiol. 2008;21(6):790-795.
6. Mathias JM. Fast action, team coordination critical when surgical fires occur. OR Manager. 2013;29(11):9-10.
7. Culp WC Jr, Kimbrough BA, Luna S. Flammability of surgical drapes and materials in varying concentrations of oxygen. Anesthesiology. 2013;119(4):770-776.
8. Apfelbaum JL, Caplan RA, Barker SJ, et al; American Society of Anesthesiologists Task Force on Operating Room Fires. Practice advisory for the prevention and management of operating room fires: an updated report by the American Society of Anesthesiologists Task Force on Operating Room Fires. Anesthesiology. 2013;118(2):271-290.
9. Barker SJ, Polson JS. Fire in the operating room: a case report and laboratory study. Anesth Analg. 2001;93(4):960-965.
10. Fire hazard created by the misuse of DuraPrep solution. Health Devices. 1998;27(11):400-402.
11. Hurt TL, Schweich PJ. Do not get burned: preventing iatrogenic fires and burns in the emergency department. Pediatr Emerg Care. 2003;19(4):255-259.
12. Prasad R, Quezado Z, St Andre A, O’Grady NP. Fires in the operating room and intensive care unit: awareness is the key to prevention. Anesth Analg. 2006;102(1):172-174.
13. Shah SC. Correspondence: operating room flash fire. Anesth Analg. 1974;53(2):288.
14. Tooher R, Maddern GJ, Simpson J. Surgical fires and alcohol-based skin preparations. ANZ J Surg. 2004;74(5):382-385.
15. Using ChloraPrep™ products and the skin prep portfolio. http://www.carefusion.com/medical-products/infection-prevention/skin-preparation/using-chloraprep.aspx. Accessed October 7, 2016.16. DePuy CMW. DePuy Orthopaedic Gentamicin Bone Cements. Blackpool, United Kingdom: DePuy International Ltd; 2008.
17. Dall’Oca C, Maluta T, Cavani F, et al. The biocompatibility of porous vs non-porous bone cements: a new methodological approach. Eur J Histochem. 2014;58(2):2255.
18. Zimmer Biomet. Bone Cement: Biomet Cement and Cementing Systems. http://www.biomet.com/wps/portal/internet/Biomet/Healthcare-Professionals/products/orthopedics. 2014. Accessed October 7, 2016.
19. Sigma-Aldrich. Methyl methacrylate. http://www.sigmaaldrich.com/catalog/product/aldrich/w400201?lang=en®ion=US. Accessed October 7, 2016.
20. DePuy Synthes. Unmedicated bone cements MSDS. Blackpool, United Kingdom: DePuy International Ltd. http://msdsdigital.com/unmedicated-bone-cements-msds. Accessed October 7, 2016.
21. Mir MR, Sun GS, Wang CM. Electrocautery. http://emedicine.medscape.com/article/2111163-overview#showall. Accessed October 7, 2016.
22. DePuy Synthes. Bone cement time setting.
23. Berry DJ, Lieberman JR, eds. Surgery of the Hip. New York, NY: Elsevier; 2011.
24. ECRI Institute. Surgical Fire Prevention. https://www.ecri.org/Accident_Investigation/Pages/Surgical-Fire-Prevention.aspx. 2014. Accessed October 7, 2016.
Approximately 600 cases of operating room (OR) fires are reported annually.1 The incidence of OR fires in the United States equals that of wrong-site surgeries, and 20% of cases have associated morbidity.1,2 The estimated mortality rate is 1 to 2 cases per year.3-5 The most commonly involved anatomical regions are the airway (33%) and the face (28%).4 Most surgical fires are reported in anesthetized patients with open oxygen delivery systems during head, neck, and upper chest surgeries; electrosurgical instruments are the ignition source in 90% of these cases.6 Despite extensive fire safety education and training, complete elimination of OR fires still has not been achieved.
Each fire requires an ignition source, a fuel source, and an oxidizer.7 In the OR, the 2 most common oxidizers are oxygen and nitrous oxide. Head and neck surgeries have a high concentration of these gases near the working field and therefore a higher risk and incidence of fires. Furthermore, surgical drapes and equipment (eg, closed or semi-closed breathing systems, masks) may potentiate this risk by reducing ventilation in areas where gases can accumulate and ignite. Ignition sources provide the energy that starts fires; common sources are electrocautery, lasers, fiber-optic light cords, drills/burrs, and defibrillator paddles. Fires are propagated by fuel sources, which encompass any flammable material, including tracheal tubes, sponges, alcohol-based solutions, hair, gastrointestinal tract gases, gloves, and packaging materials.8 Of note, alcohol-based skin-preparation agents emit flammable vapors that can ignite.9-14 Before draping or exposure to an ignition source, chlorhexidine gluconate-based preparations must be allowed to dry for at least 3 minutes after application to hairless skin and up to 1 hour after application to hair.15 Inadequate drying poses a risk of fire.10We present the case of an OR fire ignited by electrocautery near freshly applied bone cement. No patient information is disclosed in this report.
Case Report
Our patient was evaluated in clinic and scheduled for total knee arthroplasty (TKA). All preoperative safety checklists and time-out procedures were followed and documented at the start of surgery. The TKA was performed with a standard medial patellar arthrotomy. Tourniquet control was used after Esmarch exsanguination. The surgery proceeded uneventfully until just after the bone cement was applied to the tibial surface. The surgeon was using a Bovie to resect residual lateral meniscus tissue when a fire instantaneously erupted within the joint space. Fortunately, the surgeon quickly suffocated the fire with a dry towel. The ignited bone cement was removed, and the patient was examined. There was no injury to surrounding tissue or joint space. Surgery was resumed with application of new bone cement to the tibial surface. The artificial joint was then successfully implanted and the case completed without further incident. The patient was discharged from the hospital and followed up as an outpatient without any postoperative complications.
Discussion
Bone cement, which is commonly used in artificial joint anchoring, craniofacial reconstruction, and vertebroplasty, has liquid and powder components. The liquid monomer methyl methacrylate (MMA) is colorless and flammable and has a distinct odor.16 Exposure to heat or light can prematurely polymerize MMA, requiring the addition of hydroquinone to inhibit the reaction.16 The powder polymethylmethacrylate affords excellent structural support, radiopacity, and facility of use.17 Dibenzoyl peroxide and N,N-dimethyl-p-toluidine are added to the powder to facilitate the polymerization reaction at room temperature (ie, cold curing of cement). Premature application of unpolymerized cement increases the risk of fire from the volatile liquid component.
In the OR, bone cement is prepared by mixing together its powder and liquid components.18 The reaction is exothermic polymerization. The liquid is highly volatile and flammable in both liquid and vapor states.16,19 The vapors are denser than air and can concentrate in poorly ventilated areas. The OR and the application site must be adequately ventilated to eliminate any pockets of vapor accumulation.16 A vacuum mixer can be used to minimize fume exposure, enhance cement strength, and reduce fire risk while combining the 2 components.
MMA’s flash point, the temperature at which the fumes could ignite in the presence of an ignition source, is 10.5ºC. The auto-ignition point, the temperature at which MMA spontaneously combusts, is 421ºC.20 The OR is usually warmer than the flash point temperature, but the electrocautery tip can generate up to 1200ºC of heat.21 Therefore, bone cement is a potential fire hazard, and use of Bovies or other ignition sources in its vicinity must be avoided.
The Table lists the recommended times for preparing various bone cement products.22,23Mix time is the time needed to combine the liquid and powder into a homogenous putty.
For OR fires, the standard guidelines for rapid containment and safety apply. These guidelines are detailed by the American Society of Anesthesiologists.8 Briefly, delivery of all airway gases to the patient is discontinued. Any burning material is removed and extinguished by the OR staff.1 Carbon dioxide fire extinguishers are used to put out any patient fires and minimize the risk of thermal injury. (Water-mist fire extinguishers can contaminate surgical wounds and present an electric shock hazard with surgical devices and should be avoided.24) If a fire occurs in a patient’s airway, the tracheal tube is removed, and airway patency is maintained with use of other invasive or noninvasive techniques. Often, noninvasive positive pressure ventilation without supplemental oxygen is used until the fire is controlled and the patient is safe. Once the patient fire is controlled, ventilation is restarted, and the patient is evacuated from the OR and away from any other hazards, as required. Last, the patient is physically examined for any injuries and treated.24 Specific to TKA, the procedure is resumed after removal of all bone cement, inspection of the operative site, and treatment of any fire-related injuries.
We have reported the case of an OR fire during TKA. Appropriate selection and use of bone cement products, proper assessment of set time, and avoidance of electrocautery near cement application sites may dramatically reduce associated fire risks.
Am J Orthop. 2016;45(7):E512-E514. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Approximately 600 cases of operating room (OR) fires are reported annually.1 The incidence of OR fires in the United States equals that of wrong-site surgeries, and 20% of cases have associated morbidity.1,2 The estimated mortality rate is 1 to 2 cases per year.3-5 The most commonly involved anatomical regions are the airway (33%) and the face (28%).4 Most surgical fires are reported in anesthetized patients with open oxygen delivery systems during head, neck, and upper chest surgeries; electrosurgical instruments are the ignition source in 90% of these cases.6 Despite extensive fire safety education and training, complete elimination of OR fires still has not been achieved.
Each fire requires an ignition source, a fuel source, and an oxidizer.7 In the OR, the 2 most common oxidizers are oxygen and nitrous oxide. Head and neck surgeries have a high concentration of these gases near the working field and therefore a higher risk and incidence of fires. Furthermore, surgical drapes and equipment (eg, closed or semi-closed breathing systems, masks) may potentiate this risk by reducing ventilation in areas where gases can accumulate and ignite. Ignition sources provide the energy that starts fires; common sources are electrocautery, lasers, fiber-optic light cords, drills/burrs, and defibrillator paddles. Fires are propagated by fuel sources, which encompass any flammable material, including tracheal tubes, sponges, alcohol-based solutions, hair, gastrointestinal tract gases, gloves, and packaging materials.8 Of note, alcohol-based skin-preparation agents emit flammable vapors that can ignite.9-14 Before draping or exposure to an ignition source, chlorhexidine gluconate-based preparations must be allowed to dry for at least 3 minutes after application to hairless skin and up to 1 hour after application to hair.15 Inadequate drying poses a risk of fire.10We present the case of an OR fire ignited by electrocautery near freshly applied bone cement. No patient information is disclosed in this report.
Case Report
Our patient was evaluated in clinic and scheduled for total knee arthroplasty (TKA). All preoperative safety checklists and time-out procedures were followed and documented at the start of surgery. The TKA was performed with a standard medial patellar arthrotomy. Tourniquet control was used after Esmarch exsanguination. The surgery proceeded uneventfully until just after the bone cement was applied to the tibial surface. The surgeon was using a Bovie to resect residual lateral meniscus tissue when a fire instantaneously erupted within the joint space. Fortunately, the surgeon quickly suffocated the fire with a dry towel. The ignited bone cement was removed, and the patient was examined. There was no injury to surrounding tissue or joint space. Surgery was resumed with application of new bone cement to the tibial surface. The artificial joint was then successfully implanted and the case completed without further incident. The patient was discharged from the hospital and followed up as an outpatient without any postoperative complications.
Discussion
Bone cement, which is commonly used in artificial joint anchoring, craniofacial reconstruction, and vertebroplasty, has liquid and powder components. The liquid monomer methyl methacrylate (MMA) is colorless and flammable and has a distinct odor.16 Exposure to heat or light can prematurely polymerize MMA, requiring the addition of hydroquinone to inhibit the reaction.16 The powder polymethylmethacrylate affords excellent structural support, radiopacity, and facility of use.17 Dibenzoyl peroxide and N,N-dimethyl-p-toluidine are added to the powder to facilitate the polymerization reaction at room temperature (ie, cold curing of cement). Premature application of unpolymerized cement increases the risk of fire from the volatile liquid component.
In the OR, bone cement is prepared by mixing together its powder and liquid components.18 The reaction is exothermic polymerization. The liquid is highly volatile and flammable in both liquid and vapor states.16,19 The vapors are denser than air and can concentrate in poorly ventilated areas. The OR and the application site must be adequately ventilated to eliminate any pockets of vapor accumulation.16 A vacuum mixer can be used to minimize fume exposure, enhance cement strength, and reduce fire risk while combining the 2 components.
MMA’s flash point, the temperature at which the fumes could ignite in the presence of an ignition source, is 10.5ºC. The auto-ignition point, the temperature at which MMA spontaneously combusts, is 421ºC.20 The OR is usually warmer than the flash point temperature, but the electrocautery tip can generate up to 1200ºC of heat.21 Therefore, bone cement is a potential fire hazard, and use of Bovies or other ignition sources in its vicinity must be avoided.
The Table lists the recommended times for preparing various bone cement products.22,23Mix time is the time needed to combine the liquid and powder into a homogenous putty.
For OR fires, the standard guidelines for rapid containment and safety apply. These guidelines are detailed by the American Society of Anesthesiologists.8 Briefly, delivery of all airway gases to the patient is discontinued. Any burning material is removed and extinguished by the OR staff.1 Carbon dioxide fire extinguishers are used to put out any patient fires and minimize the risk of thermal injury. (Water-mist fire extinguishers can contaminate surgical wounds and present an electric shock hazard with surgical devices and should be avoided.24) If a fire occurs in a patient’s airway, the tracheal tube is removed, and airway patency is maintained with use of other invasive or noninvasive techniques. Often, noninvasive positive pressure ventilation without supplemental oxygen is used until the fire is controlled and the patient is safe. Once the patient fire is controlled, ventilation is restarted, and the patient is evacuated from the OR and away from any other hazards, as required. Last, the patient is physically examined for any injuries and treated.24 Specific to TKA, the procedure is resumed after removal of all bone cement, inspection of the operative site, and treatment of any fire-related injuries.
We have reported the case of an OR fire during TKA. Appropriate selection and use of bone cement products, proper assessment of set time, and avoidance of electrocautery near cement application sites may dramatically reduce associated fire risks.
Am J Orthop. 2016;45(7):E512-E514. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Hart SR, Yajnik A, Ashford J, Springer R, Harvey S. Operating room fire safety. Ochsner J. 2011;11(1):37-42.
2. American Society of Anesthesiologists Task Force on Operating Room Fires; Caplan RA, Barker SJ, Connis RT, et al. Practice advisory for the prevention and management of operating room fires. Anesthesiology. 2008;108(5):786-801.
3. Bruley M. Surgical fires: perioperative communication is essential to prevent this rare but devastating complication. Qual Saf HealthCare. 2004;13(6):467-471.
4. Daane SP, Toth BA. Fire in the operating room: principles and prevention. Plast Reconstr Surg. 2005;115(5):73e-75e.
5. Rinder CS. Fire safety in the operating room. Curr Opin Anaesthesiol. 2008;21(6):790-795.
6. Mathias JM. Fast action, team coordination critical when surgical fires occur. OR Manager. 2013;29(11):9-10.
7. Culp WC Jr, Kimbrough BA, Luna S. Flammability of surgical drapes and materials in varying concentrations of oxygen. Anesthesiology. 2013;119(4):770-776.
8. Apfelbaum JL, Caplan RA, Barker SJ, et al; American Society of Anesthesiologists Task Force on Operating Room Fires. Practice advisory for the prevention and management of operating room fires: an updated report by the American Society of Anesthesiologists Task Force on Operating Room Fires. Anesthesiology. 2013;118(2):271-290.
9. Barker SJ, Polson JS. Fire in the operating room: a case report and laboratory study. Anesth Analg. 2001;93(4):960-965.
10. Fire hazard created by the misuse of DuraPrep solution. Health Devices. 1998;27(11):400-402.
11. Hurt TL, Schweich PJ. Do not get burned: preventing iatrogenic fires and burns in the emergency department. Pediatr Emerg Care. 2003;19(4):255-259.
12. Prasad R, Quezado Z, St Andre A, O’Grady NP. Fires in the operating room and intensive care unit: awareness is the key to prevention. Anesth Analg. 2006;102(1):172-174.
13. Shah SC. Correspondence: operating room flash fire. Anesth Analg. 1974;53(2):288.
14. Tooher R, Maddern GJ, Simpson J. Surgical fires and alcohol-based skin preparations. ANZ J Surg. 2004;74(5):382-385.
15. Using ChloraPrep™ products and the skin prep portfolio. http://www.carefusion.com/medical-products/infection-prevention/skin-preparation/using-chloraprep.aspx. Accessed October 7, 2016.16. DePuy CMW. DePuy Orthopaedic Gentamicin Bone Cements. Blackpool, United Kingdom: DePuy International Ltd; 2008.
17. Dall’Oca C, Maluta T, Cavani F, et al. The biocompatibility of porous vs non-porous bone cements: a new methodological approach. Eur J Histochem. 2014;58(2):2255.
18. Zimmer Biomet. Bone Cement: Biomet Cement and Cementing Systems. http://www.biomet.com/wps/portal/internet/Biomet/Healthcare-Professionals/products/orthopedics. 2014. Accessed October 7, 2016.
19. Sigma-Aldrich. Methyl methacrylate. http://www.sigmaaldrich.com/catalog/product/aldrich/w400201?lang=en®ion=US. Accessed October 7, 2016.
20. DePuy Synthes. Unmedicated bone cements MSDS. Blackpool, United Kingdom: DePuy International Ltd. http://msdsdigital.com/unmedicated-bone-cements-msds. Accessed October 7, 2016.
21. Mir MR, Sun GS, Wang CM. Electrocautery. http://emedicine.medscape.com/article/2111163-overview#showall. Accessed October 7, 2016.
22. DePuy Synthes. Bone cement time setting.
23. Berry DJ, Lieberman JR, eds. Surgery of the Hip. New York, NY: Elsevier; 2011.
24. ECRI Institute. Surgical Fire Prevention. https://www.ecri.org/Accident_Investigation/Pages/Surgical-Fire-Prevention.aspx. 2014. Accessed October 7, 2016.
1. Hart SR, Yajnik A, Ashford J, Springer R, Harvey S. Operating room fire safety. Ochsner J. 2011;11(1):37-42.
2. American Society of Anesthesiologists Task Force on Operating Room Fires; Caplan RA, Barker SJ, Connis RT, et al. Practice advisory for the prevention and management of operating room fires. Anesthesiology. 2008;108(5):786-801.
3. Bruley M. Surgical fires: perioperative communication is essential to prevent this rare but devastating complication. Qual Saf HealthCare. 2004;13(6):467-471.
4. Daane SP, Toth BA. Fire in the operating room: principles and prevention. Plast Reconstr Surg. 2005;115(5):73e-75e.
5. Rinder CS. Fire safety in the operating room. Curr Opin Anaesthesiol. 2008;21(6):790-795.
6. Mathias JM. Fast action, team coordination critical when surgical fires occur. OR Manager. 2013;29(11):9-10.
7. Culp WC Jr, Kimbrough BA, Luna S. Flammability of surgical drapes and materials in varying concentrations of oxygen. Anesthesiology. 2013;119(4):770-776.
8. Apfelbaum JL, Caplan RA, Barker SJ, et al; American Society of Anesthesiologists Task Force on Operating Room Fires. Practice advisory for the prevention and management of operating room fires: an updated report by the American Society of Anesthesiologists Task Force on Operating Room Fires. Anesthesiology. 2013;118(2):271-290.
9. Barker SJ, Polson JS. Fire in the operating room: a case report and laboratory study. Anesth Analg. 2001;93(4):960-965.
10. Fire hazard created by the misuse of DuraPrep solution. Health Devices. 1998;27(11):400-402.
11. Hurt TL, Schweich PJ. Do not get burned: preventing iatrogenic fires and burns in the emergency department. Pediatr Emerg Care. 2003;19(4):255-259.
12. Prasad R, Quezado Z, St Andre A, O’Grady NP. Fires in the operating room and intensive care unit: awareness is the key to prevention. Anesth Analg. 2006;102(1):172-174.
13. Shah SC. Correspondence: operating room flash fire. Anesth Analg. 1974;53(2):288.
14. Tooher R, Maddern GJ, Simpson J. Surgical fires and alcohol-based skin preparations. ANZ J Surg. 2004;74(5):382-385.
15. Using ChloraPrep™ products and the skin prep portfolio. http://www.carefusion.com/medical-products/infection-prevention/skin-preparation/using-chloraprep.aspx. Accessed October 7, 2016.16. DePuy CMW. DePuy Orthopaedic Gentamicin Bone Cements. Blackpool, United Kingdom: DePuy International Ltd; 2008.
17. Dall’Oca C, Maluta T, Cavani F, et al. The biocompatibility of porous vs non-porous bone cements: a new methodological approach. Eur J Histochem. 2014;58(2):2255.
18. Zimmer Biomet. Bone Cement: Biomet Cement and Cementing Systems. http://www.biomet.com/wps/portal/internet/Biomet/Healthcare-Professionals/products/orthopedics. 2014. Accessed October 7, 2016.
19. Sigma-Aldrich. Methyl methacrylate. http://www.sigmaaldrich.com/catalog/product/aldrich/w400201?lang=en®ion=US. Accessed October 7, 2016.
20. DePuy Synthes. Unmedicated bone cements MSDS. Blackpool, United Kingdom: DePuy International Ltd. http://msdsdigital.com/unmedicated-bone-cements-msds. Accessed October 7, 2016.
21. Mir MR, Sun GS, Wang CM. Electrocautery. http://emedicine.medscape.com/article/2111163-overview#showall. Accessed October 7, 2016.
22. DePuy Synthes. Bone cement time setting.
23. Berry DJ, Lieberman JR, eds. Surgery of the Hip. New York, NY: Elsevier; 2011.
24. ECRI Institute. Surgical Fire Prevention. https://www.ecri.org/Accident_Investigation/Pages/Surgical-Fire-Prevention.aspx. 2014. Accessed October 7, 2016.
Biomechanics of Polyhydroxyalkanoate Mesh–Augmented Single-Row Rotator Cuff Repairs
Healing after rotator cuff repair (RCR) can be challenging, especially in cases of large and massive tears, revision repairs, and tendons with poor tissue quality.1-3 Poor tissue quality is associated with increased risk for recurrent tears, independent of age and tear size.3 Various techniques have been used to improve tendon fixation strength in these difficult situations, including augmented suture configurations (eg, massive cuff stitches, rip-stop stitches) and tissue grafts (eg, acellular dermal matrix).4-9 Clinical studies have found improved healing rates for larger tears and revision repairs using acellular dermal matrix grafts.6,10 Synthetic patches are another option for RCR augmentation, but limited clinical data and biomechanical evidence support use of synthetic grafts as an augment for RCRs.11-13
Polyhydroxyalkanoates (PHAs) are a class of biodegradable polymers that have been used as orthopedic devices, tissue scaffolds, patches, and other applications with increasing frequency over the past decade.14 In the laboratory, these implanted materials have been shown to support cell migration and growth.15 The PHA family of polymers typically degrades by hydrolytic and bacterial depolymerase mechanisms over 52-plus weeks in vivo.14PHA grafts have been studied in the setting of RCR. An expanded polytetrafluoroethylene scaffold was shown to improve repair mechanics when used as a bursal side graft in an in vitro ovine model.11 The graft increased tendon footprint contact pressure and failure loads by almost 180 N. In clinical studies, poly-L-lactic acid augmentations have been used to reinforce massive RCRs. Lenart and colleagues16 found that 38% of 16 patients with such tears had an intact rotator cuff at 1.2-year follow-up, and improvement in clinical scores. Proctor13 reported on use of a poly-L-lactic acid retrograde patch for reinforcement of massive tears with both single- and double-row repairs in 18 patients. The cohort had more favorable rates of intact cuffs at 12 months (83%) and 42 months (78%), and ASES (American Shoulder and Elbow Surgeons) scores improved from 25 before surgery to 82 at latest follow-up after surgery.
RCR augmentation traditionally has been performed with an open or mini-open technique.6 Recently, several authors have reported on arthroscopic techniques for augmentation with either acellular dermal matrix or synthetic grafts.13,17,18 Most techniques have involved “bridging” with a graft or patch used to stress-shield a single-row repair.8,9,13 This bridging typically involves placing several sutures medial to where the anchor repair stitches pass through the tendon. An alternative is to pass the repair stitches through both the tendon and the graft.17-19 The overall volume of tissue incorporated into the repair stitches (rotator cuff plus graft) is increased with the augmented technique relative to the bridging technique. Both can be technically challenging, but the augmented technique may be easier to perform arthroscopically.9,19 Regardless, these techniques are complicated and require a higher level of arthroscopic skills compared with those required in arthroscopic RCR without a graft. Simplifying arthroscopic graft augmentation likely will increase its utility because, even for skilled surgeons, adding a graft can increase operative time by 20 to 30 minutes. Simplification will also extend use of the technique to surgeons with less experience and proficiency with arthroscopic repair.
We developed a simple method for augmenting single-row RCR with a strip of bioresorbable soft-tissue scaffold. We also conducted a study to evaluate the initial biomechanical properties of single-row RCR in cadaveric shoulder specimens augmented with PHA mesh (BioFiber; Tornier) graft as compared with single-row RCR without augmentation. Both cyclic gap formation and ultimate failure loads and displacement were quantified. We hypothesized that the augmented RCRs would have decreased gap formation and increased ultimate failure loads compared with nonaugmented RCRs. This study was exempt from having to obtain Institutional Review B
Methods
Eight pairs of fresh-frozen cadaver humeri (6 male, 2 female; mean [SD] age, 61 [9] years) were dissected of all soft tissue (except rotator cuff) by Dr. Tashjian, a board-certified, fellowship-trained orthopedic surgeon. There were no qualitative differences in tendon condition between tendons within a pair. The supraspinatus muscle and tendon were separated from the other rotator cuff muscles. The infraspinatus, subscapularis, and teres minor were removed from the humerus. Last, the supraspinatus was resected at its insertion. Humeral pairs were then randomized into augmented and nonaugmented RCRs within each pair.
In the nonaugmented group, the supraspinatus was reattached to its insertion in a single-row RCR with 2 triple-loaded suture anchors (5.5-mm Insite FT Ti, No. 2 Force Fiber suture; Tornier) and 6 simple stitches (Figure 1A). Anchors were placed midway between the articular margin and the lateral edge of the greater tuberosity at about 45° to the bone surface.
In the contralateral shoulders, augmented RCRs were performed. Specimens were prepared exactly as they were for the nonaugmented RCRs, including anchor placement and suture passage. Before knot tying, RCRs were augmented with 2 strips of 13-mm × 23-mm PHA mesh (BioFiber) (Figure 1B). One strip was used to augment the 3 sutures of each anchor, overlying the residual tendon, to reinforce the tendon–knot interface. After each suture was passed through the supraspinatus tendon from the intra-articular surface, the stitch was passed through the strip of PHA mesh. Stitches were separated by 5 mm in each mesh strip. All 6 sutures were then tied with a Revo knot between the free end of each suture leg and the leg that passed through the tendon and mesh.
Each humerus was transected at the midshaft and potted and mounted in an Instron 1331 load frame with Model 8800 controller (Instron). A cryoclamp was used to grasp the supraspinatus muscle belly above the musculotendinous junction (Figure 2).
Three rows of 2-mm fiducial markers were affixed to the bone, tendon, and muscle belly with cyanoacrylate for tracking with a digital video system (DMAS Version 6.5; Spicatek) (Figure 3).21
A 0.1-MPa pre-stress (applied force/tendon cross-sectional area) was applied to each construct to determine the starting position for the deformation profile. Each repair underwent 1000 cycles of uniaxial load-controlled displacement between 0.1 and 1.0 MPa of effective stress at 1 Hz. Effective stress was determined as the ratio of applied force to cross-sectional area of the tendon at harvest to normalize the applied loads between tendons of varying size. During cyclic testing, gapping of more than 5 mm was defined as construct failure.22 After cyclic loading, each construct was loaded to failure at 1.0 mm/s. Ultimate failure load was defined as the highest load achieved at the maximum displacement before rapid decline in load supported by the construct.
Statistical Analysis
Paired t tests were used to compare the matched pairs of constructs. For all tests, significance was set at P ≤ .05. Post hoc power was calculated for significant results using G*Power Version 3.1.6.23 All data are presented as means (SDs).
Results
After 1000 cycles of displacement, mean (SD) gapping was 3.8 (0.9) mm for the nonaugmented repairs and 3.9 (1.1) mm for the PHA mesh–augmented repairs (P = .879) (Figure 4).
For the nonaugmented repairs, mean (SD) failure displacement was 6.3 (1.7) mm, and mean (SD) ultimate failure load was 472.1 (120.3) N. For the PHA-augmented repairs, failure displacement was 5.5 (1.9) mm, and ultimate failure load was 571.2 (173.0) N. There was no difference in failure displacement (P = .393), but there was a difference in ultimate failure load (P = .042; power = 0.57). During failure testing, mean (SD) tissue deformation was higher (P = .012; power = 0.83) for the PHA-augmented repairs, 1.2 (0.7) mm, than for the nonaugmented repairs, 0.8 (0.5) mm. Failures, which were consistent within pairs, were caused by tissue failure, with sutures pulling through the tissue (4 pairs) or single anchor pullout before ultimate tissue failure (4 pairs). Of the 4 failures with anchor pullout, 3 had anterior anchor pullout, and 1 had posterior anchor pullout. In all specimens with anchor pullout, the second anchor remained stable, and ultimate failure occurred with tissue tearing at the suture interface. There were no significant differences in any metrics between specimens that failed with intact anchors and specimens with single anchor pullout (P ≥ .122). Therefore, both groups were pooled for the failure analysis.
Discussion
RCR augmentation with a synthetic graft is a viable option for improving fixation strength of supraspinatus repairs, as shown in otherwise healthy tendon in the present study. Our hypothesis that there would be decreased gap formation with graft augmentation was not supported, whereas the hypothesis of increased failure loads with graft augmentation was supported. These findings may also be applicable in cases of large tears, revisions, and tendons with poor tissue quality. Simplification of graft application techniques will allow quick and easy arthroscopic augmentation.
Studies of RCRs for large or massive tears have reported retear rates of 25% to 79%.24-26 Latissimus dorsi tendon transfers also show promise in posterosuperior RCRs, with failure rates near 10%.27,28 Although use of PHA patches in RCR augmentation is relatively new, short-term and midterm failure rates are in the range of 20% to 60% in the few small cohorts currently being studied.13,16 It is possible that these rates may improve as indications, surgical experience, and techniques for use of PHA patches are further refined. Regardless, with PHA currently being used in practice, it is important to quantify the biomechanics of the augmentation as a baseline for its performance in reinforcing the tendon–suture interface.
We determined that the initial fixation strength of single-row repairs was higher with the addition of PHA synthetic grafts using a very simple technique. Single-row triple-loaded anchor repairs already provide high initial mechanical strength, and our results are similar to those of another study of this technique.29 Despite the already high mechanical strength of a triple-loaded anchor repair, PHA mesh increased ultimate strength by about 100 N (~25%). Of note, tissue elongation during failure was higher (P = .012; power = 0.83) in the PHA-augmented group (1.2 mm) than in the nonaugmented group (0.8 mm). This was not surprising—failure loads were almost 100 N higher in the PHA-augmented group than in the nonaugmented group. Consequently, much higher forces were placed on the muscle belly, likely resulting in additional elongation of the intact tissue medial to the repair construct.
The ultimate failure loads in our study compare favorably with the biomechanical strength of augmented repairs reported by others.8,9,18 Barber and colleagues18 evaluated an augmented single-row repair with 2 double-loaded suture anchors and an acellular dermal matrix graft. The ultimate failure load of the augmented repairs was 325 N. In contrast, Omae and colleagues8 tested a bridging single-row repair using 2 double-loaded suture anchors and an acellular dermal matrix graft. Ultimate failure load of the augmented repairs was 560 N, similar to our finding. Last, Shea and colleagues9 evaluated a bridging single-row repair using 2 double-loaded suture anchors and an acellular dermal matrix graft, with ultimate failure load of 429 N. The techniques in all 3 studies can be performed arthroscopically but are challenging and require multiple extra sutures and anchors that need management and tying. Our technique provides similar initial fixation strength, has no requirement for extra sutures or anchors, and is very simple to perform.
The supraspinatus tendon is estimated to fail between 800 N and 1000 N.30,31 Biomechanical shoulder simulators use supraspinatus forces in the range of 20 N to 200 N for scapular plane abduction.32-36 Therefore, the single-row repair failures in our study fell between functional and full-thickness failure loads. Studies on the mechanics of degenerated human supraspinatus tendon are limited, but there is evidence the mechanical properties of these tissues are inferior to those of healthy tendon.37 A 100-N increase in failure loads with PHA augmentation may prove highly significant in reinforcing the suture–tendon interface in degenerated tendons.
Adding the mesh did not have any effect on gapping at the repair site after cyclic loading. This finding suggests that construct gapping under cyclic loading is not a function of a reinforced knot–tendon interface but is instead caused by microtearing and cinching of the suture constructs in relation to the underlying bone. Tissue elongation likely was not a strong contributor to overall cyclic gapping, as elongation did not differ between the nonaugmented and augmented repairs (0.5 mm vs 0.7 mm; P = .276) and was small relative to the nearly 4 mm of construct gapping. Gapping may be affected by healing and integration of the mesh into the repaired tendon over time, but this effect could not be captured in the present study. Patients are initially immobilized and passive shoulder motion gradually introduced, in stark contrast to the immediate loading protocol in the present study. Regardless, the 25% increase in overall strength may be clinically important, especially in cases of difficult repair or poor tissue quality.
Our technique simplifies arthroscopic augmentation—stitches are passed through the rotator cuff in simple fashion. Before being tied, the limbs that were passed through the rotator cuff are removed through a cannula and then passed through the synthetic graft.
Study Limitations
This study had several limitations. First, it was a cadaveric biomechanical study that evaluated only time-zero biomechanical properties. Loads were normalized to tendon size, specimens were randomized between sides, and paired specimens were used to minimize the effects of tendon and bone quality on outcome metrics. In addition, donor tendons were representative of otherwise healthy tissue. Chronic tears and associated resorption/atrophy could have affected the magnitude of forces and gapping detected in this study. Theoretically, over time the tendon tissue will adhere to and grow into the mesh, which could minimize potential differences. Studies are needed to determine the effects of healing on long-term repair strength in affected patients. Last, all constructs were performed in open fashion to improve repeatability of construct placement and provide accessibility for Instron testing. Our technique did not directly replicate the arthroscopic approach, but, unlike other augmentation techniques, it is so simple that transition to all-arthroscopic augmentation is realistic.
Patch augmentation increases the cost of materials and operative time and should be considered a limitation of its utility. We do not recommend augmentation in all RCRs, as it likely is cost-ineffective. Instead, we recommend augmentation in cases of poor tissue quality, which could lead to healing failure, revision surgery, and higher overall patient costs beyond the cost of adding augmentation. Similarly, we recommend augmentation for revision cases in which tendon healing has failed and tissue quality is poor. The goal is to prevent another failure.
Conclusion
PHA graft augmentation of single-row triple-loaded anchor repairs of the supraspinatus tendon improves the overall ultimate load to failure by 25%. There was no difference in gap formation after cyclic loading between augmented and nonaugmented repairs. This technique for arthroscopic augmentation can be used to improve initial biomechanical repair strength in tears at risk for failure.
Am J Orthop. 2016;45(7):E527-E533. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. 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.
2. Keener JD, Wei AS, Kim HM, et al. Revision arthroscopic rotator cuff repair: repair integrity and clinical outcome. J Bone Joint Surg Am. 2010;92(3):590-598.
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. Barber FA, Herbert MA, Schroeder FA, Aziz-Jacobo J, Mays MM, Rapley JH. Biomechanical advantages of triple-loaded suture anchors compared with double-row rotator cuff repairs. Arthroscopy. 2010;26(3):316-323.
5. Burkhart SS, Denard PJ, Konicek J, Hanypsiak BT. Biomechanical validation of load-sharing rip-stop fixation for the repair of tissue-deficient rotator cuff tears. Am J Sports Med. 2014;42(2):457-462.
6. Gupta AK, Hug K, Boggess B, Gavigan M, Toth AP. Massive or 2-tendon rotator cuff tears in active patients with minimal glenohumeral arthritis: clinical and radiographic outcomes of reconstruction using dermal tissue matrix xenograft. Am J Sports Med. 2013;41(4):872-879.
7. Ma CB, MacGillivray JD, Clabeaux J, Lee S, Otis JC. Biomechanical evaluation of arthroscopic rotator cuff stitches. J Bone Joint Surg Am. 2004;86(6):1211-1216.
8. Omae H, Steinmann SP, Zhao C, et al. Biomechanical effect of rotator cuff augmentation with an acellular dermal matrix graft: a cadaver study. Clin Biomech. 2012;27(8):789-792.
9. Shea KP, Obopilwe E, Sperling JW, Iannotti JP. A biomechanical analysis of gap formation and failure mechanics of a xenograft-reinforced rotator cuff repair in a cadaveric model. J Shoulder Elbow Surg. 2012;21(8):1072-1079.
10. Agrawal V. Healing rates for challenging rotator cuff tears utilizing an acellular human dermal reinforcement graft. Int J Shoulder Surg. 2012;6(2):36-44.
11. Beimers L, Lam PH, Murrell GA. The biomechanical effects of polytetrafluoroethylene suture augmentations in lateral-row rotator cuff repairs in an ovine model. J Shoulder Elbow Surg. 2014;23(10):1545-1552.
12. McCarron JA, Milks RA, Chen X, Iannotti JP, Derwin KA. Improved time-zero biomechanical properties using poly-L-lactic acid graft augmentation in a cadaveric rotator cuff repair model. J Shoulder Elbow Surg. 2010;19(5):688-696.
13. Proctor CS. Long-term successful arthroscopic repair of large and massive rotator cuff tears with a functional and degradable reinforcement device. J Shoulder Elbow Surg. 2014;23(10):1508-1513.
14. Misra SK, Valappil SP, Roy I, Boccaccini AR. Polyhydroxyalkanoate (PHA)/inorganic phase composites for tissue engineering applications. Biomacromolecules. 2006;7(8):2249-2258.
15. Ellis G, Cano P, Jadraque M, et al. Laser microperforated biodegradable microbial polyhydroxyalkanoate substrates for tissue repair strategies: an infrared microspectroscopy study. Anal Bioanal Chem. 2011;399(7):2379-2388.
16. Lenart BA, Martens KA, Kearns KA, Gillespie RJ, Zoga AC, Williams GR. Treatment of massive and recurrent rotator cuff tears augmented with a poly-l-lactide graft, a preliminary study. J Shoulder Elbow Surg. 2015;24(6):915-921.
17. Barber FA, Burns JP, Deutsch A, Labbé MR, Litchfield RB. A prospective, randomized evaluation of acellular human dermal matrix augmentation for arthroscopic rotator cuff repair. Arthroscopy. 2012;28(1):8-15.
18. Barber FA, Herbert MA, Boothby MH. Ultimate tensile failure loads of a human dermal allograft rotator cuff augmentation. Arthroscopy. 2008;24(1):20-24.
19. Gilot GJ, Attia AK, Alvarez AM. Arthroscopic repair of rotator cuff tears using extracellular matrix graft. Arthrosc Tech. 2014;3(4):e487-e489.
20. Barber FA, Coons DA, Ruiz-Suarez M. Cyclic load testing of biodegradable suture anchors containing 2 high-strength sutures. Arthroscopy. 2007;23(4):355-360.
21. Kullar RS, Reagan JM, Kolz CW, Burks RT, Henninger HB. Suture placement near the musculotendinous junction in the supraspinatus: implications for rotator cuff repair. Am J Sports Med. 2015;43(1):57-62.
22. Burkhart SS, Diaz Pagàn JL, Wirth MA, Athanasiou KA. Cyclic loading of anchor-based rotator cuff repairs: confirmation of the tension overload phenomenon and comparison of suture anchor fixation with transosseous fixation. Arthroscopy. 1997;13(6):720-724.
23. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007;39(2):175-191.
24. Greenspoon JA, Petri M, Warth RJ, Millett PJ. Massive rotator cuff tears: pathomechanics, current treatment options, and clinical outcomes. J Shoulder Elbow Surg. 2015;24(9):1493-1505.
25. Hein J, Reilly JM, Chae J, Maerz T, Anderson K. Retear rates after arthroscopic single-row, double-row, and suture bridge rotator cuff repair at a minimum of 1 year of imaging follow-up: a systematic review. Arthroscopy. 2015;31(11):2274-2281.
26. Henry P, Wasserstein D, Park S, et al. Arthroscopic repair for chronic massive rotator cuff tears: a systematic review. Arthroscopy. 2015;31(12):2472-2480.
27. El-Azab HM, Rott O, Irlenbusch U. Long-term follow-up after latissimus dorsi transfer for irreparable posterosuperior rotator cuff tears. J Bone Joint Surg Am. 2015;97(6):462-469.
28. Gerber C, Rahm SA, Catanzaro S, Farshad M, Moor BK. Latissimus dorsi tendon transfer for treatment of irreparable posterosuperior rotator cuff tears: long-term results at a minimum follow-up of ten years. J Bone Joint Surg Am. 2013;95(21):1920-1926.
29. Coons DA, Barber FA, Herbert MA. Triple-loaded single-anchor stitch configurations: an analysis of cyclically loaded suture–tendon interface security. Arthroscopy. 2006;22(11):1154-1158.
30. Itoi E, Berglund LJ, Grabowski JJ, et al. Tensile properties of the supraspinatus tendon. J Orthop Res. 1995;13(4):578-584.
31. Matsuhashi T, Hooke AW, Zhao KD, et al. Tensile properties of a morphologically split supraspinatus tendon. Clin Anat. 2014;27(5):702-706.
32. Apreleva M, Parsons IM 4th, Warner JJ, Fu FH, Woo SL. Experimental investigation of reaction forces at the glenohumeral joint during active abduction. J Shoulder Elbow Surg. 2000;9(5):409-417.
33. Giles JW, Ferreira LM, Athwal GS, Johnson JA. Development and performance evaluation of a multi-PID muscle loading driven in vitro active-motion shoulder simulator and application to assessing reverse total shoulder arthroplasty. J Biomech Eng. 2014;136(12):121007.
34. Hansen ML, Otis JC, Johnson JS, Cordasco FA, Craig EV, Warren RF. Biomechanics of massive rotator cuff tears: implications for treatment. J Bone Joint Surg Am. 2008;90(2):316-325.
35. Henninger HB, Barg A, Anderson AE, Bachus KN, Tashjian RZ, Burks RT. Effect of deltoid tension and humeral version in reverse total shoulder arthroplasty: a biomechanical study. J Shoulder Elbow Surg. 2012;21(4):483-490.
36. Mihata T, Gates J, McGarry MH, Lee J, Kinoshita M, Lee TQ. Effect of rotator cuff muscle imbalance on forceful internal impingement and peel-back of the superior labrum: a cadaveric study. Am J Sports Med. 2009;37(11):2222-2227.
37. Sano H, Ishii H, Yeadon A, Backman DS, Brunet JA, Uhthoff HK. Degeneration at the insertion weakens the tensile strength of the supraspinatus tendon: a comparative mechanical and histologic study of the bone–tendon complex. J Orthop Res. 1997;15(5):719-726.
Healing after rotator cuff repair (RCR) can be challenging, especially in cases of large and massive tears, revision repairs, and tendons with poor tissue quality.1-3 Poor tissue quality is associated with increased risk for recurrent tears, independent of age and tear size.3 Various techniques have been used to improve tendon fixation strength in these difficult situations, including augmented suture configurations (eg, massive cuff stitches, rip-stop stitches) and tissue grafts (eg, acellular dermal matrix).4-9 Clinical studies have found improved healing rates for larger tears and revision repairs using acellular dermal matrix grafts.6,10 Synthetic patches are another option for RCR augmentation, but limited clinical data and biomechanical evidence support use of synthetic grafts as an augment for RCRs.11-13
Polyhydroxyalkanoates (PHAs) are a class of biodegradable polymers that have been used as orthopedic devices, tissue scaffolds, patches, and other applications with increasing frequency over the past decade.14 In the laboratory, these implanted materials have been shown to support cell migration and growth.15 The PHA family of polymers typically degrades by hydrolytic and bacterial depolymerase mechanisms over 52-plus weeks in vivo.14PHA grafts have been studied in the setting of RCR. An expanded polytetrafluoroethylene scaffold was shown to improve repair mechanics when used as a bursal side graft in an in vitro ovine model.11 The graft increased tendon footprint contact pressure and failure loads by almost 180 N. In clinical studies, poly-L-lactic acid augmentations have been used to reinforce massive RCRs. Lenart and colleagues16 found that 38% of 16 patients with such tears had an intact rotator cuff at 1.2-year follow-up, and improvement in clinical scores. Proctor13 reported on use of a poly-L-lactic acid retrograde patch for reinforcement of massive tears with both single- and double-row repairs in 18 patients. The cohort had more favorable rates of intact cuffs at 12 months (83%) and 42 months (78%), and ASES (American Shoulder and Elbow Surgeons) scores improved from 25 before surgery to 82 at latest follow-up after surgery.
RCR augmentation traditionally has been performed with an open or mini-open technique.6 Recently, several authors have reported on arthroscopic techniques for augmentation with either acellular dermal matrix or synthetic grafts.13,17,18 Most techniques have involved “bridging” with a graft or patch used to stress-shield a single-row repair.8,9,13 This bridging typically involves placing several sutures medial to where the anchor repair stitches pass through the tendon. An alternative is to pass the repair stitches through both the tendon and the graft.17-19 The overall volume of tissue incorporated into the repair stitches (rotator cuff plus graft) is increased with the augmented technique relative to the bridging technique. Both can be technically challenging, but the augmented technique may be easier to perform arthroscopically.9,19 Regardless, these techniques are complicated and require a higher level of arthroscopic skills compared with those required in arthroscopic RCR without a graft. Simplifying arthroscopic graft augmentation likely will increase its utility because, even for skilled surgeons, adding a graft can increase operative time by 20 to 30 minutes. Simplification will also extend use of the technique to surgeons with less experience and proficiency with arthroscopic repair.
We developed a simple method for augmenting single-row RCR with a strip of bioresorbable soft-tissue scaffold. We also conducted a study to evaluate the initial biomechanical properties of single-row RCR in cadaveric shoulder specimens augmented with PHA mesh (BioFiber; Tornier) graft as compared with single-row RCR without augmentation. Both cyclic gap formation and ultimate failure loads and displacement were quantified. We hypothesized that the augmented RCRs would have decreased gap formation and increased ultimate failure loads compared with nonaugmented RCRs. This study was exempt from having to obtain Institutional Review B
Methods
Eight pairs of fresh-frozen cadaver humeri (6 male, 2 female; mean [SD] age, 61 [9] years) were dissected of all soft tissue (except rotator cuff) by Dr. Tashjian, a board-certified, fellowship-trained orthopedic surgeon. There were no qualitative differences in tendon condition between tendons within a pair. The supraspinatus muscle and tendon were separated from the other rotator cuff muscles. The infraspinatus, subscapularis, and teres minor were removed from the humerus. Last, the supraspinatus was resected at its insertion. Humeral pairs were then randomized into augmented and nonaugmented RCRs within each pair.
In the nonaugmented group, the supraspinatus was reattached to its insertion in a single-row RCR with 2 triple-loaded suture anchors (5.5-mm Insite FT Ti, No. 2 Force Fiber suture; Tornier) and 6 simple stitches (Figure 1A). Anchors were placed midway between the articular margin and the lateral edge of the greater tuberosity at about 45° to the bone surface.
In the contralateral shoulders, augmented RCRs were performed. Specimens were prepared exactly as they were for the nonaugmented RCRs, including anchor placement and suture passage. Before knot tying, RCRs were augmented with 2 strips of 13-mm × 23-mm PHA mesh (BioFiber) (Figure 1B). One strip was used to augment the 3 sutures of each anchor, overlying the residual tendon, to reinforce the tendon–knot interface. After each suture was passed through the supraspinatus tendon from the intra-articular surface, the stitch was passed through the strip of PHA mesh. Stitches were separated by 5 mm in each mesh strip. All 6 sutures were then tied with a Revo knot between the free end of each suture leg and the leg that passed through the tendon and mesh.
Each humerus was transected at the midshaft and potted and mounted in an Instron 1331 load frame with Model 8800 controller (Instron). A cryoclamp was used to grasp the supraspinatus muscle belly above the musculotendinous junction (Figure 2).
Three rows of 2-mm fiducial markers were affixed to the bone, tendon, and muscle belly with cyanoacrylate for tracking with a digital video system (DMAS Version 6.5; Spicatek) (Figure 3).21
A 0.1-MPa pre-stress (applied force/tendon cross-sectional area) was applied to each construct to determine the starting position for the deformation profile. Each repair underwent 1000 cycles of uniaxial load-controlled displacement between 0.1 and 1.0 MPa of effective stress at 1 Hz. Effective stress was determined as the ratio of applied force to cross-sectional area of the tendon at harvest to normalize the applied loads between tendons of varying size. During cyclic testing, gapping of more than 5 mm was defined as construct failure.22 After cyclic loading, each construct was loaded to failure at 1.0 mm/s. Ultimate failure load was defined as the highest load achieved at the maximum displacement before rapid decline in load supported by the construct.
Statistical Analysis
Paired t tests were used to compare the matched pairs of constructs. For all tests, significance was set at P ≤ .05. Post hoc power was calculated for significant results using G*Power Version 3.1.6.23 All data are presented as means (SDs).
Results
After 1000 cycles of displacement, mean (SD) gapping was 3.8 (0.9) mm for the nonaugmented repairs and 3.9 (1.1) mm for the PHA mesh–augmented repairs (P = .879) (Figure 4).
For the nonaugmented repairs, mean (SD) failure displacement was 6.3 (1.7) mm, and mean (SD) ultimate failure load was 472.1 (120.3) N. For the PHA-augmented repairs, failure displacement was 5.5 (1.9) mm, and ultimate failure load was 571.2 (173.0) N. There was no difference in failure displacement (P = .393), but there was a difference in ultimate failure load (P = .042; power = 0.57). During failure testing, mean (SD) tissue deformation was higher (P = .012; power = 0.83) for the PHA-augmented repairs, 1.2 (0.7) mm, than for the nonaugmented repairs, 0.8 (0.5) mm. Failures, which were consistent within pairs, were caused by tissue failure, with sutures pulling through the tissue (4 pairs) or single anchor pullout before ultimate tissue failure (4 pairs). Of the 4 failures with anchor pullout, 3 had anterior anchor pullout, and 1 had posterior anchor pullout. In all specimens with anchor pullout, the second anchor remained stable, and ultimate failure occurred with tissue tearing at the suture interface. There were no significant differences in any metrics between specimens that failed with intact anchors and specimens with single anchor pullout (P ≥ .122). Therefore, both groups were pooled for the failure analysis.
Discussion
RCR augmentation with a synthetic graft is a viable option for improving fixation strength of supraspinatus repairs, as shown in otherwise healthy tendon in the present study. Our hypothesis that there would be decreased gap formation with graft augmentation was not supported, whereas the hypothesis of increased failure loads with graft augmentation was supported. These findings may also be applicable in cases of large tears, revisions, and tendons with poor tissue quality. Simplification of graft application techniques will allow quick and easy arthroscopic augmentation.
Studies of RCRs for large or massive tears have reported retear rates of 25% to 79%.24-26 Latissimus dorsi tendon transfers also show promise in posterosuperior RCRs, with failure rates near 10%.27,28 Although use of PHA patches in RCR augmentation is relatively new, short-term and midterm failure rates are in the range of 20% to 60% in the few small cohorts currently being studied.13,16 It is possible that these rates may improve as indications, surgical experience, and techniques for use of PHA patches are further refined. Regardless, with PHA currently being used in practice, it is important to quantify the biomechanics of the augmentation as a baseline for its performance in reinforcing the tendon–suture interface.
We determined that the initial fixation strength of single-row repairs was higher with the addition of PHA synthetic grafts using a very simple technique. Single-row triple-loaded anchor repairs already provide high initial mechanical strength, and our results are similar to those of another study of this technique.29 Despite the already high mechanical strength of a triple-loaded anchor repair, PHA mesh increased ultimate strength by about 100 N (~25%). Of note, tissue elongation during failure was higher (P = .012; power = 0.83) in the PHA-augmented group (1.2 mm) than in the nonaugmented group (0.8 mm). This was not surprising—failure loads were almost 100 N higher in the PHA-augmented group than in the nonaugmented group. Consequently, much higher forces were placed on the muscle belly, likely resulting in additional elongation of the intact tissue medial to the repair construct.
The ultimate failure loads in our study compare favorably with the biomechanical strength of augmented repairs reported by others.8,9,18 Barber and colleagues18 evaluated an augmented single-row repair with 2 double-loaded suture anchors and an acellular dermal matrix graft. The ultimate failure load of the augmented repairs was 325 N. In contrast, Omae and colleagues8 tested a bridging single-row repair using 2 double-loaded suture anchors and an acellular dermal matrix graft. Ultimate failure load of the augmented repairs was 560 N, similar to our finding. Last, Shea and colleagues9 evaluated a bridging single-row repair using 2 double-loaded suture anchors and an acellular dermal matrix graft, with ultimate failure load of 429 N. The techniques in all 3 studies can be performed arthroscopically but are challenging and require multiple extra sutures and anchors that need management and tying. Our technique provides similar initial fixation strength, has no requirement for extra sutures or anchors, and is very simple to perform.
The supraspinatus tendon is estimated to fail between 800 N and 1000 N.30,31 Biomechanical shoulder simulators use supraspinatus forces in the range of 20 N to 200 N for scapular plane abduction.32-36 Therefore, the single-row repair failures in our study fell between functional and full-thickness failure loads. Studies on the mechanics of degenerated human supraspinatus tendon are limited, but there is evidence the mechanical properties of these tissues are inferior to those of healthy tendon.37 A 100-N increase in failure loads with PHA augmentation may prove highly significant in reinforcing the suture–tendon interface in degenerated tendons.
Adding the mesh did not have any effect on gapping at the repair site after cyclic loading. This finding suggests that construct gapping under cyclic loading is not a function of a reinforced knot–tendon interface but is instead caused by microtearing and cinching of the suture constructs in relation to the underlying bone. Tissue elongation likely was not a strong contributor to overall cyclic gapping, as elongation did not differ between the nonaugmented and augmented repairs (0.5 mm vs 0.7 mm; P = .276) and was small relative to the nearly 4 mm of construct gapping. Gapping may be affected by healing and integration of the mesh into the repaired tendon over time, but this effect could not be captured in the present study. Patients are initially immobilized and passive shoulder motion gradually introduced, in stark contrast to the immediate loading protocol in the present study. Regardless, the 25% increase in overall strength may be clinically important, especially in cases of difficult repair or poor tissue quality.
Our technique simplifies arthroscopic augmentation—stitches are passed through the rotator cuff in simple fashion. Before being tied, the limbs that were passed through the rotator cuff are removed through a cannula and then passed through the synthetic graft.
Study Limitations
This study had several limitations. First, it was a cadaveric biomechanical study that evaluated only time-zero biomechanical properties. Loads were normalized to tendon size, specimens were randomized between sides, and paired specimens were used to minimize the effects of tendon and bone quality on outcome metrics. In addition, donor tendons were representative of otherwise healthy tissue. Chronic tears and associated resorption/atrophy could have affected the magnitude of forces and gapping detected in this study. Theoretically, over time the tendon tissue will adhere to and grow into the mesh, which could minimize potential differences. Studies are needed to determine the effects of healing on long-term repair strength in affected patients. Last, all constructs were performed in open fashion to improve repeatability of construct placement and provide accessibility for Instron testing. Our technique did not directly replicate the arthroscopic approach, but, unlike other augmentation techniques, it is so simple that transition to all-arthroscopic augmentation is realistic.
Patch augmentation increases the cost of materials and operative time and should be considered a limitation of its utility. We do not recommend augmentation in all RCRs, as it likely is cost-ineffective. Instead, we recommend augmentation in cases of poor tissue quality, which could lead to healing failure, revision surgery, and higher overall patient costs beyond the cost of adding augmentation. Similarly, we recommend augmentation for revision cases in which tendon healing has failed and tissue quality is poor. The goal is to prevent another failure.
Conclusion
PHA graft augmentation of single-row triple-loaded anchor repairs of the supraspinatus tendon improves the overall ultimate load to failure by 25%. There was no difference in gap formation after cyclic loading between augmented and nonaugmented repairs. This technique for arthroscopic augmentation can be used to improve initial biomechanical repair strength in tears at risk for failure.
Am J Orthop. 2016;45(7):E527-E533. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Healing after rotator cuff repair (RCR) can be challenging, especially in cases of large and massive tears, revision repairs, and tendons with poor tissue quality.1-3 Poor tissue quality is associated with increased risk for recurrent tears, independent of age and tear size.3 Various techniques have been used to improve tendon fixation strength in these difficult situations, including augmented suture configurations (eg, massive cuff stitches, rip-stop stitches) and tissue grafts (eg, acellular dermal matrix).4-9 Clinical studies have found improved healing rates for larger tears and revision repairs using acellular dermal matrix grafts.6,10 Synthetic patches are another option for RCR augmentation, but limited clinical data and biomechanical evidence support use of synthetic grafts as an augment for RCRs.11-13
Polyhydroxyalkanoates (PHAs) are a class of biodegradable polymers that have been used as orthopedic devices, tissue scaffolds, patches, and other applications with increasing frequency over the past decade.14 In the laboratory, these implanted materials have been shown to support cell migration and growth.15 The PHA family of polymers typically degrades by hydrolytic and bacterial depolymerase mechanisms over 52-plus weeks in vivo.14PHA grafts have been studied in the setting of RCR. An expanded polytetrafluoroethylene scaffold was shown to improve repair mechanics when used as a bursal side graft in an in vitro ovine model.11 The graft increased tendon footprint contact pressure and failure loads by almost 180 N. In clinical studies, poly-L-lactic acid augmentations have been used to reinforce massive RCRs. Lenart and colleagues16 found that 38% of 16 patients with such tears had an intact rotator cuff at 1.2-year follow-up, and improvement in clinical scores. Proctor13 reported on use of a poly-L-lactic acid retrograde patch for reinforcement of massive tears with both single- and double-row repairs in 18 patients. The cohort had more favorable rates of intact cuffs at 12 months (83%) and 42 months (78%), and ASES (American Shoulder and Elbow Surgeons) scores improved from 25 before surgery to 82 at latest follow-up after surgery.
RCR augmentation traditionally has been performed with an open or mini-open technique.6 Recently, several authors have reported on arthroscopic techniques for augmentation with either acellular dermal matrix or synthetic grafts.13,17,18 Most techniques have involved “bridging” with a graft or patch used to stress-shield a single-row repair.8,9,13 This bridging typically involves placing several sutures medial to where the anchor repair stitches pass through the tendon. An alternative is to pass the repair stitches through both the tendon and the graft.17-19 The overall volume of tissue incorporated into the repair stitches (rotator cuff plus graft) is increased with the augmented technique relative to the bridging technique. Both can be technically challenging, but the augmented technique may be easier to perform arthroscopically.9,19 Regardless, these techniques are complicated and require a higher level of arthroscopic skills compared with those required in arthroscopic RCR without a graft. Simplifying arthroscopic graft augmentation likely will increase its utility because, even for skilled surgeons, adding a graft can increase operative time by 20 to 30 minutes. Simplification will also extend use of the technique to surgeons with less experience and proficiency with arthroscopic repair.
We developed a simple method for augmenting single-row RCR with a strip of bioresorbable soft-tissue scaffold. We also conducted a study to evaluate the initial biomechanical properties of single-row RCR in cadaveric shoulder specimens augmented with PHA mesh (BioFiber; Tornier) graft as compared with single-row RCR without augmentation. Both cyclic gap formation and ultimate failure loads and displacement were quantified. We hypothesized that the augmented RCRs would have decreased gap formation and increased ultimate failure loads compared with nonaugmented RCRs. This study was exempt from having to obtain Institutional Review B
Methods
Eight pairs of fresh-frozen cadaver humeri (6 male, 2 female; mean [SD] age, 61 [9] years) were dissected of all soft tissue (except rotator cuff) by Dr. Tashjian, a board-certified, fellowship-trained orthopedic surgeon. There were no qualitative differences in tendon condition between tendons within a pair. The supraspinatus muscle and tendon were separated from the other rotator cuff muscles. The infraspinatus, subscapularis, and teres minor were removed from the humerus. Last, the supraspinatus was resected at its insertion. Humeral pairs were then randomized into augmented and nonaugmented RCRs within each pair.
In the nonaugmented group, the supraspinatus was reattached to its insertion in a single-row RCR with 2 triple-loaded suture anchors (5.5-mm Insite FT Ti, No. 2 Force Fiber suture; Tornier) and 6 simple stitches (Figure 1A). Anchors were placed midway between the articular margin and the lateral edge of the greater tuberosity at about 45° to the bone surface.
In the contralateral shoulders, augmented RCRs were performed. Specimens were prepared exactly as they were for the nonaugmented RCRs, including anchor placement and suture passage. Before knot tying, RCRs were augmented with 2 strips of 13-mm × 23-mm PHA mesh (BioFiber) (Figure 1B). One strip was used to augment the 3 sutures of each anchor, overlying the residual tendon, to reinforce the tendon–knot interface. After each suture was passed through the supraspinatus tendon from the intra-articular surface, the stitch was passed through the strip of PHA mesh. Stitches were separated by 5 mm in each mesh strip. All 6 sutures were then tied with a Revo knot between the free end of each suture leg and the leg that passed through the tendon and mesh.
Each humerus was transected at the midshaft and potted and mounted in an Instron 1331 load frame with Model 8800 controller (Instron). A cryoclamp was used to grasp the supraspinatus muscle belly above the musculotendinous junction (Figure 2).
Three rows of 2-mm fiducial markers were affixed to the bone, tendon, and muscle belly with cyanoacrylate for tracking with a digital video system (DMAS Version 6.5; Spicatek) (Figure 3).21
A 0.1-MPa pre-stress (applied force/tendon cross-sectional area) was applied to each construct to determine the starting position for the deformation profile. Each repair underwent 1000 cycles of uniaxial load-controlled displacement between 0.1 and 1.0 MPa of effective stress at 1 Hz. Effective stress was determined as the ratio of applied force to cross-sectional area of the tendon at harvest to normalize the applied loads between tendons of varying size. During cyclic testing, gapping of more than 5 mm was defined as construct failure.22 After cyclic loading, each construct was loaded to failure at 1.0 mm/s. Ultimate failure load was defined as the highest load achieved at the maximum displacement before rapid decline in load supported by the construct.
Statistical Analysis
Paired t tests were used to compare the matched pairs of constructs. For all tests, significance was set at P ≤ .05. Post hoc power was calculated for significant results using G*Power Version 3.1.6.23 All data are presented as means (SDs).
Results
After 1000 cycles of displacement, mean (SD) gapping was 3.8 (0.9) mm for the nonaugmented repairs and 3.9 (1.1) mm for the PHA mesh–augmented repairs (P = .879) (Figure 4).
For the nonaugmented repairs, mean (SD) failure displacement was 6.3 (1.7) mm, and mean (SD) ultimate failure load was 472.1 (120.3) N. For the PHA-augmented repairs, failure displacement was 5.5 (1.9) mm, and ultimate failure load was 571.2 (173.0) N. There was no difference in failure displacement (P = .393), but there was a difference in ultimate failure load (P = .042; power = 0.57). During failure testing, mean (SD) tissue deformation was higher (P = .012; power = 0.83) for the PHA-augmented repairs, 1.2 (0.7) mm, than for the nonaugmented repairs, 0.8 (0.5) mm. Failures, which were consistent within pairs, were caused by tissue failure, with sutures pulling through the tissue (4 pairs) or single anchor pullout before ultimate tissue failure (4 pairs). Of the 4 failures with anchor pullout, 3 had anterior anchor pullout, and 1 had posterior anchor pullout. In all specimens with anchor pullout, the second anchor remained stable, and ultimate failure occurred with tissue tearing at the suture interface. There were no significant differences in any metrics between specimens that failed with intact anchors and specimens with single anchor pullout (P ≥ .122). Therefore, both groups were pooled for the failure analysis.
Discussion
RCR augmentation with a synthetic graft is a viable option for improving fixation strength of supraspinatus repairs, as shown in otherwise healthy tendon in the present study. Our hypothesis that there would be decreased gap formation with graft augmentation was not supported, whereas the hypothesis of increased failure loads with graft augmentation was supported. These findings may also be applicable in cases of large tears, revisions, and tendons with poor tissue quality. Simplification of graft application techniques will allow quick and easy arthroscopic augmentation.
Studies of RCRs for large or massive tears have reported retear rates of 25% to 79%.24-26 Latissimus dorsi tendon transfers also show promise in posterosuperior RCRs, with failure rates near 10%.27,28 Although use of PHA patches in RCR augmentation is relatively new, short-term and midterm failure rates are in the range of 20% to 60% in the few small cohorts currently being studied.13,16 It is possible that these rates may improve as indications, surgical experience, and techniques for use of PHA patches are further refined. Regardless, with PHA currently being used in practice, it is important to quantify the biomechanics of the augmentation as a baseline for its performance in reinforcing the tendon–suture interface.
We determined that the initial fixation strength of single-row repairs was higher with the addition of PHA synthetic grafts using a very simple technique. Single-row triple-loaded anchor repairs already provide high initial mechanical strength, and our results are similar to those of another study of this technique.29 Despite the already high mechanical strength of a triple-loaded anchor repair, PHA mesh increased ultimate strength by about 100 N (~25%). Of note, tissue elongation during failure was higher (P = .012; power = 0.83) in the PHA-augmented group (1.2 mm) than in the nonaugmented group (0.8 mm). This was not surprising—failure loads were almost 100 N higher in the PHA-augmented group than in the nonaugmented group. Consequently, much higher forces were placed on the muscle belly, likely resulting in additional elongation of the intact tissue medial to the repair construct.
The ultimate failure loads in our study compare favorably with the biomechanical strength of augmented repairs reported by others.8,9,18 Barber and colleagues18 evaluated an augmented single-row repair with 2 double-loaded suture anchors and an acellular dermal matrix graft. The ultimate failure load of the augmented repairs was 325 N. In contrast, Omae and colleagues8 tested a bridging single-row repair using 2 double-loaded suture anchors and an acellular dermal matrix graft. Ultimate failure load of the augmented repairs was 560 N, similar to our finding. Last, Shea and colleagues9 evaluated a bridging single-row repair using 2 double-loaded suture anchors and an acellular dermal matrix graft, with ultimate failure load of 429 N. The techniques in all 3 studies can be performed arthroscopically but are challenging and require multiple extra sutures and anchors that need management and tying. Our technique provides similar initial fixation strength, has no requirement for extra sutures or anchors, and is very simple to perform.
The supraspinatus tendon is estimated to fail between 800 N and 1000 N.30,31 Biomechanical shoulder simulators use supraspinatus forces in the range of 20 N to 200 N for scapular plane abduction.32-36 Therefore, the single-row repair failures in our study fell between functional and full-thickness failure loads. Studies on the mechanics of degenerated human supraspinatus tendon are limited, but there is evidence the mechanical properties of these tissues are inferior to those of healthy tendon.37 A 100-N increase in failure loads with PHA augmentation may prove highly significant in reinforcing the suture–tendon interface in degenerated tendons.
Adding the mesh did not have any effect on gapping at the repair site after cyclic loading. This finding suggests that construct gapping under cyclic loading is not a function of a reinforced knot–tendon interface but is instead caused by microtearing and cinching of the suture constructs in relation to the underlying bone. Tissue elongation likely was not a strong contributor to overall cyclic gapping, as elongation did not differ between the nonaugmented and augmented repairs (0.5 mm vs 0.7 mm; P = .276) and was small relative to the nearly 4 mm of construct gapping. Gapping may be affected by healing and integration of the mesh into the repaired tendon over time, but this effect could not be captured in the present study. Patients are initially immobilized and passive shoulder motion gradually introduced, in stark contrast to the immediate loading protocol in the present study. Regardless, the 25% increase in overall strength may be clinically important, especially in cases of difficult repair or poor tissue quality.
Our technique simplifies arthroscopic augmentation—stitches are passed through the rotator cuff in simple fashion. Before being tied, the limbs that were passed through the rotator cuff are removed through a cannula and then passed through the synthetic graft.
Study Limitations
This study had several limitations. First, it was a cadaveric biomechanical study that evaluated only time-zero biomechanical properties. Loads were normalized to tendon size, specimens were randomized between sides, and paired specimens were used to minimize the effects of tendon and bone quality on outcome metrics. In addition, donor tendons were representative of otherwise healthy tissue. Chronic tears and associated resorption/atrophy could have affected the magnitude of forces and gapping detected in this study. Theoretically, over time the tendon tissue will adhere to and grow into the mesh, which could minimize potential differences. Studies are needed to determine the effects of healing on long-term repair strength in affected patients. Last, all constructs were performed in open fashion to improve repeatability of construct placement and provide accessibility for Instron testing. Our technique did not directly replicate the arthroscopic approach, but, unlike other augmentation techniques, it is so simple that transition to all-arthroscopic augmentation is realistic.
Patch augmentation increases the cost of materials and operative time and should be considered a limitation of its utility. We do not recommend augmentation in all RCRs, as it likely is cost-ineffective. Instead, we recommend augmentation in cases of poor tissue quality, which could lead to healing failure, revision surgery, and higher overall patient costs beyond the cost of adding augmentation. Similarly, we recommend augmentation for revision cases in which tendon healing has failed and tissue quality is poor. The goal is to prevent another failure.
Conclusion
PHA graft augmentation of single-row triple-loaded anchor repairs of the supraspinatus tendon improves the overall ultimate load to failure by 25%. There was no difference in gap formation after cyclic loading between augmented and nonaugmented repairs. This technique for arthroscopic augmentation can be used to improve initial biomechanical repair strength in tears at risk for failure.
Am J Orthop. 2016;45(7):E527-E533. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. 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.
2. Keener JD, Wei AS, Kim HM, et al. Revision arthroscopic rotator cuff repair: repair integrity and clinical outcome. J Bone Joint Surg Am. 2010;92(3):590-598.
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. Barber FA, Herbert MA, Schroeder FA, Aziz-Jacobo J, Mays MM, Rapley JH. Biomechanical advantages of triple-loaded suture anchors compared with double-row rotator cuff repairs. Arthroscopy. 2010;26(3):316-323.
5. Burkhart SS, Denard PJ, Konicek J, Hanypsiak BT. Biomechanical validation of load-sharing rip-stop fixation for the repair of tissue-deficient rotator cuff tears. Am J Sports Med. 2014;42(2):457-462.
6. Gupta AK, Hug K, Boggess B, Gavigan M, Toth AP. Massive or 2-tendon rotator cuff tears in active patients with minimal glenohumeral arthritis: clinical and radiographic outcomes of reconstruction using dermal tissue matrix xenograft. Am J Sports Med. 2013;41(4):872-879.
7. Ma CB, MacGillivray JD, Clabeaux J, Lee S, Otis JC. Biomechanical evaluation of arthroscopic rotator cuff stitches. J Bone Joint Surg Am. 2004;86(6):1211-1216.
8. Omae H, Steinmann SP, Zhao C, et al. Biomechanical effect of rotator cuff augmentation with an acellular dermal matrix graft: a cadaver study. Clin Biomech. 2012;27(8):789-792.
9. Shea KP, Obopilwe E, Sperling JW, Iannotti JP. A biomechanical analysis of gap formation and failure mechanics of a xenograft-reinforced rotator cuff repair in a cadaveric model. J Shoulder Elbow Surg. 2012;21(8):1072-1079.
10. Agrawal V. Healing rates for challenging rotator cuff tears utilizing an acellular human dermal reinforcement graft. Int J Shoulder Surg. 2012;6(2):36-44.
11. Beimers L, Lam PH, Murrell GA. The biomechanical effects of polytetrafluoroethylene suture augmentations in lateral-row rotator cuff repairs in an ovine model. J Shoulder Elbow Surg. 2014;23(10):1545-1552.
12. McCarron JA, Milks RA, Chen X, Iannotti JP, Derwin KA. Improved time-zero biomechanical properties using poly-L-lactic acid graft augmentation in a cadaveric rotator cuff repair model. J Shoulder Elbow Surg. 2010;19(5):688-696.
13. Proctor CS. Long-term successful arthroscopic repair of large and massive rotator cuff tears with a functional and degradable reinforcement device. J Shoulder Elbow Surg. 2014;23(10):1508-1513.
14. Misra SK, Valappil SP, Roy I, Boccaccini AR. Polyhydroxyalkanoate (PHA)/inorganic phase composites for tissue engineering applications. Biomacromolecules. 2006;7(8):2249-2258.
15. Ellis G, Cano P, Jadraque M, et al. Laser microperforated biodegradable microbial polyhydroxyalkanoate substrates for tissue repair strategies: an infrared microspectroscopy study. Anal Bioanal Chem. 2011;399(7):2379-2388.
16. Lenart BA, Martens KA, Kearns KA, Gillespie RJ, Zoga AC, Williams GR. Treatment of massive and recurrent rotator cuff tears augmented with a poly-l-lactide graft, a preliminary study. J Shoulder Elbow Surg. 2015;24(6):915-921.
17. Barber FA, Burns JP, Deutsch A, Labbé MR, Litchfield RB. A prospective, randomized evaluation of acellular human dermal matrix augmentation for arthroscopic rotator cuff repair. Arthroscopy. 2012;28(1):8-15.
18. Barber FA, Herbert MA, Boothby MH. Ultimate tensile failure loads of a human dermal allograft rotator cuff augmentation. Arthroscopy. 2008;24(1):20-24.
19. Gilot GJ, Attia AK, Alvarez AM. Arthroscopic repair of rotator cuff tears using extracellular matrix graft. Arthrosc Tech. 2014;3(4):e487-e489.
20. Barber FA, Coons DA, Ruiz-Suarez M. Cyclic load testing of biodegradable suture anchors containing 2 high-strength sutures. Arthroscopy. 2007;23(4):355-360.
21. Kullar RS, Reagan JM, Kolz CW, Burks RT, Henninger HB. Suture placement near the musculotendinous junction in the supraspinatus: implications for rotator cuff repair. Am J Sports Med. 2015;43(1):57-62.
22. Burkhart SS, Diaz Pagàn JL, Wirth MA, Athanasiou KA. Cyclic loading of anchor-based rotator cuff repairs: confirmation of the tension overload phenomenon and comparison of suture anchor fixation with transosseous fixation. Arthroscopy. 1997;13(6):720-724.
23. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007;39(2):175-191.
24. Greenspoon JA, Petri M, Warth RJ, Millett PJ. Massive rotator cuff tears: pathomechanics, current treatment options, and clinical outcomes. J Shoulder Elbow Surg. 2015;24(9):1493-1505.
25. Hein J, Reilly JM, Chae J, Maerz T, Anderson K. Retear rates after arthroscopic single-row, double-row, and suture bridge rotator cuff repair at a minimum of 1 year of imaging follow-up: a systematic review. Arthroscopy. 2015;31(11):2274-2281.
26. Henry P, Wasserstein D, Park S, et al. Arthroscopic repair for chronic massive rotator cuff tears: a systematic review. Arthroscopy. 2015;31(12):2472-2480.
27. El-Azab HM, Rott O, Irlenbusch U. Long-term follow-up after latissimus dorsi transfer for irreparable posterosuperior rotator cuff tears. J Bone Joint Surg Am. 2015;97(6):462-469.
28. Gerber C, Rahm SA, Catanzaro S, Farshad M, Moor BK. Latissimus dorsi tendon transfer for treatment of irreparable posterosuperior rotator cuff tears: long-term results at a minimum follow-up of ten years. J Bone Joint Surg Am. 2013;95(21):1920-1926.
29. Coons DA, Barber FA, Herbert MA. Triple-loaded single-anchor stitch configurations: an analysis of cyclically loaded suture–tendon interface security. Arthroscopy. 2006;22(11):1154-1158.
30. Itoi E, Berglund LJ, Grabowski JJ, et al. Tensile properties of the supraspinatus tendon. J Orthop Res. 1995;13(4):578-584.
31. Matsuhashi T, Hooke AW, Zhao KD, et al. Tensile properties of a morphologically split supraspinatus tendon. Clin Anat. 2014;27(5):702-706.
32. Apreleva M, Parsons IM 4th, Warner JJ, Fu FH, Woo SL. Experimental investigation of reaction forces at the glenohumeral joint during active abduction. J Shoulder Elbow Surg. 2000;9(5):409-417.
33. Giles JW, Ferreira LM, Athwal GS, Johnson JA. Development and performance evaluation of a multi-PID muscle loading driven in vitro active-motion shoulder simulator and application to assessing reverse total shoulder arthroplasty. J Biomech Eng. 2014;136(12):121007.
34. Hansen ML, Otis JC, Johnson JS, Cordasco FA, Craig EV, Warren RF. Biomechanics of massive rotator cuff tears: implications for treatment. J Bone Joint Surg Am. 2008;90(2):316-325.
35. Henninger HB, Barg A, Anderson AE, Bachus KN, Tashjian RZ, Burks RT. Effect of deltoid tension and humeral version in reverse total shoulder arthroplasty: a biomechanical study. J Shoulder Elbow Surg. 2012;21(4):483-490.
36. Mihata T, Gates J, McGarry MH, Lee J, Kinoshita M, Lee TQ. Effect of rotator cuff muscle imbalance on forceful internal impingement and peel-back of the superior labrum: a cadaveric study. Am J Sports Med. 2009;37(11):2222-2227.
37. Sano H, Ishii H, Yeadon A, Backman DS, Brunet JA, Uhthoff HK. Degeneration at the insertion weakens the tensile strength of the supraspinatus tendon: a comparative mechanical and histologic study of the bone–tendon complex. J Orthop Res. 1997;15(5):719-726.
1. 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.
2. Keener JD, Wei AS, Kim HM, et al. Revision arthroscopic rotator cuff repair: repair integrity and clinical outcome. J Bone Joint Surg Am. 2010;92(3):590-598.
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. Barber FA, Herbert MA, Schroeder FA, Aziz-Jacobo J, Mays MM, Rapley JH. Biomechanical advantages of triple-loaded suture anchors compared with double-row rotator cuff repairs. Arthroscopy. 2010;26(3):316-323.
5. Burkhart SS, Denard PJ, Konicek J, Hanypsiak BT. Biomechanical validation of load-sharing rip-stop fixation for the repair of tissue-deficient rotator cuff tears. Am J Sports Med. 2014;42(2):457-462.
6. Gupta AK, Hug K, Boggess B, Gavigan M, Toth AP. Massive or 2-tendon rotator cuff tears in active patients with minimal glenohumeral arthritis: clinical and radiographic outcomes of reconstruction using dermal tissue matrix xenograft. Am J Sports Med. 2013;41(4):872-879.
7. Ma CB, MacGillivray JD, Clabeaux J, Lee S, Otis JC. Biomechanical evaluation of arthroscopic rotator cuff stitches. J Bone Joint Surg Am. 2004;86(6):1211-1216.
8. Omae H, Steinmann SP, Zhao C, et al. Biomechanical effect of rotator cuff augmentation with an acellular dermal matrix graft: a cadaver study. Clin Biomech. 2012;27(8):789-792.
9. Shea KP, Obopilwe E, Sperling JW, Iannotti JP. A biomechanical analysis of gap formation and failure mechanics of a xenograft-reinforced rotator cuff repair in a cadaveric model. J Shoulder Elbow Surg. 2012;21(8):1072-1079.
10. Agrawal V. Healing rates for challenging rotator cuff tears utilizing an acellular human dermal reinforcement graft. Int J Shoulder Surg. 2012;6(2):36-44.
11. Beimers L, Lam PH, Murrell GA. The biomechanical effects of polytetrafluoroethylene suture augmentations in lateral-row rotator cuff repairs in an ovine model. J Shoulder Elbow Surg. 2014;23(10):1545-1552.
12. McCarron JA, Milks RA, Chen X, Iannotti JP, Derwin KA. Improved time-zero biomechanical properties using poly-L-lactic acid graft augmentation in a cadaveric rotator cuff repair model. J Shoulder Elbow Surg. 2010;19(5):688-696.
13. Proctor CS. Long-term successful arthroscopic repair of large and massive rotator cuff tears with a functional and degradable reinforcement device. J Shoulder Elbow Surg. 2014;23(10):1508-1513.
14. Misra SK, Valappil SP, Roy I, Boccaccini AR. Polyhydroxyalkanoate (PHA)/inorganic phase composites for tissue engineering applications. Biomacromolecules. 2006;7(8):2249-2258.
15. Ellis G, Cano P, Jadraque M, et al. Laser microperforated biodegradable microbial polyhydroxyalkanoate substrates for tissue repair strategies: an infrared microspectroscopy study. Anal Bioanal Chem. 2011;399(7):2379-2388.
16. Lenart BA, Martens KA, Kearns KA, Gillespie RJ, Zoga AC, Williams GR. Treatment of massive and recurrent rotator cuff tears augmented with a poly-l-lactide graft, a preliminary study. J Shoulder Elbow Surg. 2015;24(6):915-921.
17. Barber FA, Burns JP, Deutsch A, Labbé MR, Litchfield RB. A prospective, randomized evaluation of acellular human dermal matrix augmentation for arthroscopic rotator cuff repair. Arthroscopy. 2012;28(1):8-15.
18. Barber FA, Herbert MA, Boothby MH. Ultimate tensile failure loads of a human dermal allograft rotator cuff augmentation. Arthroscopy. 2008;24(1):20-24.
19. Gilot GJ, Attia AK, Alvarez AM. Arthroscopic repair of rotator cuff tears using extracellular matrix graft. Arthrosc Tech. 2014;3(4):e487-e489.
20. Barber FA, Coons DA, Ruiz-Suarez M. Cyclic load testing of biodegradable suture anchors containing 2 high-strength sutures. Arthroscopy. 2007;23(4):355-360.
21. Kullar RS, Reagan JM, Kolz CW, Burks RT, Henninger HB. Suture placement near the musculotendinous junction in the supraspinatus: implications for rotator cuff repair. Am J Sports Med. 2015;43(1):57-62.
22. Burkhart SS, Diaz Pagàn JL, Wirth MA, Athanasiou KA. Cyclic loading of anchor-based rotator cuff repairs: confirmation of the tension overload phenomenon and comparison of suture anchor fixation with transosseous fixation. Arthroscopy. 1997;13(6):720-724.
23. Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007;39(2):175-191.
24. Greenspoon JA, Petri M, Warth RJ, Millett PJ. Massive rotator cuff tears: pathomechanics, current treatment options, and clinical outcomes. J Shoulder Elbow Surg. 2015;24(9):1493-1505.
25. Hein J, Reilly JM, Chae J, Maerz T, Anderson K. Retear rates after arthroscopic single-row, double-row, and suture bridge rotator cuff repair at a minimum of 1 year of imaging follow-up: a systematic review. Arthroscopy. 2015;31(11):2274-2281.
26. Henry P, Wasserstein D, Park S, et al. Arthroscopic repair for chronic massive rotator cuff tears: a systematic review. Arthroscopy. 2015;31(12):2472-2480.
27. El-Azab HM, Rott O, Irlenbusch U. Long-term follow-up after latissimus dorsi transfer for irreparable posterosuperior rotator cuff tears. J Bone Joint Surg Am. 2015;97(6):462-469.
28. Gerber C, Rahm SA, Catanzaro S, Farshad M, Moor BK. Latissimus dorsi tendon transfer for treatment of irreparable posterosuperior rotator cuff tears: long-term results at a minimum follow-up of ten years. J Bone Joint Surg Am. 2013;95(21):1920-1926.
29. Coons DA, Barber FA, Herbert MA. Triple-loaded single-anchor stitch configurations: an analysis of cyclically loaded suture–tendon interface security. Arthroscopy. 2006;22(11):1154-1158.
30. Itoi E, Berglund LJ, Grabowski JJ, et al. Tensile properties of the supraspinatus tendon. J Orthop Res. 1995;13(4):578-584.
31. Matsuhashi T, Hooke AW, Zhao KD, et al. Tensile properties of a morphologically split supraspinatus tendon. Clin Anat. 2014;27(5):702-706.
32. Apreleva M, Parsons IM 4th, Warner JJ, Fu FH, Woo SL. Experimental investigation of reaction forces at the glenohumeral joint during active abduction. J Shoulder Elbow Surg. 2000;9(5):409-417.
33. Giles JW, Ferreira LM, Athwal GS, Johnson JA. Development and performance evaluation of a multi-PID muscle loading driven in vitro active-motion shoulder simulator and application to assessing reverse total shoulder arthroplasty. J Biomech Eng. 2014;136(12):121007.
34. Hansen ML, Otis JC, Johnson JS, Cordasco FA, Craig EV, Warren RF. Biomechanics of massive rotator cuff tears: implications for treatment. J Bone Joint Surg Am. 2008;90(2):316-325.
35. Henninger HB, Barg A, Anderson AE, Bachus KN, Tashjian RZ, Burks RT. Effect of deltoid tension and humeral version in reverse total shoulder arthroplasty: a biomechanical study. J Shoulder Elbow Surg. 2012;21(4):483-490.
36. Mihata T, Gates J, McGarry MH, Lee J, Kinoshita M, Lee TQ. Effect of rotator cuff muscle imbalance on forceful internal impingement and peel-back of the superior labrum: a cadaveric study. Am J Sports Med. 2009;37(11):2222-2227.
37. Sano H, Ishii H, Yeadon A, Backman DS, Brunet JA, Uhthoff HK. Degeneration at the insertion weakens the tensile strength of the supraspinatus tendon: a comparative mechanical and histologic study of the bone–tendon complex. J Orthop Res. 1997;15(5):719-726.
T-Capsulotomy to Improve Visualization of the Peripheral Compartment and Repair
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The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
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An Update on Management of Syndesmosis Injury: A National US Database Study
Acute ankle injuries are common problems treated by orthopedic surgeons. In the United States, nearly 2 million ankle sprains occur each year,1 and ankle fractures account for 9% to 18% of all fractures treated in emergency departments.2,3 Ankle injuries that involve the syndesmotic ligaments may result in instability and require specific treatment beyond fixation of the malleolar fractures.
The usual mechanism of syndesmotic injury is external rotation of the ankle with hyperdorsiflexion of a pronated or supinated foot.4,5 Syndesmotic injuries are estimated to occur in up to 10% of ankle sprains6 and up to 23% of all ankle fractures.7 Overall US incidence of syndesmotic injury is estimated at 6445 injuries per year.8 Syndesmotic injury occurs in 39% to 45% of supination-external rotation IV ankle fractures.9,10 Pronation-external rotation ankle fractures have the highest rate of syndesmotic injury. Syndesmotic injury may be less common in other types of malleolar fracture, but the exact incidence has not been reliably reported.
Traditionally, isolated nondisplaced syndesmotic injuries are treated nonoperatively, and syndesmotic injuries with concomitant malleolar fractures are treated surgically. Various options are available for syndesmotic fixation. The gold standard is syndesmotic screw placement from the lateral aspect of the fibula through the tibia. Fixation may be achieved with screws in a variety of configurations and formats. However, fixation with two 4.5-mm screws is stronger.11,12 Functional outcomes are similar, regardless of screw material,13-16 number of cortices,17 or number of screws.18 Disadvantages specific to screw fixation include altered ankle biomechanics,19,20 potential for screw breakage,21 and need for implant removal.3Alternatively, suture button fixation is said to be equally as effective as screw fixation in achieving syndesmotic reduction, and their functional outcomes are similar.22,23 The initial cost of suture button fixation is higher than that of screw fixation, but the difference may be offset by potential elimination of a second surgery for syndesmotic screw removal.24 Soft-tissue irritation caused by the suture material and local osteolysis are reported complications of suture button fixation.25-27
Regardless of fixation method used, achieving anatomical reduction of the syndesmosis is considered the most important factor in optimizing functional outcomes.28-31 However, achieving and verifying anatomical reduction of the syndesmosis during surgery can be quite challenging.30,32-34 Various methods of lowering the malreduction risk, including direct visualization of the tibiofibular joint during reduction30,35 and intraoperative 3-dimensional imaging,33,36 have been proposed.
In the study reported here, we used a US insurance database to determine the incidence and rate of syndesmotic stabilization within various ankle injuries and fracture patterns.
Materials and Methods
All data for this study were obtained from a publicly available for-fee healthcare database, the PearlDiver Patient Records Database, which includes procedural volumes and demographic information for patients with International Classification of Diseases, Ninth Revision (ICD-9) diagnoses and procedures or Current Procedural Terminology (CPT) codes. Data for the study were derived from 2 databases within PearlDiver: a private-payer database, which has its largest contribution (>30 million individual patient records for 2007-2011) from United HealthCare, and a Medicare database (>50 million patient records for 2007-2011). Access to the database was granted by PearlDiver Technologies for the purpose of academic research. The database was stored on a password-protected server maintained by PearlDiver.
We searched the database for cases of ankle fracture fixation, including fixation of isolated lateral malleolus (CPT 27792), bimalleolar (CPT 27814), and trimalleolar (CPTs 27822 and 27823) fractures. CPT 27829 was used to search for syndesmotic fixation, and CPT 20680 for implant removal. These codes were used individually and in combination.
Overall procedural volume data are reported as number of patients with the given CPT(s) in the database output and as incidence, calculated as number of patients with the CPT of interest normalized to total number of patients in the database for that particular subgroup. Results of age group and sex analyses are reported as number of patients reported in the database output and as percentage of patients who had the CPT procedure of interest that year. As United HealthCare is the largest contributor to the private-payer portion of the database and is represented most prominently in the southern region, data for the regional analysis are presented only as incidence. This incidence was calculated as number of patients in a particular region and year normalized to total number of patients in the database for that region or year. The regions were Midwest (IA, IL, IN, KS, MI, MN, MO, ND, NE, OH, SD, WI), Northeast (CT, MA, ME, NH, NJ, NY, PA, RI, VT), South (AL, AR, DC, DE, FL, GA, KY, LA, MD, MI, NC, OK, SC, TN, TX, VA, WV), and West (AK, AZ, CA, CO, HI, ID, MT, NM, NV, OR, UT, WA, WY).
Chi-square linear-by-linear association analysis was used to determine the statistical significance of time trends in procedural volume, sex, age group, and region. For all statistical comparisons, P < .05 was considered significant.
Results
Number of open reduction and internal fixation (ORIF) procedures increased for all ankle fracture types over the period 2007 to 2011 (Table 1).
ORIF was performed for an ankle injury in 54,767 patients during the period 2007 to 2011, resulting in a cumulative incidence of 64.2 per 1000 patients (Table 2).
More ankle ORIF procedures were performed in females (33,565) than in males (21,202); incidence of ankle ORIF procedures was higher in females (68.6/1000 patients) than in males (58.4/1000 patients) (Table 2); percentages of bimalleolar and trimalleolar fractures were higher in females (bi, 40.6%; tri, 27.8%) than in males (bi, 34.6%; tri, 15.2%); and percentage of lateral malleolus fractures was higher in males (50.2%) than in females (31.6%).
Incidence of ankle ORIF procedures was similar in the South (69.6/1000 patients), Midwest (69.4/100 patients), and West (65.1/1000 patients) but lower in the Northeast (43.3/1000 patients) (Table 2). Lateral malleolus fractures were the most common ankle fractures in the Midwest (40.7%) and West (41.3%), followed by bimalleolar fractures (Midwest, 36.3%; West 36.0%) and trimalleolar fractures (Midwest, 23.0%; West, 22.7%). Bimalleolar fractures were most common in the Northeast (40.2%) and South (39.8%), followed by lateral malleolus fractures (Northeast, 34.4%; South, 38.0%) and trimalleolar fractures (Northeast, 25.4%; South, 22.3%).
Discussion
The present study found no significant change in number of lateral malleolus, bimalleolar, and trimalleolar ankle fracture ORIF procedures performed over the period 2007 to 2011. However, over the same period, incidence of syndesmosis fixation increased significantly in patients with isolated syndesmotic injuries and in patients with concomitant ankle fracture and syndesmotic injury. The largest percentage change was found in the bimalleolar ORIF group, which showed nearly a doubling of syndesmotic fixation over the 4-year study period, followed by a 38.1% increase in syndesmotic fixation in the trimalleolar ORIF group. Both groups had a syndesmotic fixation percentage change about twice that seen in the isolated lateral malleolus group.
There are several explanations for these trends. First, bimalleolar and trimalleolar fractures are more severe ankle fractures that tend to result from a more forceful mechanism, allowing for a higher rate of syndesmotic injury. Second, these trends likely do not reflect a true increase in the rate of syndesmosis injury but, rather, increased recognition of syndesmotic injury. Third, the data likely reflect a well-established approach to ankle fracture fixation and an increase in thinking that syndesmotic injuries should be stabilized in the setting of ankle fixation.
Incidence of syndesmotic injury as indicated by stabilization procedures can be compared with the data of Vosseller and colleagues,8 who reported an incidence of 6445 syndesmotic injuries per year in the United States. Our data showed fewer syndesmotic injuries, which may be related to use of CPT codes rather than ICD-9 codes for database searches, such that only operative syndesmotic injuries are represented in our data. Population differences between the 2 studies could also account for some of the differences in syndesmotic injury incidence.
We also found a significant change in the rate of hardware removal after syndesmosis ORIF. Across all treatment groups, incidence of screw removal decreased—a trend likely reflecting a change in attitude about the need for routine screw removal. Studies have shown that patients have favorable outcomes in the setting of syndesmotic screw loosening and screw breakage.37 Some authors have suggested that screw breakage or removal could be advantageous, as it allows the syndesmosis to settle into a more anatomical position after imperfect reduction.38 In addition, the trend of decreased syndesmotic screw removal could also have resulted from increased suture button fixation, which may less frequently require implant removal. Regardless, the overall trend is that routine syndesmotic implant removal has become less common.
This study had several limitations. First are the many limitations inherent to all studies that use large administrative databases, such as PearlDiver. The power of analysis depends on data quality; potential sources of error include accuracy of billing codes and physicians’ miscoding or noncoding. Although we tried to accurately represent a large population of interest through use of this database, we cannot be sure that the database represents a true cross-section of the United States. In addition, as we could not determine the method of syndesmotic fixation—the same CPT code is used for both suture button fixation and screw fixation—we could not establish trends for the rate of each method. More research is needed to establish these trends, and this research likely will require analysis of data from a large trauma center or from multiple centers.
Potential regional differences are another limitation. In the PearlDiver database, the South and Midwest are highly represented, the Northeast and West much less so. The South, Midwest, and West (but not the Northeast) had similar overall incidence and subgroup incidence of ankle ORIF. However, any regional differences in the rate of syndesmotic fixation could have skewed our data.
Ankle fractures and associated syndesmotic injuries remain a common problem. Although the prevalence of ankle fracture fixation has been relatively constant, the rate of syndesmosis stabilization has increased significantly. Young adults have the highest incidence of ankle fracture and associated syndesmotic fixation, but more ankle fractures occur in the large and growing elderly population. Increased awareness of syndesmotic injury likely has contributed to the recent rise in syndesmosis fixation seen in the present study. Given this trend, we recommend further analysis of outcome data and to establish treatment guidelines.
Am J Orthop. 2016;45(7):E472-E477. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Waterman BR, Owens BD, Davey S, Zacchilli MA, Belmont PJ Jr. The epidemiology of ankle sprains in the United States. J Bone Joint Surg Am. 2010;92(13):2279-2284.
2. Court-Brown CM, Caesar B. Epidemiology of adult fractures: a review. Injury. 2006;37(8):691-697.
3. Miller AN, Paul O, Boraiah S, Parker RJ, Helfet DL, Lorich DG. Functional outcomes after syndesmotic screw fixation and removal. J Orthop Trauma. 2010;24(1):12-16.
4. Edwards GS Jr, DeLee JC. Ankle diastasis without fracture. Foot Ankle. 1984;4(6):305-312.
5. Norkus SA, Floyd RT. The anatomy and mechanisms of syndesmotic ankle sprains. J Athl Train. 2001;36(1):68-73.
6. Brosky T, Nyland J, Nitz A, Caborn DN. The ankle ligaments: consideration of syndesmotic injury and implications for rehabilitation. J Orthop Sports Phys Ther. 1995;21(4):197-205.
7. Purvis GD. Displaced, unstable ankle fractures: classification, incidence, and management of a consecutive series. Clin Orthop Relat Res. 1982;(165):91-98.
8. Vosseller JT, Karl JW, Greisberg JK. Incidence of syndesmotic injury. Orthopedics. 2014;37(3):e226-e229.
9. Stark E, Tornetta P 3rd, Creevy WR. Syndesmotic instability in Weber B ankle fractures: a clinical evaluation. J Orthop Trauma. 2007;21(9):643-646.
10. Tornetta P 3rd, Axelrad TW, Sibai TA, Creevy WR. Treatment of the stress positive ligamentous SE4 ankle fracture: incidence of syndesmotic injury and clinical decision making. J Orthop Trauma. 2012;26(11):659-661.
11. Xenos JS, Hopkinson WJ, Mulligan ME, Olson EJ, Popovic NA. The tibiofibular syndesmosis. Evaluation of the ligamentous structures, methods of fixation, and radiographic assessment. J Bone Joint Surg Am. 1995;77(6):847-856.
12. Ebraheim NA, Lu J, Yang H, Mekhail AO, Yeasting RA. Radiographic and CT evaluation of tibiofibular syndesmotic diastasis: a cadaver study. Foot Ankle Int. 1997;18(11):693-698.
13. Ahmad J, Raikin SM, Pour AE, Haytmanek C. Bioabsorbable screw fixation of the syndesmosis in unstable ankle injuries. Foot Ankle Int. 2009;30(2):99-105.
14. Hovis WD, Kaiser BW, Watson JT, Bucholz RW. Treatment of syndesmotic disruptions of the ankle with bioabsorbable screw fixation. J Bone Joint Surg Am. 2002;84(1):26-31.
15. Kaukonen JP, Lamberg T, Korkala O, Pajarinen J. Fixation of syndesmotic ruptures in 38 patients with a malleolar fracture: a randomized study comparing a metallic and a bioabsorbable screw. J Orthop Trauma. 2005;19(6):392-395.
16. Thordarson DB, Samuelson M, Shepherd LE, Merkle PF, Lee J. Bioabsorbable versus stainless steel screw fixation of the syndesmosis in pronation-lateral rotation ankle fractures: a prospective randomized trial. Foot Ankle Int. 2001;22(4):335-338.
17. Moore JA Jr, Shank JR, Morgan SJ, Smith WR. Syndesmosis fixation: a comparison of three and four cortices of screw fixation without hardware removal. Foot Ankle Int. 2006;27(8):567-572.
18. Høiness P, Strømsøe K. Tricortical versus quadricortical syndesmosis fixation in ankle fractures: a prospective, randomized study comparing two methods of syndesmosis fixation. J Orthop Trauma. 2004;18(6):331-337.
19. Huber T, Schmoelz W, Bölderl A. Motion of the fibula relative to the tibia and its alterations with syndesmosis screws: a cadaver study. Foot Ankle Surg. 2012;18(3):203-209.
20. Needleman RL, Skrade DA, Stiehl JB. Effect of the syndesmotic screw on ankle motion. Foot Ankle. 1989;10(1):17-24.
21. Mendelsohn ES, Hoshino CM, Harris TG, Zinar DM. The effect of obesity on early failure after operative syndesmosis injuries. J Orthop Trauma. 2013;27(4):201-206.
22. Schepers T. Acute distal tibiofibular syndesmosis injury: a systematic review of suture-button versus syndesmotic screw repair. Int Orthop. 2012;36(6):1199-1206.
23. Cottom JM, Hyer CF, Philbin TM, Berlet GC. Transosseous fixation of the distal tibiofibular syndesmosis: comparison of an interosseous suture and Endobutton to traditional screw fixation in 50 cases. J Foot Ankle Surg. 2009;48(6):620-630.
24. Thornes B, Shannon F, Guiney AM, Hession P, Masterson E. Suture-button syndesmosis fixation: accelerated rehabilitation and improved outcomes. Clin Orthop Relat Res. 2005;(431):207-212.
25. Willmott HJ, Singh B, David LA. Outcome and complications of treatment of ankle diastasis with tightrope fixation. Injury. 2009;40(11):1204-1206.
26. Qamar F, Kadakia A, Venkateswaran B. An anatomical way of treating ankle syndesmotic injuries. J Foot Ankle Surg. 2011;50(6):762-765.
27. Degroot H, Al-Omari AA, El Ghazaly SA. Outcomes of suture button repair of the distal tibiofibular syndesmosis. Foot Ankle Int. 2011;32(3):250-256.
28. Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg Am. 1976;58(3):356-357.
29. Weening B, Bhandari M. Predictors of functional outcome following transsyndesmotic screw fixation of ankle fractures. J Orthop Trauma. 2005;19(2):102-108.
30. Sagi HC, Shah AR, Sanders RW. The functional consequence of syndesmotic joint malreduction at a minimum 2-year follow-up. J Orthop Trauma. 2012;26(7):439-443.
31. Naqvi GA, Cunningham P, Lynch B, Galvin R, Awan N. Fixation of ankle syndesmotic injuries: comparison of tightrope fixation and syndesmotic screw fixation for accuracy of syndesmotic reduction. Am J Sports Med. 2012;40(12):2828-2835.
32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.
33. Franke J, von Recum J, Suda AJ, Grützner PA, Wendl K. Intraoperative three-dimensional imaging in the treatment of acute unstable syndesmotic injuries. J Bone Joint Surg Am. 2012;94(15):1386-1390.
34. Gardner MJ, Demetrakopoulos D, Briggs SM, Helfet DL, Lorich DG. Malreduction of the tibiofibular syndesmosis in ankle fractures. Foot Ankle Int. 2006;27(10):788-792.
35. Miller AN, Carroll EA, Parker RJ, Boraiah S, Helfet DL, Lorich DG. Direct visualization for syndesmotic stabilization of ankle fractures. Foot Ankle Int. 2009;30(5):419-426.
36. Ruan Z, Luo C, Shi Z, Zhang B, Zeng B, Zhang C. Intraoperative reduction of distal tibiofibular joint aided by three-dimensional fluoroscopy. Technol Health Care. 2011;19(3):161-166.
37. Hamid N, Loeffler BJ, Braddy W, Kellam JF, Cohen BE, Bosse MJ. Outcome after fixation of ankle fractures with an injury to the syndesmosis: the effect of the syndesmosis screw. J Bone Joint Surg Br. 2009;91(8):1069-1073.
38. Song DJ, Lanzi JT, Groth AT, et al. The effect of syndesmosis screw removal on the reduction of the distal tibiofibular joint: a prospective radiographic study. Foot Ankle Int. 2014;35(6):543-548.
Acute ankle injuries are common problems treated by orthopedic surgeons. In the United States, nearly 2 million ankle sprains occur each year,1 and ankle fractures account for 9% to 18% of all fractures treated in emergency departments.2,3 Ankle injuries that involve the syndesmotic ligaments may result in instability and require specific treatment beyond fixation of the malleolar fractures.
The usual mechanism of syndesmotic injury is external rotation of the ankle with hyperdorsiflexion of a pronated or supinated foot.4,5 Syndesmotic injuries are estimated to occur in up to 10% of ankle sprains6 and up to 23% of all ankle fractures.7 Overall US incidence of syndesmotic injury is estimated at 6445 injuries per year.8 Syndesmotic injury occurs in 39% to 45% of supination-external rotation IV ankle fractures.9,10 Pronation-external rotation ankle fractures have the highest rate of syndesmotic injury. Syndesmotic injury may be less common in other types of malleolar fracture, but the exact incidence has not been reliably reported.
Traditionally, isolated nondisplaced syndesmotic injuries are treated nonoperatively, and syndesmotic injuries with concomitant malleolar fractures are treated surgically. Various options are available for syndesmotic fixation. The gold standard is syndesmotic screw placement from the lateral aspect of the fibula through the tibia. Fixation may be achieved with screws in a variety of configurations and formats. However, fixation with two 4.5-mm screws is stronger.11,12 Functional outcomes are similar, regardless of screw material,13-16 number of cortices,17 or number of screws.18 Disadvantages specific to screw fixation include altered ankle biomechanics,19,20 potential for screw breakage,21 and need for implant removal.3Alternatively, suture button fixation is said to be equally as effective as screw fixation in achieving syndesmotic reduction, and their functional outcomes are similar.22,23 The initial cost of suture button fixation is higher than that of screw fixation, but the difference may be offset by potential elimination of a second surgery for syndesmotic screw removal.24 Soft-tissue irritation caused by the suture material and local osteolysis are reported complications of suture button fixation.25-27
Regardless of fixation method used, achieving anatomical reduction of the syndesmosis is considered the most important factor in optimizing functional outcomes.28-31 However, achieving and verifying anatomical reduction of the syndesmosis during surgery can be quite challenging.30,32-34 Various methods of lowering the malreduction risk, including direct visualization of the tibiofibular joint during reduction30,35 and intraoperative 3-dimensional imaging,33,36 have been proposed.
In the study reported here, we used a US insurance database to determine the incidence and rate of syndesmotic stabilization within various ankle injuries and fracture patterns.
Materials and Methods
All data for this study were obtained from a publicly available for-fee healthcare database, the PearlDiver Patient Records Database, which includes procedural volumes and demographic information for patients with International Classification of Diseases, Ninth Revision (ICD-9) diagnoses and procedures or Current Procedural Terminology (CPT) codes. Data for the study were derived from 2 databases within PearlDiver: a private-payer database, which has its largest contribution (>30 million individual patient records for 2007-2011) from United HealthCare, and a Medicare database (>50 million patient records for 2007-2011). Access to the database was granted by PearlDiver Technologies for the purpose of academic research. The database was stored on a password-protected server maintained by PearlDiver.
We searched the database for cases of ankle fracture fixation, including fixation of isolated lateral malleolus (CPT 27792), bimalleolar (CPT 27814), and trimalleolar (CPTs 27822 and 27823) fractures. CPT 27829 was used to search for syndesmotic fixation, and CPT 20680 for implant removal. These codes were used individually and in combination.
Overall procedural volume data are reported as number of patients with the given CPT(s) in the database output and as incidence, calculated as number of patients with the CPT of interest normalized to total number of patients in the database for that particular subgroup. Results of age group and sex analyses are reported as number of patients reported in the database output and as percentage of patients who had the CPT procedure of interest that year. As United HealthCare is the largest contributor to the private-payer portion of the database and is represented most prominently in the southern region, data for the regional analysis are presented only as incidence. This incidence was calculated as number of patients in a particular region and year normalized to total number of patients in the database for that region or year. The regions were Midwest (IA, IL, IN, KS, MI, MN, MO, ND, NE, OH, SD, WI), Northeast (CT, MA, ME, NH, NJ, NY, PA, RI, VT), South (AL, AR, DC, DE, FL, GA, KY, LA, MD, MI, NC, OK, SC, TN, TX, VA, WV), and West (AK, AZ, CA, CO, HI, ID, MT, NM, NV, OR, UT, WA, WY).
Chi-square linear-by-linear association analysis was used to determine the statistical significance of time trends in procedural volume, sex, age group, and region. For all statistical comparisons, P < .05 was considered significant.
Results
Number of open reduction and internal fixation (ORIF) procedures increased for all ankle fracture types over the period 2007 to 2011 (Table 1).
ORIF was performed for an ankle injury in 54,767 patients during the period 2007 to 2011, resulting in a cumulative incidence of 64.2 per 1000 patients (Table 2).
More ankle ORIF procedures were performed in females (33,565) than in males (21,202); incidence of ankle ORIF procedures was higher in females (68.6/1000 patients) than in males (58.4/1000 patients) (Table 2); percentages of bimalleolar and trimalleolar fractures were higher in females (bi, 40.6%; tri, 27.8%) than in males (bi, 34.6%; tri, 15.2%); and percentage of lateral malleolus fractures was higher in males (50.2%) than in females (31.6%).
Incidence of ankle ORIF procedures was similar in the South (69.6/1000 patients), Midwest (69.4/100 patients), and West (65.1/1000 patients) but lower in the Northeast (43.3/1000 patients) (Table 2). Lateral malleolus fractures were the most common ankle fractures in the Midwest (40.7%) and West (41.3%), followed by bimalleolar fractures (Midwest, 36.3%; West 36.0%) and trimalleolar fractures (Midwest, 23.0%; West, 22.7%). Bimalleolar fractures were most common in the Northeast (40.2%) and South (39.8%), followed by lateral malleolus fractures (Northeast, 34.4%; South, 38.0%) and trimalleolar fractures (Northeast, 25.4%; South, 22.3%).
Discussion
The present study found no significant change in number of lateral malleolus, bimalleolar, and trimalleolar ankle fracture ORIF procedures performed over the period 2007 to 2011. However, over the same period, incidence of syndesmosis fixation increased significantly in patients with isolated syndesmotic injuries and in patients with concomitant ankle fracture and syndesmotic injury. The largest percentage change was found in the bimalleolar ORIF group, which showed nearly a doubling of syndesmotic fixation over the 4-year study period, followed by a 38.1% increase in syndesmotic fixation in the trimalleolar ORIF group. Both groups had a syndesmotic fixation percentage change about twice that seen in the isolated lateral malleolus group.
There are several explanations for these trends. First, bimalleolar and trimalleolar fractures are more severe ankle fractures that tend to result from a more forceful mechanism, allowing for a higher rate of syndesmotic injury. Second, these trends likely do not reflect a true increase in the rate of syndesmosis injury but, rather, increased recognition of syndesmotic injury. Third, the data likely reflect a well-established approach to ankle fracture fixation and an increase in thinking that syndesmotic injuries should be stabilized in the setting of ankle fixation.
Incidence of syndesmotic injury as indicated by stabilization procedures can be compared with the data of Vosseller and colleagues,8 who reported an incidence of 6445 syndesmotic injuries per year in the United States. Our data showed fewer syndesmotic injuries, which may be related to use of CPT codes rather than ICD-9 codes for database searches, such that only operative syndesmotic injuries are represented in our data. Population differences between the 2 studies could also account for some of the differences in syndesmotic injury incidence.
We also found a significant change in the rate of hardware removal after syndesmosis ORIF. Across all treatment groups, incidence of screw removal decreased—a trend likely reflecting a change in attitude about the need for routine screw removal. Studies have shown that patients have favorable outcomes in the setting of syndesmotic screw loosening and screw breakage.37 Some authors have suggested that screw breakage or removal could be advantageous, as it allows the syndesmosis to settle into a more anatomical position after imperfect reduction.38 In addition, the trend of decreased syndesmotic screw removal could also have resulted from increased suture button fixation, which may less frequently require implant removal. Regardless, the overall trend is that routine syndesmotic implant removal has become less common.
This study had several limitations. First are the many limitations inherent to all studies that use large administrative databases, such as PearlDiver. The power of analysis depends on data quality; potential sources of error include accuracy of billing codes and physicians’ miscoding or noncoding. Although we tried to accurately represent a large population of interest through use of this database, we cannot be sure that the database represents a true cross-section of the United States. In addition, as we could not determine the method of syndesmotic fixation—the same CPT code is used for both suture button fixation and screw fixation—we could not establish trends for the rate of each method. More research is needed to establish these trends, and this research likely will require analysis of data from a large trauma center or from multiple centers.
Potential regional differences are another limitation. In the PearlDiver database, the South and Midwest are highly represented, the Northeast and West much less so. The South, Midwest, and West (but not the Northeast) had similar overall incidence and subgroup incidence of ankle ORIF. However, any regional differences in the rate of syndesmotic fixation could have skewed our data.
Ankle fractures and associated syndesmotic injuries remain a common problem. Although the prevalence of ankle fracture fixation has been relatively constant, the rate of syndesmosis stabilization has increased significantly. Young adults have the highest incidence of ankle fracture and associated syndesmotic fixation, but more ankle fractures occur in the large and growing elderly population. Increased awareness of syndesmotic injury likely has contributed to the recent rise in syndesmosis fixation seen in the present study. Given this trend, we recommend further analysis of outcome data and to establish treatment guidelines.
Am J Orthop. 2016;45(7):E472-E477. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Acute ankle injuries are common problems treated by orthopedic surgeons. In the United States, nearly 2 million ankle sprains occur each year,1 and ankle fractures account for 9% to 18% of all fractures treated in emergency departments.2,3 Ankle injuries that involve the syndesmotic ligaments may result in instability and require specific treatment beyond fixation of the malleolar fractures.
The usual mechanism of syndesmotic injury is external rotation of the ankle with hyperdorsiflexion of a pronated or supinated foot.4,5 Syndesmotic injuries are estimated to occur in up to 10% of ankle sprains6 and up to 23% of all ankle fractures.7 Overall US incidence of syndesmotic injury is estimated at 6445 injuries per year.8 Syndesmotic injury occurs in 39% to 45% of supination-external rotation IV ankle fractures.9,10 Pronation-external rotation ankle fractures have the highest rate of syndesmotic injury. Syndesmotic injury may be less common in other types of malleolar fracture, but the exact incidence has not been reliably reported.
Traditionally, isolated nondisplaced syndesmotic injuries are treated nonoperatively, and syndesmotic injuries with concomitant malleolar fractures are treated surgically. Various options are available for syndesmotic fixation. The gold standard is syndesmotic screw placement from the lateral aspect of the fibula through the tibia. Fixation may be achieved with screws in a variety of configurations and formats. However, fixation with two 4.5-mm screws is stronger.11,12 Functional outcomes are similar, regardless of screw material,13-16 number of cortices,17 or number of screws.18 Disadvantages specific to screw fixation include altered ankle biomechanics,19,20 potential for screw breakage,21 and need for implant removal.3Alternatively, suture button fixation is said to be equally as effective as screw fixation in achieving syndesmotic reduction, and their functional outcomes are similar.22,23 The initial cost of suture button fixation is higher than that of screw fixation, but the difference may be offset by potential elimination of a second surgery for syndesmotic screw removal.24 Soft-tissue irritation caused by the suture material and local osteolysis are reported complications of suture button fixation.25-27
Regardless of fixation method used, achieving anatomical reduction of the syndesmosis is considered the most important factor in optimizing functional outcomes.28-31 However, achieving and verifying anatomical reduction of the syndesmosis during surgery can be quite challenging.30,32-34 Various methods of lowering the malreduction risk, including direct visualization of the tibiofibular joint during reduction30,35 and intraoperative 3-dimensional imaging,33,36 have been proposed.
In the study reported here, we used a US insurance database to determine the incidence and rate of syndesmotic stabilization within various ankle injuries and fracture patterns.
Materials and Methods
All data for this study were obtained from a publicly available for-fee healthcare database, the PearlDiver Patient Records Database, which includes procedural volumes and demographic information for patients with International Classification of Diseases, Ninth Revision (ICD-9) diagnoses and procedures or Current Procedural Terminology (CPT) codes. Data for the study were derived from 2 databases within PearlDiver: a private-payer database, which has its largest contribution (>30 million individual patient records for 2007-2011) from United HealthCare, and a Medicare database (>50 million patient records for 2007-2011). Access to the database was granted by PearlDiver Technologies for the purpose of academic research. The database was stored on a password-protected server maintained by PearlDiver.
We searched the database for cases of ankle fracture fixation, including fixation of isolated lateral malleolus (CPT 27792), bimalleolar (CPT 27814), and trimalleolar (CPTs 27822 and 27823) fractures. CPT 27829 was used to search for syndesmotic fixation, and CPT 20680 for implant removal. These codes were used individually and in combination.
Overall procedural volume data are reported as number of patients with the given CPT(s) in the database output and as incidence, calculated as number of patients with the CPT of interest normalized to total number of patients in the database for that particular subgroup. Results of age group and sex analyses are reported as number of patients reported in the database output and as percentage of patients who had the CPT procedure of interest that year. As United HealthCare is the largest contributor to the private-payer portion of the database and is represented most prominently in the southern region, data for the regional analysis are presented only as incidence. This incidence was calculated as number of patients in a particular region and year normalized to total number of patients in the database for that region or year. The regions were Midwest (IA, IL, IN, KS, MI, MN, MO, ND, NE, OH, SD, WI), Northeast (CT, MA, ME, NH, NJ, NY, PA, RI, VT), South (AL, AR, DC, DE, FL, GA, KY, LA, MD, MI, NC, OK, SC, TN, TX, VA, WV), and West (AK, AZ, CA, CO, HI, ID, MT, NM, NV, OR, UT, WA, WY).
Chi-square linear-by-linear association analysis was used to determine the statistical significance of time trends in procedural volume, sex, age group, and region. For all statistical comparisons, P < .05 was considered significant.
Results
Number of open reduction and internal fixation (ORIF) procedures increased for all ankle fracture types over the period 2007 to 2011 (Table 1).
ORIF was performed for an ankle injury in 54,767 patients during the period 2007 to 2011, resulting in a cumulative incidence of 64.2 per 1000 patients (Table 2).
More ankle ORIF procedures were performed in females (33,565) than in males (21,202); incidence of ankle ORIF procedures was higher in females (68.6/1000 patients) than in males (58.4/1000 patients) (Table 2); percentages of bimalleolar and trimalleolar fractures were higher in females (bi, 40.6%; tri, 27.8%) than in males (bi, 34.6%; tri, 15.2%); and percentage of lateral malleolus fractures was higher in males (50.2%) than in females (31.6%).
Incidence of ankle ORIF procedures was similar in the South (69.6/1000 patients), Midwest (69.4/100 patients), and West (65.1/1000 patients) but lower in the Northeast (43.3/1000 patients) (Table 2). Lateral malleolus fractures were the most common ankle fractures in the Midwest (40.7%) and West (41.3%), followed by bimalleolar fractures (Midwest, 36.3%; West 36.0%) and trimalleolar fractures (Midwest, 23.0%; West, 22.7%). Bimalleolar fractures were most common in the Northeast (40.2%) and South (39.8%), followed by lateral malleolus fractures (Northeast, 34.4%; South, 38.0%) and trimalleolar fractures (Northeast, 25.4%; South, 22.3%).
Discussion
The present study found no significant change in number of lateral malleolus, bimalleolar, and trimalleolar ankle fracture ORIF procedures performed over the period 2007 to 2011. However, over the same period, incidence of syndesmosis fixation increased significantly in patients with isolated syndesmotic injuries and in patients with concomitant ankle fracture and syndesmotic injury. The largest percentage change was found in the bimalleolar ORIF group, which showed nearly a doubling of syndesmotic fixation over the 4-year study period, followed by a 38.1% increase in syndesmotic fixation in the trimalleolar ORIF group. Both groups had a syndesmotic fixation percentage change about twice that seen in the isolated lateral malleolus group.
There are several explanations for these trends. First, bimalleolar and trimalleolar fractures are more severe ankle fractures that tend to result from a more forceful mechanism, allowing for a higher rate of syndesmotic injury. Second, these trends likely do not reflect a true increase in the rate of syndesmosis injury but, rather, increased recognition of syndesmotic injury. Third, the data likely reflect a well-established approach to ankle fracture fixation and an increase in thinking that syndesmotic injuries should be stabilized in the setting of ankle fixation.
Incidence of syndesmotic injury as indicated by stabilization procedures can be compared with the data of Vosseller and colleagues,8 who reported an incidence of 6445 syndesmotic injuries per year in the United States. Our data showed fewer syndesmotic injuries, which may be related to use of CPT codes rather than ICD-9 codes for database searches, such that only operative syndesmotic injuries are represented in our data. Population differences between the 2 studies could also account for some of the differences in syndesmotic injury incidence.
We also found a significant change in the rate of hardware removal after syndesmosis ORIF. Across all treatment groups, incidence of screw removal decreased—a trend likely reflecting a change in attitude about the need for routine screw removal. Studies have shown that patients have favorable outcomes in the setting of syndesmotic screw loosening and screw breakage.37 Some authors have suggested that screw breakage or removal could be advantageous, as it allows the syndesmosis to settle into a more anatomical position after imperfect reduction.38 In addition, the trend of decreased syndesmotic screw removal could also have resulted from increased suture button fixation, which may less frequently require implant removal. Regardless, the overall trend is that routine syndesmotic implant removal has become less common.
This study had several limitations. First are the many limitations inherent to all studies that use large administrative databases, such as PearlDiver. The power of analysis depends on data quality; potential sources of error include accuracy of billing codes and physicians’ miscoding or noncoding. Although we tried to accurately represent a large population of interest through use of this database, we cannot be sure that the database represents a true cross-section of the United States. In addition, as we could not determine the method of syndesmotic fixation—the same CPT code is used for both suture button fixation and screw fixation—we could not establish trends for the rate of each method. More research is needed to establish these trends, and this research likely will require analysis of data from a large trauma center or from multiple centers.
Potential regional differences are another limitation. In the PearlDiver database, the South and Midwest are highly represented, the Northeast and West much less so. The South, Midwest, and West (but not the Northeast) had similar overall incidence and subgroup incidence of ankle ORIF. However, any regional differences in the rate of syndesmotic fixation could have skewed our data.
Ankle fractures and associated syndesmotic injuries remain a common problem. Although the prevalence of ankle fracture fixation has been relatively constant, the rate of syndesmosis stabilization has increased significantly. Young adults have the highest incidence of ankle fracture and associated syndesmotic fixation, but more ankle fractures occur in the large and growing elderly population. Increased awareness of syndesmotic injury likely has contributed to the recent rise in syndesmosis fixation seen in the present study. Given this trend, we recommend further analysis of outcome data and to establish treatment guidelines.
Am J Orthop. 2016;45(7):E472-E477. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Waterman BR, Owens BD, Davey S, Zacchilli MA, Belmont PJ Jr. The epidemiology of ankle sprains in the United States. J Bone Joint Surg Am. 2010;92(13):2279-2284.
2. Court-Brown CM, Caesar B. Epidemiology of adult fractures: a review. Injury. 2006;37(8):691-697.
3. Miller AN, Paul O, Boraiah S, Parker RJ, Helfet DL, Lorich DG. Functional outcomes after syndesmotic screw fixation and removal. J Orthop Trauma. 2010;24(1):12-16.
4. Edwards GS Jr, DeLee JC. Ankle diastasis without fracture. Foot Ankle. 1984;4(6):305-312.
5. Norkus SA, Floyd RT. The anatomy and mechanisms of syndesmotic ankle sprains. J Athl Train. 2001;36(1):68-73.
6. Brosky T, Nyland J, Nitz A, Caborn DN. The ankle ligaments: consideration of syndesmotic injury and implications for rehabilitation. J Orthop Sports Phys Ther. 1995;21(4):197-205.
7. Purvis GD. Displaced, unstable ankle fractures: classification, incidence, and management of a consecutive series. Clin Orthop Relat Res. 1982;(165):91-98.
8. Vosseller JT, Karl JW, Greisberg JK. Incidence of syndesmotic injury. Orthopedics. 2014;37(3):e226-e229.
9. Stark E, Tornetta P 3rd, Creevy WR. Syndesmotic instability in Weber B ankle fractures: a clinical evaluation. J Orthop Trauma. 2007;21(9):643-646.
10. Tornetta P 3rd, Axelrad TW, Sibai TA, Creevy WR. Treatment of the stress positive ligamentous SE4 ankle fracture: incidence of syndesmotic injury and clinical decision making. J Orthop Trauma. 2012;26(11):659-661.
11. Xenos JS, Hopkinson WJ, Mulligan ME, Olson EJ, Popovic NA. The tibiofibular syndesmosis. Evaluation of the ligamentous structures, methods of fixation, and radiographic assessment. J Bone Joint Surg Am. 1995;77(6):847-856.
12. Ebraheim NA, Lu J, Yang H, Mekhail AO, Yeasting RA. Radiographic and CT evaluation of tibiofibular syndesmotic diastasis: a cadaver study. Foot Ankle Int. 1997;18(11):693-698.
13. Ahmad J, Raikin SM, Pour AE, Haytmanek C. Bioabsorbable screw fixation of the syndesmosis in unstable ankle injuries. Foot Ankle Int. 2009;30(2):99-105.
14. Hovis WD, Kaiser BW, Watson JT, Bucholz RW. Treatment of syndesmotic disruptions of the ankle with bioabsorbable screw fixation. J Bone Joint Surg Am. 2002;84(1):26-31.
15. Kaukonen JP, Lamberg T, Korkala O, Pajarinen J. Fixation of syndesmotic ruptures in 38 patients with a malleolar fracture: a randomized study comparing a metallic and a bioabsorbable screw. J Orthop Trauma. 2005;19(6):392-395.
16. Thordarson DB, Samuelson M, Shepherd LE, Merkle PF, Lee J. Bioabsorbable versus stainless steel screw fixation of the syndesmosis in pronation-lateral rotation ankle fractures: a prospective randomized trial. Foot Ankle Int. 2001;22(4):335-338.
17. Moore JA Jr, Shank JR, Morgan SJ, Smith WR. Syndesmosis fixation: a comparison of three and four cortices of screw fixation without hardware removal. Foot Ankle Int. 2006;27(8):567-572.
18. Høiness P, Strømsøe K. Tricortical versus quadricortical syndesmosis fixation in ankle fractures: a prospective, randomized study comparing two methods of syndesmosis fixation. J Orthop Trauma. 2004;18(6):331-337.
19. Huber T, Schmoelz W, Bölderl A. Motion of the fibula relative to the tibia and its alterations with syndesmosis screws: a cadaver study. Foot Ankle Surg. 2012;18(3):203-209.
20. Needleman RL, Skrade DA, Stiehl JB. Effect of the syndesmotic screw on ankle motion. Foot Ankle. 1989;10(1):17-24.
21. Mendelsohn ES, Hoshino CM, Harris TG, Zinar DM. The effect of obesity on early failure after operative syndesmosis injuries. J Orthop Trauma. 2013;27(4):201-206.
22. Schepers T. Acute distal tibiofibular syndesmosis injury: a systematic review of suture-button versus syndesmotic screw repair. Int Orthop. 2012;36(6):1199-1206.
23. Cottom JM, Hyer CF, Philbin TM, Berlet GC. Transosseous fixation of the distal tibiofibular syndesmosis: comparison of an interosseous suture and Endobutton to traditional screw fixation in 50 cases. J Foot Ankle Surg. 2009;48(6):620-630.
24. Thornes B, Shannon F, Guiney AM, Hession P, Masterson E. Suture-button syndesmosis fixation: accelerated rehabilitation and improved outcomes. Clin Orthop Relat Res. 2005;(431):207-212.
25. Willmott HJ, Singh B, David LA. Outcome and complications of treatment of ankle diastasis with tightrope fixation. Injury. 2009;40(11):1204-1206.
26. Qamar F, Kadakia A, Venkateswaran B. An anatomical way of treating ankle syndesmotic injuries. J Foot Ankle Surg. 2011;50(6):762-765.
27. Degroot H, Al-Omari AA, El Ghazaly SA. Outcomes of suture button repair of the distal tibiofibular syndesmosis. Foot Ankle Int. 2011;32(3):250-256.
28. Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg Am. 1976;58(3):356-357.
29. Weening B, Bhandari M. Predictors of functional outcome following transsyndesmotic screw fixation of ankle fractures. J Orthop Trauma. 2005;19(2):102-108.
30. Sagi HC, Shah AR, Sanders RW. The functional consequence of syndesmotic joint malreduction at a minimum 2-year follow-up. J Orthop Trauma. 2012;26(7):439-443.
31. Naqvi GA, Cunningham P, Lynch B, Galvin R, Awan N. Fixation of ankle syndesmotic injuries: comparison of tightrope fixation and syndesmotic screw fixation for accuracy of syndesmotic reduction. Am J Sports Med. 2012;40(12):2828-2835.
32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.
33. Franke J, von Recum J, Suda AJ, Grützner PA, Wendl K. Intraoperative three-dimensional imaging in the treatment of acute unstable syndesmotic injuries. J Bone Joint Surg Am. 2012;94(15):1386-1390.
34. Gardner MJ, Demetrakopoulos D, Briggs SM, Helfet DL, Lorich DG. Malreduction of the tibiofibular syndesmosis in ankle fractures. Foot Ankle Int. 2006;27(10):788-792.
35. Miller AN, Carroll EA, Parker RJ, Boraiah S, Helfet DL, Lorich DG. Direct visualization for syndesmotic stabilization of ankle fractures. Foot Ankle Int. 2009;30(5):419-426.
36. Ruan Z, Luo C, Shi Z, Zhang B, Zeng B, Zhang C. Intraoperative reduction of distal tibiofibular joint aided by three-dimensional fluoroscopy. Technol Health Care. 2011;19(3):161-166.
37. Hamid N, Loeffler BJ, Braddy W, Kellam JF, Cohen BE, Bosse MJ. Outcome after fixation of ankle fractures with an injury to the syndesmosis: the effect of the syndesmosis screw. J Bone Joint Surg Br. 2009;91(8):1069-1073.
38. Song DJ, Lanzi JT, Groth AT, et al. The effect of syndesmosis screw removal on the reduction of the distal tibiofibular joint: a prospective radiographic study. Foot Ankle Int. 2014;35(6):543-548.
1. Waterman BR, Owens BD, Davey S, Zacchilli MA, Belmont PJ Jr. The epidemiology of ankle sprains in the United States. J Bone Joint Surg Am. 2010;92(13):2279-2284.
2. Court-Brown CM, Caesar B. Epidemiology of adult fractures: a review. Injury. 2006;37(8):691-697.
3. Miller AN, Paul O, Boraiah S, Parker RJ, Helfet DL, Lorich DG. Functional outcomes after syndesmotic screw fixation and removal. J Orthop Trauma. 2010;24(1):12-16.
4. Edwards GS Jr, DeLee JC. Ankle diastasis without fracture. Foot Ankle. 1984;4(6):305-312.
5. Norkus SA, Floyd RT. The anatomy and mechanisms of syndesmotic ankle sprains. J Athl Train. 2001;36(1):68-73.
6. Brosky T, Nyland J, Nitz A, Caborn DN. The ankle ligaments: consideration of syndesmotic injury and implications for rehabilitation. J Orthop Sports Phys Ther. 1995;21(4):197-205.
7. Purvis GD. Displaced, unstable ankle fractures: classification, incidence, and management of a consecutive series. Clin Orthop Relat Res. 1982;(165):91-98.
8. Vosseller JT, Karl JW, Greisberg JK. Incidence of syndesmotic injury. Orthopedics. 2014;37(3):e226-e229.
9. Stark E, Tornetta P 3rd, Creevy WR. Syndesmotic instability in Weber B ankle fractures: a clinical evaluation. J Orthop Trauma. 2007;21(9):643-646.
10. Tornetta P 3rd, Axelrad TW, Sibai TA, Creevy WR. Treatment of the stress positive ligamentous SE4 ankle fracture: incidence of syndesmotic injury and clinical decision making. J Orthop Trauma. 2012;26(11):659-661.
11. Xenos JS, Hopkinson WJ, Mulligan ME, Olson EJ, Popovic NA. The tibiofibular syndesmosis. Evaluation of the ligamentous structures, methods of fixation, and radiographic assessment. J Bone Joint Surg Am. 1995;77(6):847-856.
12. Ebraheim NA, Lu J, Yang H, Mekhail AO, Yeasting RA. Radiographic and CT evaluation of tibiofibular syndesmotic diastasis: a cadaver study. Foot Ankle Int. 1997;18(11):693-698.
13. Ahmad J, Raikin SM, Pour AE, Haytmanek C. Bioabsorbable screw fixation of the syndesmosis in unstable ankle injuries. Foot Ankle Int. 2009;30(2):99-105.
14. Hovis WD, Kaiser BW, Watson JT, Bucholz RW. Treatment of syndesmotic disruptions of the ankle with bioabsorbable screw fixation. J Bone Joint Surg Am. 2002;84(1):26-31.
15. Kaukonen JP, Lamberg T, Korkala O, Pajarinen J. Fixation of syndesmotic ruptures in 38 patients with a malleolar fracture: a randomized study comparing a metallic and a bioabsorbable screw. J Orthop Trauma. 2005;19(6):392-395.
16. Thordarson DB, Samuelson M, Shepherd LE, Merkle PF, Lee J. Bioabsorbable versus stainless steel screw fixation of the syndesmosis in pronation-lateral rotation ankle fractures: a prospective randomized trial. Foot Ankle Int. 2001;22(4):335-338.
17. Moore JA Jr, Shank JR, Morgan SJ, Smith WR. Syndesmosis fixation: a comparison of three and four cortices of screw fixation without hardware removal. Foot Ankle Int. 2006;27(8):567-572.
18. Høiness P, Strømsøe K. Tricortical versus quadricortical syndesmosis fixation in ankle fractures: a prospective, randomized study comparing two methods of syndesmosis fixation. J Orthop Trauma. 2004;18(6):331-337.
19. Huber T, Schmoelz W, Bölderl A. Motion of the fibula relative to the tibia and its alterations with syndesmosis screws: a cadaver study. Foot Ankle Surg. 2012;18(3):203-209.
20. Needleman RL, Skrade DA, Stiehl JB. Effect of the syndesmotic screw on ankle motion. Foot Ankle. 1989;10(1):17-24.
21. Mendelsohn ES, Hoshino CM, Harris TG, Zinar DM. The effect of obesity on early failure after operative syndesmosis injuries. J Orthop Trauma. 2013;27(4):201-206.
22. Schepers T. Acute distal tibiofibular syndesmosis injury: a systematic review of suture-button versus syndesmotic screw repair. Int Orthop. 2012;36(6):1199-1206.
23. Cottom JM, Hyer CF, Philbin TM, Berlet GC. Transosseous fixation of the distal tibiofibular syndesmosis: comparison of an interosseous suture and Endobutton to traditional screw fixation in 50 cases. J Foot Ankle Surg. 2009;48(6):620-630.
24. Thornes B, Shannon F, Guiney AM, Hession P, Masterson E. Suture-button syndesmosis fixation: accelerated rehabilitation and improved outcomes. Clin Orthop Relat Res. 2005;(431):207-212.
25. Willmott HJ, Singh B, David LA. Outcome and complications of treatment of ankle diastasis with tightrope fixation. Injury. 2009;40(11):1204-1206.
26. Qamar F, Kadakia A, Venkateswaran B. An anatomical way of treating ankle syndesmotic injuries. J Foot Ankle Surg. 2011;50(6):762-765.
27. Degroot H, Al-Omari AA, El Ghazaly SA. Outcomes of suture button repair of the distal tibiofibular syndesmosis. Foot Ankle Int. 2011;32(3):250-256.
28. Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg Am. 1976;58(3):356-357.
29. Weening B, Bhandari M. Predictors of functional outcome following transsyndesmotic screw fixation of ankle fractures. J Orthop Trauma. 2005;19(2):102-108.
30. Sagi HC, Shah AR, Sanders RW. The functional consequence of syndesmotic joint malreduction at a minimum 2-year follow-up. J Orthop Trauma. 2012;26(7):439-443.
31. Naqvi GA, Cunningham P, Lynch B, Galvin R, Awan N. Fixation of ankle syndesmotic injuries: comparison of tightrope fixation and syndesmotic screw fixation for accuracy of syndesmotic reduction. Am J Sports Med. 2012;40(12):2828-2835.
32. Marmor M, Hansen E, Han HK, Buckley J, Matityahu A. Limitations of standard fluoroscopy in detecting rotational malreduction of the syndesmosis in an ankle fracture model. Foot Ankle Int. 2011;32(6):616-622.
33. Franke J, von Recum J, Suda AJ, Grützner PA, Wendl K. Intraoperative three-dimensional imaging in the treatment of acute unstable syndesmotic injuries. J Bone Joint Surg Am. 2012;94(15):1386-1390.
34. Gardner MJ, Demetrakopoulos D, Briggs SM, Helfet DL, Lorich DG. Malreduction of the tibiofibular syndesmosis in ankle fractures. Foot Ankle Int. 2006;27(10):788-792.
35. Miller AN, Carroll EA, Parker RJ, Boraiah S, Helfet DL, Lorich DG. Direct visualization for syndesmotic stabilization of ankle fractures. Foot Ankle Int. 2009;30(5):419-426.
36. Ruan Z, Luo C, Shi Z, Zhang B, Zeng B, Zhang C. Intraoperative reduction of distal tibiofibular joint aided by three-dimensional fluoroscopy. Technol Health Care. 2011;19(3):161-166.
37. Hamid N, Loeffler BJ, Braddy W, Kellam JF, Cohen BE, Bosse MJ. Outcome after fixation of ankle fractures with an injury to the syndesmosis: the effect of the syndesmosis screw. J Bone Joint Surg Br. 2009;91(8):1069-1073.
38. Song DJ, Lanzi JT, Groth AT, et al. The effect of syndesmosis screw removal on the reduction of the distal tibiofibular joint: a prospective radiographic study. Foot Ankle Int. 2014;35(6):543-548.
Tenotomy, Tenodesis, Transfer: A Review of Treatment Options for Biceps-Labrum Complex Disease
Pathology of the biceps-labrum complex (BLC) can be an important source of shoulder pain. Discussion of pathoanatomy, imaging, and surgical intervention is facilitated by distinguishing the anatomical zones of the BLC: inside, junction, and bicipital tunnel (extra-articular), parts of which cannot be visualized with standard diagnostic arthroscopy.
The recent literature indicates that bicipital tunnel lesions are common and perhaps overlooked. Systematic reviews suggest improvement in outcomes of BLC operations when the bicipital tunnel is decompressed. Higher-level clinical and basic science studies are needed to fully elucidate the role of the bicipital tunnel, but it is evident that a comprehensive physical examination and an understanding of the limits of advanced imaging are necessary to correctly diagnose and treat BLC-related shoulder pain.
Anatomy of Biceps-Labrum Complex
The long head of the biceps tendon (LHBT) and the glenoid labrum work as an interdependent functional unit, the biceps-labrum complex (BLC). The BLC is divided into 3 distinct anatomical zones: inside, junction, and bicipital tunnel.1,2
Inside
The inside includes the superior labrum and biceps attachment. The LHBT most commonly originates in the superior labrum.3-5 Vangsness and colleagues3 described 4 types of LHBT origins: Type I biceps attaches solely to the posterior labrum, type II predominantly posterior, type III equally to the anterior and posterior labrum, and type IV mostly to the anterior labrum. The LHBT can also originate in the supraglenoid tubercle or the inferior border of the supraspinatus.3,6
Junction
Junction is the intra-articular segment of the LHBT and the biceps pulley. The LHBT traverses the glenohumeral joint en route to the extra-articular bicipital tunnel.2 The LHBT is enveloped in synovium that extends into part of the bicipital tunnel.2 The intra-articular segment of the LHBT is about 25 mm in length7 and has a diameter of 5 mm to 6 mm.8
A cadaveric study found that the average length of the LHBT that can be arthroscopically visualized at rest is 35.6 mm, or only 40% of the total length of the LHBT with respect to the proximal margin of the pectoralis major tendon.1 When the LHBT was pulled into the joint, more tendon (another 14 mm) was visualized.1 Therefore, diagnostic arthroscopy of the glenohumeral joint visualizes about 50% of the LHBT.9The morphology of the LHBT varies by location. The intra-articular portion of the LHBT is wide and flat, whereas the extra-articular portion is round.8 The tendon becomes smoother and more avascular as it exits the joint to promote gliding within its sheath in the bicipital groove.10 The proximal LHBT receives its vascular supply from superior labrum tributaries, and distally the LHBT is supplied by ascending branches of the anterior humeral circumflex artery.4 There is a hypovascular zone, created by this dual blood supply, about 12 mm to 30 mm from the LHBT origin, predisposing the tendon to rupture or fray in this region.11The LHBT makes a 30° turn into the biceps pulley system as it exits the glenohumeral joint. The fibrous pulley system that stabilizes the LHBT in this region has contributions from the coracohumeral ligament, the superior glenohumeral ligament, and the supraspinatus tendon.12-14
Bicipital Tunnel
The bicipital tunnel, the third portion of the BLC, remains largely hidden from standard diagnostic glenohumeral arthroscopy. The bicipital tunnel is an extra-articular, closed space that constrains the LHBT from the articular margin through the subpectoral region.2
Zone 1 is the traditional bicipital groove or “bony groove” that extends from the articular margin to the distal margin of the subscapularis tendon. The floor consists of a deep osseous groove covered by a continuation of subscapularis tendon fibers and periosteum.2Zone 2, “no man’s land,” extends from the distal margin of the subscapularis tendon to the proximal margin of the pectoralis major (PMPM). The LHBT in this zone cannot be visualized during a pull test at arthroscopy, yet lesions commonly occur here.1 Zones 1 and 2 have a similar histology and contain synovium.2Zone 3 is the subpectoral region distal to the PMPM. Fibers of the latissimus dorsi form the flat floor of zone 3, and the pectoralis major inserts lateral to the LHBT on the humerus in this zone. The synovium encapsulating the LHBT in zones 1 and 2 rarely extends past the PMPM. Taylor and colleagues2 found a higher percentage of unoccupied tunnel space in zone 3 than in zones 1 and 2, which results in a “functional bottleneck” between zones 2 and 3 represented by the PMPM.
Pathoanatomy
BLC lesions may occur in isolation or concomitantly across multiple anatomical zones. In a series of 277 chronically symptomatic shoulders that underwent transfer of the LHBT to the conjoint tendon with subdeltoid arthroscopy, Taylor and colleagues1 found 47% incidence of bicipital tunnel lesions, 44% incidence of junctional lesions, and 35% incidence of inside lesions. In their series, 37% of patients had concomitant lesions involving more than 1 anatomical zone.
Inside Lesions
Inside lesions involve the superior labrum, the LHBT origin, or both. Superior labrum anterior-posterior (SLAP) tears are included as inside BLC lesions. Snyder and colleagues16 originally identified 4 broad categories of SLAP tears, but Powell and colleagues17 described up to 10 variations. Type II lesions, which are the most common, destabilize the biceps anchor.
Dynamic incarceration of the biceps between the humeral head and the glenoid labrum is another inside lesion that can be identified during routine diagnostic glenohumeral arthroscopy. The arthroscopic active compression test, as described by Verma and colleagues,18 can be used during surgery to demonstrate incarceration of the biceps tendon.
Medial biceps chondromalacia, attritional chondral wear along the anteromedial aspect of the humeral head, occurs secondary to a windshield wiper effect of the LHBT in the setting of an incarcerating LHBT or may be associated with destabilization of the biceps pulley.
Junctional Lesions
Junctional lesions, which include lesions that affect the intra-articular LHBT, can be visualized during routine glenohumeral arthroscopy. They include partial and complete biceps tears, biceps pulley lesions, and junctional biceps chondromalacia.
Biceps pulley injuries and/or tears of the upper subscapularis tendon can destabilize the biceps as it exits the joint, and this destabilization may result in medial subluxation of the tendon and the aforementioned medial biceps chondromalacia.10,19 Junctional biceps chondromalacia is attritional chondral wear of the humeral head from abnormal tracking of the LHBT deep to the LHBT near the articular margin.
Recently elucidated is the limited ability of diagnostic glenohumeral arthroscopy to fully identify the extent of BLC pathology.1,20-22 Gilmer and colleagues20 found that diagnostic arthroscopy identified only 67% of biceps pathology and underestimated its extent in 56% of patients in their series. Similarly, Moon and colleagues21 found that 79% of proximal LHBT tears propagated distally into the bicipital tunnel and were incompletely visualized with standard arthroscopy.
Bicipital Tunnel Lesions
Recent evidence indicates that the bicipital tunnel is a closed space that often conceals space-occupying lesions, including scar, synovitis, loose bodies, and osteophytes, which can become trapped in the tunnel. The functional bottleneck between zones 2 and 3 of the bicipital tunnel explains the aggregation of loose bodies in this region.2 Similarly, as the percentage of free space within the bicipital tunnel increases, space-occupying lesions (eg scar, loose bodies, osteophytes) may exude a compressive and/or abrasive force within zones 1 and 2, but not as commonly within zone 3.2
Physical Examination of Biceps-Labrum Complex
Accurate diagnosis of BLC disease is crucial in selecting an optimal intervention, but challenging. Beyond identifying biceps pathology, specific examination maneuvers may help distinguish between lesions of the intra-articular BLC and lesions of the extra-articular bicipital tunnel.23
Traditional examination maneuvers for biceps-related shoulder pain include the Speed test, the full can test, and the Yergason test.24,25 For the Speed test, the patient forward-flexes the shoulder to 60° to 90°, extends the arm at the elbow, and supinates the forearm. The clinician applies a downward force as the patient resists. The reported sensitivity of the Speed test ranges from 37% to 63%, and specificity is 60% to 88%.25,26 In the full can test, with the patient’s arm in the plane of the scapula, the shoulder abducted to 90°, and the forearm in neutral rotation, a downward force is applied against resistance. Sensitivity of the full can test is 60% to 67%, and specificity is 76% to 84%.24 The Yergason test is performed with the patient’s arm at his or her side, the elbow flexed to 90°, and the forearm pronated. The patient supinates the forearm against the clinician’s resistance. Sensitivity of the Yergason test is 19% to 32%, and specificity is 70% to 100%.25,26 The Yergason test has a positive predictive value of 92% for bicipital tunnel disease.
O’Brien and colleagues23,26 introduced a “3-pack” physical examination designed to elicit BLC symptoms. In this examination, the LHBT is palpated along its course within the bicipital tunnel. Reproduction of the patient’s pain by palpation had a sensitivity of 98% for bicipital tunnel disease but was less specific (70%). Gill and colleagues27 reported low sensitivity (53%) and low specificity (54%) for biceps palpation, and they used arthroscopy as a gold standard. Since then, multiple studies have demonstrated that glenohumeral arthroscopy fails to identify lesions concealed within the bicipital tunnel.20-22The second part of the 3-pack examination is the active compression test. A downward force is applied as the patient resists with his or her arm forward-flexed to 90° and adducted 10° to 15° with the thumb pointing downward.28 This action is repeated with the humerus externally rotated and the forearm supinated. A positive test is indicated by reproduction of symptoms with the thumb down, and elimination or reduction of symptoms with the palm up. Test sensitivity is 88% to 96%, and specificity is 46% to 64% for BLC lesions, but for bicipital tunnel disease sensitivity is higher (96%), and the negative predictive value is 93%.26The third component of the 3-pack examination is the throwing test. A late-cocking throwing position is re-created with the shoulder externally rotated and abducted to 90° and the elbow flexed to 90°. The patient steps forward with the contralateral leg and moves into the acceleration phase of throwing while the clinician provides isometric resistance. If this maneuver reproduces pain, the test is positive. As Taylor and colleagues26 reported, the throwing test has sensitivity of 73% to 77% and specificity of 65% to 79% for BLC pathology. This test has moderate sensitivity and negative predictive value for bicipital tunnel disease but may be the only positive test on physical examination in the setting of LHBT instability.
Imaging of Biceps-Labrum Complex
Plain anteroposterior, lateral, and axillary radiographs of the shoulder should be obtained for all patients having an orthopedic examination for shoulder pain. Magnetic resonance imaging (MRI) and ultrasound are the advanced modalities most commonly used for diagnostic imaging. These modalities should be considered in conjunction with, not in place of, a comprehensive history and physical examination.
MRI has sensitivity of 9% to 89% for LHBT pathology29-37 and 38% to 98% for SLAP pathology.35,38-41 The wide range of reported sensitivity and specificity might be attributed to the varying criteria for what constitutes a BLC lesion. Some authors include biceps chondromalacia, dynamic incarceration of LHBT, and extra-articular bicipital tunnel lesions, while others historically have included only intra-articular LHBT lesions that can be directly visualized arthroscopically.
In their retrospective review of 277 shoulders with chronic refractory BLC symptoms treated with subdeltoid transfer of the LHBT to the conjoint tendon, Taylor and colleagues30 reported MRI was more sensitive for inside BLC lesions than for junctional or bicipital tunnel lesions (77% vs 43% and 50%, respectively).
Treatment Options for Biceps-Labrum Complex Lesions
A diagnosis of BLC disease warrants a trial of conservative (nonoperative) management for at least 3 months. Many patients improve with activity modification, use of oral anti-inflammatory medication, and structured physical therapy focused on dynamic stabilizers and range of motion. If pain persists, local anesthetic and corticosteroid can be injected under ultrasound guidance into the bicipital tunnel; this injection has the advantage of being both diagnostic and therapeutic. Hashiuchi and colleagues42 found ultrasound-guided injections are 87% successful in achieving intra-sheath placement (injections without ultrasound guidance are only 27% successful).
If the 3-month trial of conservative management fails, surgical intervention should be considered. The goal in treating BLC pain is to maximize clinical function and alleviate pain in a predictable manner while minimizing technical demands and morbidity. A singular solution has not been identified. Furthermore, 3 systematic reviews failed to identify a difference between the most commonly used techniques, biceps tenodesis and tenotomy.43-45 These reviews grouped all tenotomy procedures together and compared them with all tenodesis procedures. A limitation of these systematic reviews is that they did not differentiate tenodesis techniques. We prefer to classify techniques according to whether or not they decompress zones 1 and 2 of the bicipital tunnel.
Bicipital Tunnel Nondecompressing Techniques
Release of the biceps tendon, a biceps tenotomy, is a simple procedure that potentially avoids open surgery and provides patients with a quick return to activity. Disadvantages of tenotomy include cosmetic (Popeye) deformity after surgery, potential cramping and fatigue, and biomechanical changes in the humeral head,46-48 particularly among patients younger than 65 years. High rates of revision after tenotomy have been reported.43,49 Incomplete retraction of the LHBT and/or residual synovium may be responsible for refractory pain following biceps tenotomy.49 We hypothesize that failure of tenotomy may be related to unaddressed bicipital tunnel disease.
Proximal nondecompressing tenodesis techniques may be performed either on soft tissue in the interval or rotator cuff or on bone at the articular margin or within zone 1 of the bicipital tunnel.50-52 These techniques can be performed with standard glenohumeral arthroscopy and generally are fast and well tolerated and have limited operative morbidity. Advantages of these techniques over simple tenotomy are lower rates of cosmetic deformity and lower rates of cramping and fatigue pain, likely resulting from maintenance of the muscle tension relationship of the LHBT. Disadvantages of proximal tenodesis techniques include introduction of hardware for bony fixation, longer postoperative rehabilitation to protect repairs, and failure to address hidden bicipital tunnel disease. Furthermore, the rate of stiffness in patients who undergo proximal tenodesis without decompression of the bicipital tunnel may be as high as 18%.53
Bicipital Tunnel Decompressing Techniques
Surgical techniques that decompress the bicipital tunnel include proximal techniques that release the bicipital sheath within zones 1 and 2 of the bicipital tunnel (to the level of the proximal margin of the pectoralis major tendon) and certain arthroscopic suprapectoral techniques,54 open subpectoral tenodeses,55-57 and arthroscopic transfer of the LHBT to the conjoint tendon.58,59
Open subpectoral tenodesis techniques have the advantage of maintaining the length-tension relationship of the LHBT and preventing Popeye deformity. However, these techniques require making an incision near the axilla, which may introduce an unnecessary source of infection. Furthermore, open subpectoral tenodesis requires drilling the humerus and placing a screw for bony fixation of the LHBT, which can create a risk of neurovascular injury, given the proximity of neurovascular structures,60-62 and humeral shaft fracture, particularly in athletes.63,64Our preferred method is transfer of the LHBT to the conjoint tendon (Figure 3).59
Am J Orthop. 2016;45(7):E503-E511. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
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25. Chen HS, Lin SH, Hsu YH, Chen SC, Kang JH. A comparison of physical examinations with musculoskeletal ultrasound in the diagnosis of biceps long head tendinitis. Ultrasound Med Biol. 2011;37(9):1392-1398.
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29. Zanetti M, Weishaupt D, Gerber C, Hodler J. Tendinopathy and rupture of the tendon of the long head of the biceps brachii muscle: evaluation with MR arthrography. AJR Am J Roentgenol. 1998;170(6):1557-1561.
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31. Malavolta EA, Assunção JH, Guglielmetti CL, de Souza FF, Gracitelli ME, Ferreira Neto AA. Accuracy of preoperative MRI in the diagnosis of disorders of the long head of the biceps tendon. Eur J Radiol. 2015;84(11):2250-2254.
32. Dubrow SA, Streit JJ, Shishani Y, Robbin MR, Gobezie R. Diagnostic accuracy in detecting tears in the proximal biceps tendon using standard nonenhancing shoulder MRI. Open Access J Sports Med. 2014;5:81-87.
33. Nourissat G, Tribot-Laspiere Q, Aim F, Radier C. Contribution of MRI and CT arthrography to the diagnosis of intra-articular tendinopathy of the long head of the biceps. Orthop Traumatol Surg Res. 2014;100(8 suppl):S391-S394.
34. De Maeseneer M, Boulet C, Pouliart N, et al. Assessment of the long head of the biceps tendon of the shoulder with 3T magnetic resonance arthrography and CT arthrography. Eur J Radiol. 2012;81(5):934-939.
35. Houtz CG, Schwartzberg RS, Barry JA, Reuss BL, Papa L. Shoulder MRI accuracy in the community setting. J Shoulder Elbow Surg. 2011;20(4):537-542.
36. Buck FM, Grehn H, Hilbe M, Pfirrmann CW, Manzanell S, Hodler J. Degeneration of the long biceps tendon: comparison of MRI with gross anatomy and histology. AJR Am J Roentgenol. 2009;193(5):1367-1375.
37. Mohtadi NG, Vellet AD, Clark ML, et al. A prospective, double-blind comparison of magnetic resonance imaging and arthroscopy in the evaluation of patients presenting with shoulder pain. J Shoulder Elbow Surg. 2004;13(3):258-265.
38. Sheridan K, Kreulen C, Kim S, Mak W, Lewis K, Marder R. Accuracy of magnetic resonance imaging to diagnose superior labrum anterior-posterior tears. Knee Surg Sports Traumatol Arthrosc. 2015;23(9):2645-2650.
39. Connolly KP, Schwartzberg RS, Reuss B, Crumbie D Jr, Homan BM. Sensitivity and specificity of noncontrast magnetic resonance imaging reports in the diagnosis of type-II superior labral anterior-posterior lesions in the community setting. J Bone Joint Surg Am. 2013;95(4):308-313.
40. Reuss BL, Schwartzberg R, Zlatkin MB, Cooperman A, Dixon JR. Magnetic resonance imaging accuracy for the diagnosis of superior labrum anterior-posterior lesions in the community setting: eighty-three arthroscopically confirmed cases. J Shoulder Elbow Surg. 2006;15(5):580-585.
41. Connell DA, Potter HG, Wickiewicz TL, Altchek DW, Warren RF. Noncontrast magnetic resonance imaging of superior labral lesions. 102 cases confirmed at arthroscopic surgery. Am J Sports Med. 1999;27(2):208-213.
42. Hashiuchi T, Sakurai G, Morimoto M, Komei T, Takakura Y, Tanaka Y. Accuracy of the biceps tendon sheath injection: ultrasound-guided or unguided injection? A randomized controlled trial. J Shoulder Elbow Surg. 2011;20(7):1069-1073.
43. Hsu AR, Ghodadra NS, Provencher MT, Lewis PB, Bach BR. Biceps tenotomy versus tenodesis: a review of clinical outcomes and biomechanical results. J Shoulder Elbow Surg. 2011;20(2):326-332.
44. Slenker NR, Lawson K, Ciccotti MG, Dodson CC, Cohen SB. Biceps tenotomy versus tenodesis: clinical outcomes. Arthroscopy. 2012;28(4):576-582.
45. Frost A, Zafar MS, Maffulli N. Tenotomy versus tenodesis in the management of pathologic lesions of the tendon of the long head of the biceps brachii. Am J Sports Med. 2009;37(4):828-833.
46. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
47. Berlemann U, Bayley I. Tenodesis of the long head of biceps brachii in the painful shoulder: improving results in the long term. J Shoulder Elbow Surg. 1995;4(6):429-435.
48. Gill TJ, McIrvin E, Mair SD, Hawkins RJ. Results of biceps tenotomy for treatment of pathology of the long head of the biceps brachii. J Shoulder Elbow Surg. 2001;10(3):247-249.
49. Sanders B, Lavery KP, Pennington S, Warner JJ. Clinical success of biceps tenodesis with and without release of the transverse humeral ligament. J Shoulder Elbow Surg. 2012;21(1):66-71.
50. Gartsman GM, Hammerman SM. Arthroscopic biceps tenodesis: operative technique. Arthroscopy. 2000;16(5):550-552.
51. Richards DP, Burkhart SS. Arthroscopic-assisted biceps tenodesis for ruptures of the long head of biceps brachii: the cobra procedure. Arthroscopy. 2004;20(suppl 2):201-207.
52. Klepps S, Hazrati Y, Flatow E. Arthroscopic biceps tenodesis. Arthroscopy. 2002;18(9):1040-1045.
53. Werner BC, Pehlivan HC, Hart JM, et al. Increased incidence of postoperative stiffness after arthroscopic compared with open biceps tenodesis. Arthroscopy. 2014;30(9):1075-1084.54. Werner BC, Lyons ML, Evans CL, et al. Arthroscopic suprapectoral and open subpectoral biceps tenodesis: a comparison of restoration of length-tension and mechanical strength between techniques. Arthroscopy. 2015;31(4):620-627.
55. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
56. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
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58. Taylor SA, Fabricant PD, Baret NJ, et al. Midterm clinical outcomes for arthroscopic subdeltoid transfer of the long head of the biceps tendon to the conjoint tendon. Arthroscopy. 2014;30(12):1574-1581.
59. Drakos MC, Verma NN, Gulotta LV, et al. Arthroscopic transfer of the long head of the biceps tendon: functional outcome and clinical results. Arthroscopy. 2008;24(2):217-223.
60. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
61. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
62. Ma H, Van Heest A, Glisson C, Patel S. Musculocutaneous nerve entrapment: an unusual complication after biceps tenodesis. Am J Sports Med. 2009;37(12):2467-2469.
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66. Urch E, Taylor SA, Ramkumar PN, et al. Biceps tenodesis: a comparison of tendon-to-bone and tendon-to-tendon healing in a rat model. Paper presented at: Closed Meeting of the American Shoulder and Elbow Surgeons; October 10, 2015; Asheville, NC. Paper 26.
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Pathology of the biceps-labrum complex (BLC) can be an important source of shoulder pain. Discussion of pathoanatomy, imaging, and surgical intervention is facilitated by distinguishing the anatomical zones of the BLC: inside, junction, and bicipital tunnel (extra-articular), parts of which cannot be visualized with standard diagnostic arthroscopy.
The recent literature indicates that bicipital tunnel lesions are common and perhaps overlooked. Systematic reviews suggest improvement in outcomes of BLC operations when the bicipital tunnel is decompressed. Higher-level clinical and basic science studies are needed to fully elucidate the role of the bicipital tunnel, but it is evident that a comprehensive physical examination and an understanding of the limits of advanced imaging are necessary to correctly diagnose and treat BLC-related shoulder pain.
Anatomy of Biceps-Labrum Complex
The long head of the biceps tendon (LHBT) and the glenoid labrum work as an interdependent functional unit, the biceps-labrum complex (BLC). The BLC is divided into 3 distinct anatomical zones: inside, junction, and bicipital tunnel.1,2
Inside
The inside includes the superior labrum and biceps attachment. The LHBT most commonly originates in the superior labrum.3-5 Vangsness and colleagues3 described 4 types of LHBT origins: Type I biceps attaches solely to the posterior labrum, type II predominantly posterior, type III equally to the anterior and posterior labrum, and type IV mostly to the anterior labrum. The LHBT can also originate in the supraglenoid tubercle or the inferior border of the supraspinatus.3,6
Junction
Junction is the intra-articular segment of the LHBT and the biceps pulley. The LHBT traverses the glenohumeral joint en route to the extra-articular bicipital tunnel.2 The LHBT is enveloped in synovium that extends into part of the bicipital tunnel.2 The intra-articular segment of the LHBT is about 25 mm in length7 and has a diameter of 5 mm to 6 mm.8
A cadaveric study found that the average length of the LHBT that can be arthroscopically visualized at rest is 35.6 mm, or only 40% of the total length of the LHBT with respect to the proximal margin of the pectoralis major tendon.1 When the LHBT was pulled into the joint, more tendon (another 14 mm) was visualized.1 Therefore, diagnostic arthroscopy of the glenohumeral joint visualizes about 50% of the LHBT.9The morphology of the LHBT varies by location. The intra-articular portion of the LHBT is wide and flat, whereas the extra-articular portion is round.8 The tendon becomes smoother and more avascular as it exits the joint to promote gliding within its sheath in the bicipital groove.10 The proximal LHBT receives its vascular supply from superior labrum tributaries, and distally the LHBT is supplied by ascending branches of the anterior humeral circumflex artery.4 There is a hypovascular zone, created by this dual blood supply, about 12 mm to 30 mm from the LHBT origin, predisposing the tendon to rupture or fray in this region.11The LHBT makes a 30° turn into the biceps pulley system as it exits the glenohumeral joint. The fibrous pulley system that stabilizes the LHBT in this region has contributions from the coracohumeral ligament, the superior glenohumeral ligament, and the supraspinatus tendon.12-14
Bicipital Tunnel
The bicipital tunnel, the third portion of the BLC, remains largely hidden from standard diagnostic glenohumeral arthroscopy. The bicipital tunnel is an extra-articular, closed space that constrains the LHBT from the articular margin through the subpectoral region.2
Zone 1 is the traditional bicipital groove or “bony groove” that extends from the articular margin to the distal margin of the subscapularis tendon. The floor consists of a deep osseous groove covered by a continuation of subscapularis tendon fibers and periosteum.2Zone 2, “no man’s land,” extends from the distal margin of the subscapularis tendon to the proximal margin of the pectoralis major (PMPM). The LHBT in this zone cannot be visualized during a pull test at arthroscopy, yet lesions commonly occur here.1 Zones 1 and 2 have a similar histology and contain synovium.2Zone 3 is the subpectoral region distal to the PMPM. Fibers of the latissimus dorsi form the flat floor of zone 3, and the pectoralis major inserts lateral to the LHBT on the humerus in this zone. The synovium encapsulating the LHBT in zones 1 and 2 rarely extends past the PMPM. Taylor and colleagues2 found a higher percentage of unoccupied tunnel space in zone 3 than in zones 1 and 2, which results in a “functional bottleneck” between zones 2 and 3 represented by the PMPM.
Pathoanatomy
BLC lesions may occur in isolation or concomitantly across multiple anatomical zones. In a series of 277 chronically symptomatic shoulders that underwent transfer of the LHBT to the conjoint tendon with subdeltoid arthroscopy, Taylor and colleagues1 found 47% incidence of bicipital tunnel lesions, 44% incidence of junctional lesions, and 35% incidence of inside lesions. In their series, 37% of patients had concomitant lesions involving more than 1 anatomical zone.
Inside Lesions
Inside lesions involve the superior labrum, the LHBT origin, or both. Superior labrum anterior-posterior (SLAP) tears are included as inside BLC lesions. Snyder and colleagues16 originally identified 4 broad categories of SLAP tears, but Powell and colleagues17 described up to 10 variations. Type II lesions, which are the most common, destabilize the biceps anchor.
Dynamic incarceration of the biceps between the humeral head and the glenoid labrum is another inside lesion that can be identified during routine diagnostic glenohumeral arthroscopy. The arthroscopic active compression test, as described by Verma and colleagues,18 can be used during surgery to demonstrate incarceration of the biceps tendon.
Medial biceps chondromalacia, attritional chondral wear along the anteromedial aspect of the humeral head, occurs secondary to a windshield wiper effect of the LHBT in the setting of an incarcerating LHBT or may be associated with destabilization of the biceps pulley.
Junctional Lesions
Junctional lesions, which include lesions that affect the intra-articular LHBT, can be visualized during routine glenohumeral arthroscopy. They include partial and complete biceps tears, biceps pulley lesions, and junctional biceps chondromalacia.
Biceps pulley injuries and/or tears of the upper subscapularis tendon can destabilize the biceps as it exits the joint, and this destabilization may result in medial subluxation of the tendon and the aforementioned medial biceps chondromalacia.10,19 Junctional biceps chondromalacia is attritional chondral wear of the humeral head from abnormal tracking of the LHBT deep to the LHBT near the articular margin.
Recently elucidated is the limited ability of diagnostic glenohumeral arthroscopy to fully identify the extent of BLC pathology.1,20-22 Gilmer and colleagues20 found that diagnostic arthroscopy identified only 67% of biceps pathology and underestimated its extent in 56% of patients in their series. Similarly, Moon and colleagues21 found that 79% of proximal LHBT tears propagated distally into the bicipital tunnel and were incompletely visualized with standard arthroscopy.
Bicipital Tunnel Lesions
Recent evidence indicates that the bicipital tunnel is a closed space that often conceals space-occupying lesions, including scar, synovitis, loose bodies, and osteophytes, which can become trapped in the tunnel. The functional bottleneck between zones 2 and 3 of the bicipital tunnel explains the aggregation of loose bodies in this region.2 Similarly, as the percentage of free space within the bicipital tunnel increases, space-occupying lesions (eg scar, loose bodies, osteophytes) may exude a compressive and/or abrasive force within zones 1 and 2, but not as commonly within zone 3.2
Physical Examination of Biceps-Labrum Complex
Accurate diagnosis of BLC disease is crucial in selecting an optimal intervention, but challenging. Beyond identifying biceps pathology, specific examination maneuvers may help distinguish between lesions of the intra-articular BLC and lesions of the extra-articular bicipital tunnel.23
Traditional examination maneuvers for biceps-related shoulder pain include the Speed test, the full can test, and the Yergason test.24,25 For the Speed test, the patient forward-flexes the shoulder to 60° to 90°, extends the arm at the elbow, and supinates the forearm. The clinician applies a downward force as the patient resists. The reported sensitivity of the Speed test ranges from 37% to 63%, and specificity is 60% to 88%.25,26 In the full can test, with the patient’s arm in the plane of the scapula, the shoulder abducted to 90°, and the forearm in neutral rotation, a downward force is applied against resistance. Sensitivity of the full can test is 60% to 67%, and specificity is 76% to 84%.24 The Yergason test is performed with the patient’s arm at his or her side, the elbow flexed to 90°, and the forearm pronated. The patient supinates the forearm against the clinician’s resistance. Sensitivity of the Yergason test is 19% to 32%, and specificity is 70% to 100%.25,26 The Yergason test has a positive predictive value of 92% for bicipital tunnel disease.
O’Brien and colleagues23,26 introduced a “3-pack” physical examination designed to elicit BLC symptoms. In this examination, the LHBT is palpated along its course within the bicipital tunnel. Reproduction of the patient’s pain by palpation had a sensitivity of 98% for bicipital tunnel disease but was less specific (70%). Gill and colleagues27 reported low sensitivity (53%) and low specificity (54%) for biceps palpation, and they used arthroscopy as a gold standard. Since then, multiple studies have demonstrated that glenohumeral arthroscopy fails to identify lesions concealed within the bicipital tunnel.20-22The second part of the 3-pack examination is the active compression test. A downward force is applied as the patient resists with his or her arm forward-flexed to 90° and adducted 10° to 15° with the thumb pointing downward.28 This action is repeated with the humerus externally rotated and the forearm supinated. A positive test is indicated by reproduction of symptoms with the thumb down, and elimination or reduction of symptoms with the palm up. Test sensitivity is 88% to 96%, and specificity is 46% to 64% for BLC lesions, but for bicipital tunnel disease sensitivity is higher (96%), and the negative predictive value is 93%.26The third component of the 3-pack examination is the throwing test. A late-cocking throwing position is re-created with the shoulder externally rotated and abducted to 90° and the elbow flexed to 90°. The patient steps forward with the contralateral leg and moves into the acceleration phase of throwing while the clinician provides isometric resistance. If this maneuver reproduces pain, the test is positive. As Taylor and colleagues26 reported, the throwing test has sensitivity of 73% to 77% and specificity of 65% to 79% for BLC pathology. This test has moderate sensitivity and negative predictive value for bicipital tunnel disease but may be the only positive test on physical examination in the setting of LHBT instability.
Imaging of Biceps-Labrum Complex
Plain anteroposterior, lateral, and axillary radiographs of the shoulder should be obtained for all patients having an orthopedic examination for shoulder pain. Magnetic resonance imaging (MRI) and ultrasound are the advanced modalities most commonly used for diagnostic imaging. These modalities should be considered in conjunction with, not in place of, a comprehensive history and physical examination.
MRI has sensitivity of 9% to 89% for LHBT pathology29-37 and 38% to 98% for SLAP pathology.35,38-41 The wide range of reported sensitivity and specificity might be attributed to the varying criteria for what constitutes a BLC lesion. Some authors include biceps chondromalacia, dynamic incarceration of LHBT, and extra-articular bicipital tunnel lesions, while others historically have included only intra-articular LHBT lesions that can be directly visualized arthroscopically.
In their retrospective review of 277 shoulders with chronic refractory BLC symptoms treated with subdeltoid transfer of the LHBT to the conjoint tendon, Taylor and colleagues30 reported MRI was more sensitive for inside BLC lesions than for junctional or bicipital tunnel lesions (77% vs 43% and 50%, respectively).
Treatment Options for Biceps-Labrum Complex Lesions
A diagnosis of BLC disease warrants a trial of conservative (nonoperative) management for at least 3 months. Many patients improve with activity modification, use of oral anti-inflammatory medication, and structured physical therapy focused on dynamic stabilizers and range of motion. If pain persists, local anesthetic and corticosteroid can be injected under ultrasound guidance into the bicipital tunnel; this injection has the advantage of being both diagnostic and therapeutic. Hashiuchi and colleagues42 found ultrasound-guided injections are 87% successful in achieving intra-sheath placement (injections without ultrasound guidance are only 27% successful).
If the 3-month trial of conservative management fails, surgical intervention should be considered. The goal in treating BLC pain is to maximize clinical function and alleviate pain in a predictable manner while minimizing technical demands and morbidity. A singular solution has not been identified. Furthermore, 3 systematic reviews failed to identify a difference between the most commonly used techniques, biceps tenodesis and tenotomy.43-45 These reviews grouped all tenotomy procedures together and compared them with all tenodesis procedures. A limitation of these systematic reviews is that they did not differentiate tenodesis techniques. We prefer to classify techniques according to whether or not they decompress zones 1 and 2 of the bicipital tunnel.
Bicipital Tunnel Nondecompressing Techniques
Release of the biceps tendon, a biceps tenotomy, is a simple procedure that potentially avoids open surgery and provides patients with a quick return to activity. Disadvantages of tenotomy include cosmetic (Popeye) deformity after surgery, potential cramping and fatigue, and biomechanical changes in the humeral head,46-48 particularly among patients younger than 65 years. High rates of revision after tenotomy have been reported.43,49 Incomplete retraction of the LHBT and/or residual synovium may be responsible for refractory pain following biceps tenotomy.49 We hypothesize that failure of tenotomy may be related to unaddressed bicipital tunnel disease.
Proximal nondecompressing tenodesis techniques may be performed either on soft tissue in the interval or rotator cuff or on bone at the articular margin or within zone 1 of the bicipital tunnel.50-52 These techniques can be performed with standard glenohumeral arthroscopy and generally are fast and well tolerated and have limited operative morbidity. Advantages of these techniques over simple tenotomy are lower rates of cosmetic deformity and lower rates of cramping and fatigue pain, likely resulting from maintenance of the muscle tension relationship of the LHBT. Disadvantages of proximal tenodesis techniques include introduction of hardware for bony fixation, longer postoperative rehabilitation to protect repairs, and failure to address hidden bicipital tunnel disease. Furthermore, the rate of stiffness in patients who undergo proximal tenodesis without decompression of the bicipital tunnel may be as high as 18%.53
Bicipital Tunnel Decompressing Techniques
Surgical techniques that decompress the bicipital tunnel include proximal techniques that release the bicipital sheath within zones 1 and 2 of the bicipital tunnel (to the level of the proximal margin of the pectoralis major tendon) and certain arthroscopic suprapectoral techniques,54 open subpectoral tenodeses,55-57 and arthroscopic transfer of the LHBT to the conjoint tendon.58,59
Open subpectoral tenodesis techniques have the advantage of maintaining the length-tension relationship of the LHBT and preventing Popeye deformity. However, these techniques require making an incision near the axilla, which may introduce an unnecessary source of infection. Furthermore, open subpectoral tenodesis requires drilling the humerus and placing a screw for bony fixation of the LHBT, which can create a risk of neurovascular injury, given the proximity of neurovascular structures,60-62 and humeral shaft fracture, particularly in athletes.63,64Our preferred method is transfer of the LHBT to the conjoint tendon (Figure 3).59
Am J Orthop. 2016;45(7):E503-E511. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Pathology of the biceps-labrum complex (BLC) can be an important source of shoulder pain. Discussion of pathoanatomy, imaging, and surgical intervention is facilitated by distinguishing the anatomical zones of the BLC: inside, junction, and bicipital tunnel (extra-articular), parts of which cannot be visualized with standard diagnostic arthroscopy.
The recent literature indicates that bicipital tunnel lesions are common and perhaps overlooked. Systematic reviews suggest improvement in outcomes of BLC operations when the bicipital tunnel is decompressed. Higher-level clinical and basic science studies are needed to fully elucidate the role of the bicipital tunnel, but it is evident that a comprehensive physical examination and an understanding of the limits of advanced imaging are necessary to correctly diagnose and treat BLC-related shoulder pain.
Anatomy of Biceps-Labrum Complex
The long head of the biceps tendon (LHBT) and the glenoid labrum work as an interdependent functional unit, the biceps-labrum complex (BLC). The BLC is divided into 3 distinct anatomical zones: inside, junction, and bicipital tunnel.1,2
Inside
The inside includes the superior labrum and biceps attachment. The LHBT most commonly originates in the superior labrum.3-5 Vangsness and colleagues3 described 4 types of LHBT origins: Type I biceps attaches solely to the posterior labrum, type II predominantly posterior, type III equally to the anterior and posterior labrum, and type IV mostly to the anterior labrum. The LHBT can also originate in the supraglenoid tubercle or the inferior border of the supraspinatus.3,6
Junction
Junction is the intra-articular segment of the LHBT and the biceps pulley. The LHBT traverses the glenohumeral joint en route to the extra-articular bicipital tunnel.2 The LHBT is enveloped in synovium that extends into part of the bicipital tunnel.2 The intra-articular segment of the LHBT is about 25 mm in length7 and has a diameter of 5 mm to 6 mm.8
A cadaveric study found that the average length of the LHBT that can be arthroscopically visualized at rest is 35.6 mm, or only 40% of the total length of the LHBT with respect to the proximal margin of the pectoralis major tendon.1 When the LHBT was pulled into the joint, more tendon (another 14 mm) was visualized.1 Therefore, diagnostic arthroscopy of the glenohumeral joint visualizes about 50% of the LHBT.9The morphology of the LHBT varies by location. The intra-articular portion of the LHBT is wide and flat, whereas the extra-articular portion is round.8 The tendon becomes smoother and more avascular as it exits the joint to promote gliding within its sheath in the bicipital groove.10 The proximal LHBT receives its vascular supply from superior labrum tributaries, and distally the LHBT is supplied by ascending branches of the anterior humeral circumflex artery.4 There is a hypovascular zone, created by this dual blood supply, about 12 mm to 30 mm from the LHBT origin, predisposing the tendon to rupture or fray in this region.11The LHBT makes a 30° turn into the biceps pulley system as it exits the glenohumeral joint. The fibrous pulley system that stabilizes the LHBT in this region has contributions from the coracohumeral ligament, the superior glenohumeral ligament, and the supraspinatus tendon.12-14
Bicipital Tunnel
The bicipital tunnel, the third portion of the BLC, remains largely hidden from standard diagnostic glenohumeral arthroscopy. The bicipital tunnel is an extra-articular, closed space that constrains the LHBT from the articular margin through the subpectoral region.2
Zone 1 is the traditional bicipital groove or “bony groove” that extends from the articular margin to the distal margin of the subscapularis tendon. The floor consists of a deep osseous groove covered by a continuation of subscapularis tendon fibers and periosteum.2Zone 2, “no man’s land,” extends from the distal margin of the subscapularis tendon to the proximal margin of the pectoralis major (PMPM). The LHBT in this zone cannot be visualized during a pull test at arthroscopy, yet lesions commonly occur here.1 Zones 1 and 2 have a similar histology and contain synovium.2Zone 3 is the subpectoral region distal to the PMPM. Fibers of the latissimus dorsi form the flat floor of zone 3, and the pectoralis major inserts lateral to the LHBT on the humerus in this zone. The synovium encapsulating the LHBT in zones 1 and 2 rarely extends past the PMPM. Taylor and colleagues2 found a higher percentage of unoccupied tunnel space in zone 3 than in zones 1 and 2, which results in a “functional bottleneck” between zones 2 and 3 represented by the PMPM.
Pathoanatomy
BLC lesions may occur in isolation or concomitantly across multiple anatomical zones. In a series of 277 chronically symptomatic shoulders that underwent transfer of the LHBT to the conjoint tendon with subdeltoid arthroscopy, Taylor and colleagues1 found 47% incidence of bicipital tunnel lesions, 44% incidence of junctional lesions, and 35% incidence of inside lesions. In their series, 37% of patients had concomitant lesions involving more than 1 anatomical zone.
Inside Lesions
Inside lesions involve the superior labrum, the LHBT origin, or both. Superior labrum anterior-posterior (SLAP) tears are included as inside BLC lesions. Snyder and colleagues16 originally identified 4 broad categories of SLAP tears, but Powell and colleagues17 described up to 10 variations. Type II lesions, which are the most common, destabilize the biceps anchor.
Dynamic incarceration of the biceps between the humeral head and the glenoid labrum is another inside lesion that can be identified during routine diagnostic glenohumeral arthroscopy. The arthroscopic active compression test, as described by Verma and colleagues,18 can be used during surgery to demonstrate incarceration of the biceps tendon.
Medial biceps chondromalacia, attritional chondral wear along the anteromedial aspect of the humeral head, occurs secondary to a windshield wiper effect of the LHBT in the setting of an incarcerating LHBT or may be associated with destabilization of the biceps pulley.
Junctional Lesions
Junctional lesions, which include lesions that affect the intra-articular LHBT, can be visualized during routine glenohumeral arthroscopy. They include partial and complete biceps tears, biceps pulley lesions, and junctional biceps chondromalacia.
Biceps pulley injuries and/or tears of the upper subscapularis tendon can destabilize the biceps as it exits the joint, and this destabilization may result in medial subluxation of the tendon and the aforementioned medial biceps chondromalacia.10,19 Junctional biceps chondromalacia is attritional chondral wear of the humeral head from abnormal tracking of the LHBT deep to the LHBT near the articular margin.
Recently elucidated is the limited ability of diagnostic glenohumeral arthroscopy to fully identify the extent of BLC pathology.1,20-22 Gilmer and colleagues20 found that diagnostic arthroscopy identified only 67% of biceps pathology and underestimated its extent in 56% of patients in their series. Similarly, Moon and colleagues21 found that 79% of proximal LHBT tears propagated distally into the bicipital tunnel and were incompletely visualized with standard arthroscopy.
Bicipital Tunnel Lesions
Recent evidence indicates that the bicipital tunnel is a closed space that often conceals space-occupying lesions, including scar, synovitis, loose bodies, and osteophytes, which can become trapped in the tunnel. The functional bottleneck between zones 2 and 3 of the bicipital tunnel explains the aggregation of loose bodies in this region.2 Similarly, as the percentage of free space within the bicipital tunnel increases, space-occupying lesions (eg scar, loose bodies, osteophytes) may exude a compressive and/or abrasive force within zones 1 and 2, but not as commonly within zone 3.2
Physical Examination of Biceps-Labrum Complex
Accurate diagnosis of BLC disease is crucial in selecting an optimal intervention, but challenging. Beyond identifying biceps pathology, specific examination maneuvers may help distinguish between lesions of the intra-articular BLC and lesions of the extra-articular bicipital tunnel.23
Traditional examination maneuvers for biceps-related shoulder pain include the Speed test, the full can test, and the Yergason test.24,25 For the Speed test, the patient forward-flexes the shoulder to 60° to 90°, extends the arm at the elbow, and supinates the forearm. The clinician applies a downward force as the patient resists. The reported sensitivity of the Speed test ranges from 37% to 63%, and specificity is 60% to 88%.25,26 In the full can test, with the patient’s arm in the plane of the scapula, the shoulder abducted to 90°, and the forearm in neutral rotation, a downward force is applied against resistance. Sensitivity of the full can test is 60% to 67%, and specificity is 76% to 84%.24 The Yergason test is performed with the patient’s arm at his or her side, the elbow flexed to 90°, and the forearm pronated. The patient supinates the forearm against the clinician’s resistance. Sensitivity of the Yergason test is 19% to 32%, and specificity is 70% to 100%.25,26 The Yergason test has a positive predictive value of 92% for bicipital tunnel disease.
O’Brien and colleagues23,26 introduced a “3-pack” physical examination designed to elicit BLC symptoms. In this examination, the LHBT is palpated along its course within the bicipital tunnel. Reproduction of the patient’s pain by palpation had a sensitivity of 98% for bicipital tunnel disease but was less specific (70%). Gill and colleagues27 reported low sensitivity (53%) and low specificity (54%) for biceps palpation, and they used arthroscopy as a gold standard. Since then, multiple studies have demonstrated that glenohumeral arthroscopy fails to identify lesions concealed within the bicipital tunnel.20-22The second part of the 3-pack examination is the active compression test. A downward force is applied as the patient resists with his or her arm forward-flexed to 90° and adducted 10° to 15° with the thumb pointing downward.28 This action is repeated with the humerus externally rotated and the forearm supinated. A positive test is indicated by reproduction of symptoms with the thumb down, and elimination or reduction of symptoms with the palm up. Test sensitivity is 88% to 96%, and specificity is 46% to 64% for BLC lesions, but for bicipital tunnel disease sensitivity is higher (96%), and the negative predictive value is 93%.26The third component of the 3-pack examination is the throwing test. A late-cocking throwing position is re-created with the shoulder externally rotated and abducted to 90° and the elbow flexed to 90°. The patient steps forward with the contralateral leg and moves into the acceleration phase of throwing while the clinician provides isometric resistance. If this maneuver reproduces pain, the test is positive. As Taylor and colleagues26 reported, the throwing test has sensitivity of 73% to 77% and specificity of 65% to 79% for BLC pathology. This test has moderate sensitivity and negative predictive value for bicipital tunnel disease but may be the only positive test on physical examination in the setting of LHBT instability.
Imaging of Biceps-Labrum Complex
Plain anteroposterior, lateral, and axillary radiographs of the shoulder should be obtained for all patients having an orthopedic examination for shoulder pain. Magnetic resonance imaging (MRI) and ultrasound are the advanced modalities most commonly used for diagnostic imaging. These modalities should be considered in conjunction with, not in place of, a comprehensive history and physical examination.
MRI has sensitivity of 9% to 89% for LHBT pathology29-37 and 38% to 98% for SLAP pathology.35,38-41 The wide range of reported sensitivity and specificity might be attributed to the varying criteria for what constitutes a BLC lesion. Some authors include biceps chondromalacia, dynamic incarceration of LHBT, and extra-articular bicipital tunnel lesions, while others historically have included only intra-articular LHBT lesions that can be directly visualized arthroscopically.
In their retrospective review of 277 shoulders with chronic refractory BLC symptoms treated with subdeltoid transfer of the LHBT to the conjoint tendon, Taylor and colleagues30 reported MRI was more sensitive for inside BLC lesions than for junctional or bicipital tunnel lesions (77% vs 43% and 50%, respectively).
Treatment Options for Biceps-Labrum Complex Lesions
A diagnosis of BLC disease warrants a trial of conservative (nonoperative) management for at least 3 months. Many patients improve with activity modification, use of oral anti-inflammatory medication, and structured physical therapy focused on dynamic stabilizers and range of motion. If pain persists, local anesthetic and corticosteroid can be injected under ultrasound guidance into the bicipital tunnel; this injection has the advantage of being both diagnostic and therapeutic. Hashiuchi and colleagues42 found ultrasound-guided injections are 87% successful in achieving intra-sheath placement (injections without ultrasound guidance are only 27% successful).
If the 3-month trial of conservative management fails, surgical intervention should be considered. The goal in treating BLC pain is to maximize clinical function and alleviate pain in a predictable manner while minimizing technical demands and morbidity. A singular solution has not been identified. Furthermore, 3 systematic reviews failed to identify a difference between the most commonly used techniques, biceps tenodesis and tenotomy.43-45 These reviews grouped all tenotomy procedures together and compared them with all tenodesis procedures. A limitation of these systematic reviews is that they did not differentiate tenodesis techniques. We prefer to classify techniques according to whether or not they decompress zones 1 and 2 of the bicipital tunnel.
Bicipital Tunnel Nondecompressing Techniques
Release of the biceps tendon, a biceps tenotomy, is a simple procedure that potentially avoids open surgery and provides patients with a quick return to activity. Disadvantages of tenotomy include cosmetic (Popeye) deformity after surgery, potential cramping and fatigue, and biomechanical changes in the humeral head,46-48 particularly among patients younger than 65 years. High rates of revision after tenotomy have been reported.43,49 Incomplete retraction of the LHBT and/or residual synovium may be responsible for refractory pain following biceps tenotomy.49 We hypothesize that failure of tenotomy may be related to unaddressed bicipital tunnel disease.
Proximal nondecompressing tenodesis techniques may be performed either on soft tissue in the interval or rotator cuff or on bone at the articular margin or within zone 1 of the bicipital tunnel.50-52 These techniques can be performed with standard glenohumeral arthroscopy and generally are fast and well tolerated and have limited operative morbidity. Advantages of these techniques over simple tenotomy are lower rates of cosmetic deformity and lower rates of cramping and fatigue pain, likely resulting from maintenance of the muscle tension relationship of the LHBT. Disadvantages of proximal tenodesis techniques include introduction of hardware for bony fixation, longer postoperative rehabilitation to protect repairs, and failure to address hidden bicipital tunnel disease. Furthermore, the rate of stiffness in patients who undergo proximal tenodesis without decompression of the bicipital tunnel may be as high as 18%.53
Bicipital Tunnel Decompressing Techniques
Surgical techniques that decompress the bicipital tunnel include proximal techniques that release the bicipital sheath within zones 1 and 2 of the bicipital tunnel (to the level of the proximal margin of the pectoralis major tendon) and certain arthroscopic suprapectoral techniques,54 open subpectoral tenodeses,55-57 and arthroscopic transfer of the LHBT to the conjoint tendon.58,59
Open subpectoral tenodesis techniques have the advantage of maintaining the length-tension relationship of the LHBT and preventing Popeye deformity. However, these techniques require making an incision near the axilla, which may introduce an unnecessary source of infection. Furthermore, open subpectoral tenodesis requires drilling the humerus and placing a screw for bony fixation of the LHBT, which can create a risk of neurovascular injury, given the proximity of neurovascular structures,60-62 and humeral shaft fracture, particularly in athletes.63,64Our preferred method is transfer of the LHBT to the conjoint tendon (Figure 3).59
Am J Orthop. 2016;45(7):E503-E511. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Taylor SA, Khair MM, Gulotta LV, et al. Diagnostic glenohumeral arthroscopy fails to fully evaluate the biceps-labral complex. Arthroscopy. 2015;31(2):215-224.
2. Taylor SA, Fabricant PD, Bansal M, et al. The anatomy and histology of the bicipital tunnel of the shoulder. J Shoulder Elbow Surg. 2015;24(4):511-519.
3. Vangsness CT Jr, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
4. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, DiCarlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. an anatomical study. J Bone Joint Surg Am. 1992;74(1):46-52.
5. Tuoheti Y, Itoi E, Minagawa H, et al. Attachment types of the long head of the biceps tendon to the glenoid labrum and their relationships with the glenohumeral ligaments. Arthroscopy. 2005;21(10):1242-1249.
6. Dierickx C, Ceccarelli E, Conti M, Vanlommel J, Castagna A. Variations of the intra-articular portion of the long head of the biceps tendon: a classification of embryologically explained variations. J Shoulder Elbow Surg. 2009;18(4):556-565.
7. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length-tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
8. Ahrens PM, Boileau P. The long head of biceps and associated tendinopathy. J Bone Joint Surg Br. 2007;89(8):1001-1009.
9. Hart ND, Golish SR, Dragoo JL. Effects of arm position on maximizing intra-articular visualization of the biceps tendon: a cadaveric study. Arthroscopy. 2012;28(4):481-485.
10. Elser F, Braun S, Dewing CB, Giphart JE, Millett PJ. Anatomy, function, injuries, and treatment of the long head of the biceps brachii tendon. Arthroscopy. 2011;27(4):581-592.
11. Cheng NM, Pan WR, Vally F, Le Roux CM, Richardson MD. The arterial supply of the long head of biceps tendon: anatomical study with implications for tendon rupture. Clin Anat. 2010;23(6):683-692.
12. Habermeyer P, Magosch P, Pritsch M, Scheibel MT, Lichtenberg S. Anterosuperior impingement of the shoulder as a result of pulley lesions: a prospective arthroscopic study. J Shoulder Elbow Surg. 2004;13(1):5-12.
13. Gohlke F, Daum P, Bushe C. The stabilizing function of the glenohumeral joint capsule. Current aspects of the biomechanics of instability [in German]. Z Orthop Ihre Grenzgeb. 1994;132(2):112-119.
14. Arai R, Mochizuki T, Yamaguchi K, et al. Functional anatomy of the superior glenohumeral and coracohumeral ligaments and the subscapularis tendon in view of stabilization of the long head of the biceps tendon. J Shoulder Elbow Surg. 2010;19(1):58-64.
15. Busconi BB, DeAngelis N, Guerrero PE. The proximal biceps tendon: tricks and pearls. Sports Med Arthrosc. 2008;16(3):187-194.
16. Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274-279.
17. Powell SE, Nord KD, Ryu RKN. The diagnosis, classification, and treatment of SLAP lesions. Oper Tech Sports Med. 2004;12(2):99-110.
18. Verma NN, Drakos M, O’Brien SJ. The arthroscopic active compression test. Arthroscopy. 2005;21(5):634.
19. Walch G, Nove-Josserand L, Levigne C, Renaud E. Tears of the supraspinatus tendon associated with “hidden” lesions of the rotator interval. J Shoulder Elbow Surg. 1994;3(6):353-360.
20. Gilmer BB, DeMers AM, Guerrero D, Reid JB 3rd, Lubowitz JH, Guttmann D. Arthroscopic versus open comparison of long head of biceps tendon visualization and pathology in patients requiring tenodesis. Arthroscopy. 2015;31(1):29-34.
21. Moon SC, Cho NS, Rhee YG. Analysis of “hidden lesions” of the extra-articular biceps after subpectoral biceps tenodesis: the subpectoral portion as the optimal tenodesis site. Am J Sports Med. 2015;43(1):63-68.
22. Festa A, Allert J, Issa K, Tasto JP, Myer JJ. Visualization of the extra-articular portion of the long head of the biceps tendon during intra-articular shoulder arthroscopy. Arthroscopy. 2014;30(11):1413-1417.
23. O’Brien SJ, Newman AM, Taylor SA, et al. The accurate diagnosis of biceps-labral complex lesions with MRI and “3-pack” physical examination: a retrospective analysis with prospective validation. Orthop J Sports Med. 2013;1(4 suppl). doi:10.1177/2325967113S00018.
24. Hegedus EJ, Goode AP, Cook CE, et al. Which physical examination tests provide clinicians with the most value when examining the shoulder? Update of a systematic review with meta-analysis of individual tests. Br J Sports Med. 2012;46(14):964-978.
25. Chen HS, Lin SH, Hsu YH, Chen SC, Kang JH. A comparison of physical examinations with musculoskeletal ultrasound in the diagnosis of biceps long head tendinitis. Ultrasound Med Biol. 2011;37(9):1392-1398.
26. Taylor SA, Newman AM, Dawson C, et al. The “3-Pack” examination is critical for comprehensive evaluation of the biceps-labrum complex and the bicipital tunnel: a prospective study. Arthroscopy. 2016 Jul 20. [Epub ahead of print]
27. Gill HS, El Rassi G, Bahk MS, Castillo RC, McFarland EG. Physical examination for partial tears of the biceps tendon. Am J Sports Med. 2007;35(8):1334-1340.
28. O’Brien SJ, Pagnani MJ, Fealy S, McGlynn SR, Wilson JB. The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med. 1998;26(5):610-613.
29. Zanetti M, Weishaupt D, Gerber C, Hodler J. Tendinopathy and rupture of the tendon of the long head of the biceps brachii muscle: evaluation with MR arthrography. AJR Am J Roentgenol. 1998;170(6):1557-1561.
30. Taylor SA, Newman AM, Nguyen J, et al. Magnetic resonance imaging currently fails to fully evaluate the biceps-labrum complex and bicipital tunnel. Arthroscopy. 2016;32(2):238-244.
31. Malavolta EA, Assunção JH, Guglielmetti CL, de Souza FF, Gracitelli ME, Ferreira Neto AA. Accuracy of preoperative MRI in the diagnosis of disorders of the long head of the biceps tendon. Eur J Radiol. 2015;84(11):2250-2254.
32. Dubrow SA, Streit JJ, Shishani Y, Robbin MR, Gobezie R. Diagnostic accuracy in detecting tears in the proximal biceps tendon using standard nonenhancing shoulder MRI. Open Access J Sports Med. 2014;5:81-87.
33. Nourissat G, Tribot-Laspiere Q, Aim F, Radier C. Contribution of MRI and CT arthrography to the diagnosis of intra-articular tendinopathy of the long head of the biceps. Orthop Traumatol Surg Res. 2014;100(8 suppl):S391-S394.
34. De Maeseneer M, Boulet C, Pouliart N, et al. Assessment of the long head of the biceps tendon of the shoulder with 3T magnetic resonance arthrography and CT arthrography. Eur J Radiol. 2012;81(5):934-939.
35. Houtz CG, Schwartzberg RS, Barry JA, Reuss BL, Papa L. Shoulder MRI accuracy in the community setting. J Shoulder Elbow Surg. 2011;20(4):537-542.
36. Buck FM, Grehn H, Hilbe M, Pfirrmann CW, Manzanell S, Hodler J. Degeneration of the long biceps tendon: comparison of MRI with gross anatomy and histology. AJR Am J Roentgenol. 2009;193(5):1367-1375.
37. Mohtadi NG, Vellet AD, Clark ML, et al. A prospective, double-blind comparison of magnetic resonance imaging and arthroscopy in the evaluation of patients presenting with shoulder pain. J Shoulder Elbow Surg. 2004;13(3):258-265.
38. Sheridan K, Kreulen C, Kim S, Mak W, Lewis K, Marder R. Accuracy of magnetic resonance imaging to diagnose superior labrum anterior-posterior tears. Knee Surg Sports Traumatol Arthrosc. 2015;23(9):2645-2650.
39. Connolly KP, Schwartzberg RS, Reuss B, Crumbie D Jr, Homan BM. Sensitivity and specificity of noncontrast magnetic resonance imaging reports in the diagnosis of type-II superior labral anterior-posterior lesions in the community setting. J Bone Joint Surg Am. 2013;95(4):308-313.
40. Reuss BL, Schwartzberg R, Zlatkin MB, Cooperman A, Dixon JR. Magnetic resonance imaging accuracy for the diagnosis of superior labrum anterior-posterior lesions in the community setting: eighty-three arthroscopically confirmed cases. J Shoulder Elbow Surg. 2006;15(5):580-585.
41. Connell DA, Potter HG, Wickiewicz TL, Altchek DW, Warren RF. Noncontrast magnetic resonance imaging of superior labral lesions. 102 cases confirmed at arthroscopic surgery. Am J Sports Med. 1999;27(2):208-213.
42. Hashiuchi T, Sakurai G, Morimoto M, Komei T, Takakura Y, Tanaka Y. Accuracy of the biceps tendon sheath injection: ultrasound-guided or unguided injection? A randomized controlled trial. J Shoulder Elbow Surg. 2011;20(7):1069-1073.
43. Hsu AR, Ghodadra NS, Provencher MT, Lewis PB, Bach BR. Biceps tenotomy versus tenodesis: a review of clinical outcomes and biomechanical results. J Shoulder Elbow Surg. 2011;20(2):326-332.
44. Slenker NR, Lawson K, Ciccotti MG, Dodson CC, Cohen SB. Biceps tenotomy versus tenodesis: clinical outcomes. Arthroscopy. 2012;28(4):576-582.
45. Frost A, Zafar MS, Maffulli N. Tenotomy versus tenodesis in the management of pathologic lesions of the tendon of the long head of the biceps brachii. Am J Sports Med. 2009;37(4):828-833.
46. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
47. Berlemann U, Bayley I. Tenodesis of the long head of biceps brachii in the painful shoulder: improving results in the long term. J Shoulder Elbow Surg. 1995;4(6):429-435.
48. Gill TJ, McIrvin E, Mair SD, Hawkins RJ. Results of biceps tenotomy for treatment of pathology of the long head of the biceps brachii. J Shoulder Elbow Surg. 2001;10(3):247-249.
49. Sanders B, Lavery KP, Pennington S, Warner JJ. Clinical success of biceps tenodesis with and without release of the transverse humeral ligament. J Shoulder Elbow Surg. 2012;21(1):66-71.
50. Gartsman GM, Hammerman SM. Arthroscopic biceps tenodesis: operative technique. Arthroscopy. 2000;16(5):550-552.
51. Richards DP, Burkhart SS. Arthroscopic-assisted biceps tenodesis for ruptures of the long head of biceps brachii: the cobra procedure. Arthroscopy. 2004;20(suppl 2):201-207.
52. Klepps S, Hazrati Y, Flatow E. Arthroscopic biceps tenodesis. Arthroscopy. 2002;18(9):1040-1045.
53. Werner BC, Pehlivan HC, Hart JM, et al. Increased incidence of postoperative stiffness after arthroscopic compared with open biceps tenodesis. Arthroscopy. 2014;30(9):1075-1084.54. Werner BC, Lyons ML, Evans CL, et al. Arthroscopic suprapectoral and open subpectoral biceps tenodesis: a comparison of restoration of length-tension and mechanical strength between techniques. Arthroscopy. 2015;31(4):620-627.
55. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
56. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
57. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc. 2008;16(3):170-176.
58. Taylor SA, Fabricant PD, Baret NJ, et al. Midterm clinical outcomes for arthroscopic subdeltoid transfer of the long head of the biceps tendon to the conjoint tendon. Arthroscopy. 2014;30(12):1574-1581.
59. Drakos MC, Verma NN, Gulotta LV, et al. Arthroscopic transfer of the long head of the biceps tendon: functional outcome and clinical results. Arthroscopy. 2008;24(2):217-223.
60. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
61. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
62. Ma H, Van Heest A, Glisson C, Patel S. Musculocutaneous nerve entrapment: an unusual complication after biceps tenodesis. Am J Sports Med. 2009;37(12):2467-2469.
63. Dein EJ, Huri G, Gordon JC, McFarland EG. A humerus fracture in a baseball pitcher after biceps tenodesis. Am J Sports Med. 2014;42(4):877-879.
64. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
65. O’Brien SJ, Taylor SA, DiPietro JR, Newman AM, Drakos MC, Voos JE. The arthroscopic “subdeltoid approach” to the anterior shoulder. J Shoulder Elbow Surg. 2013;22(4):e6-e10.
66. Urch E, Taylor SA, Ramkumar PN, et al. Biceps tenodesis: a comparison of tendon-to-bone and tendon-to-tendon healing in a rat model. Paper presented at: Closed Meeting of the American Shoulder and Elbow Surgeons; October 10, 2015; Asheville, NC. Paper 26.
67. Taylor SA, Ramkumar PN, Fabricant PD, et al. The clinical impact of bicipital tunnel decompression during long head of the biceps tendon surgery: a systematic review and meta-analysis. Arthroscopy. 2016;32(6):1155-1164.
1. Taylor SA, Khair MM, Gulotta LV, et al. Diagnostic glenohumeral arthroscopy fails to fully evaluate the biceps-labral complex. Arthroscopy. 2015;31(2):215-224.
2. Taylor SA, Fabricant PD, Bansal M, et al. The anatomy and histology of the bicipital tunnel of the shoulder. J Shoulder Elbow Surg. 2015;24(4):511-519.
3. Vangsness CT Jr, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
4. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, DiCarlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. an anatomical study. J Bone Joint Surg Am. 1992;74(1):46-52.
5. Tuoheti Y, Itoi E, Minagawa H, et al. Attachment types of the long head of the biceps tendon to the glenoid labrum and their relationships with the glenohumeral ligaments. Arthroscopy. 2005;21(10):1242-1249.
6. Dierickx C, Ceccarelli E, Conti M, Vanlommel J, Castagna A. Variations of the intra-articular portion of the long head of the biceps tendon: a classification of embryologically explained variations. J Shoulder Elbow Surg. 2009;18(4):556-565.
7. Denard PJ, Dai X, Hanypsiak BT, Burkhart SS. Anatomy of the biceps tendon: implications for restoring physiological length-tension relation during biceps tenodesis with interference screw fixation. Arthroscopy. 2012;28(10):1352-1358.
8. Ahrens PM, Boileau P. The long head of biceps and associated tendinopathy. J Bone Joint Surg Br. 2007;89(8):1001-1009.
9. Hart ND, Golish SR, Dragoo JL. Effects of arm position on maximizing intra-articular visualization of the biceps tendon: a cadaveric study. Arthroscopy. 2012;28(4):481-485.
10. Elser F, Braun S, Dewing CB, Giphart JE, Millett PJ. Anatomy, function, injuries, and treatment of the long head of the biceps brachii tendon. Arthroscopy. 2011;27(4):581-592.
11. Cheng NM, Pan WR, Vally F, Le Roux CM, Richardson MD. The arterial supply of the long head of biceps tendon: anatomical study with implications for tendon rupture. Clin Anat. 2010;23(6):683-692.
12. Habermeyer P, Magosch P, Pritsch M, Scheibel MT, Lichtenberg S. Anterosuperior impingement of the shoulder as a result of pulley lesions: a prospective arthroscopic study. J Shoulder Elbow Surg. 2004;13(1):5-12.
13. Gohlke F, Daum P, Bushe C. The stabilizing function of the glenohumeral joint capsule. Current aspects of the biomechanics of instability [in German]. Z Orthop Ihre Grenzgeb. 1994;132(2):112-119.
14. Arai R, Mochizuki T, Yamaguchi K, et al. Functional anatomy of the superior glenohumeral and coracohumeral ligaments and the subscapularis tendon in view of stabilization of the long head of the biceps tendon. J Shoulder Elbow Surg. 2010;19(1):58-64.
15. Busconi BB, DeAngelis N, Guerrero PE. The proximal biceps tendon: tricks and pearls. Sports Med Arthrosc. 2008;16(3):187-194.
16. Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274-279.
17. Powell SE, Nord KD, Ryu RKN. The diagnosis, classification, and treatment of SLAP lesions. Oper Tech Sports Med. 2004;12(2):99-110.
18. Verma NN, Drakos M, O’Brien SJ. The arthroscopic active compression test. Arthroscopy. 2005;21(5):634.
19. Walch G, Nove-Josserand L, Levigne C, Renaud E. Tears of the supraspinatus tendon associated with “hidden” lesions of the rotator interval. J Shoulder Elbow Surg. 1994;3(6):353-360.
20. Gilmer BB, DeMers AM, Guerrero D, Reid JB 3rd, Lubowitz JH, Guttmann D. Arthroscopic versus open comparison of long head of biceps tendon visualization and pathology in patients requiring tenodesis. Arthroscopy. 2015;31(1):29-34.
21. Moon SC, Cho NS, Rhee YG. Analysis of “hidden lesions” of the extra-articular biceps after subpectoral biceps tenodesis: the subpectoral portion as the optimal tenodesis site. Am J Sports Med. 2015;43(1):63-68.
22. Festa A, Allert J, Issa K, Tasto JP, Myer JJ. Visualization of the extra-articular portion of the long head of the biceps tendon during intra-articular shoulder arthroscopy. Arthroscopy. 2014;30(11):1413-1417.
23. O’Brien SJ, Newman AM, Taylor SA, et al. The accurate diagnosis of biceps-labral complex lesions with MRI and “3-pack” physical examination: a retrospective analysis with prospective validation. Orthop J Sports Med. 2013;1(4 suppl). doi:10.1177/2325967113S00018.
24. Hegedus EJ, Goode AP, Cook CE, et al. Which physical examination tests provide clinicians with the most value when examining the shoulder? Update of a systematic review with meta-analysis of individual tests. Br J Sports Med. 2012;46(14):964-978.
25. Chen HS, Lin SH, Hsu YH, Chen SC, Kang JH. A comparison of physical examinations with musculoskeletal ultrasound in the diagnosis of biceps long head tendinitis. Ultrasound Med Biol. 2011;37(9):1392-1398.
26. Taylor SA, Newman AM, Dawson C, et al. The “3-Pack” examination is critical for comprehensive evaluation of the biceps-labrum complex and the bicipital tunnel: a prospective study. Arthroscopy. 2016 Jul 20. [Epub ahead of print]
27. Gill HS, El Rassi G, Bahk MS, Castillo RC, McFarland EG. Physical examination for partial tears of the biceps tendon. Am J Sports Med. 2007;35(8):1334-1340.
28. O’Brien SJ, Pagnani MJ, Fealy S, McGlynn SR, Wilson JB. The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med. 1998;26(5):610-613.
29. Zanetti M, Weishaupt D, Gerber C, Hodler J. Tendinopathy and rupture of the tendon of the long head of the biceps brachii muscle: evaluation with MR arthrography. AJR Am J Roentgenol. 1998;170(6):1557-1561.
30. Taylor SA, Newman AM, Nguyen J, et al. Magnetic resonance imaging currently fails to fully evaluate the biceps-labrum complex and bicipital tunnel. Arthroscopy. 2016;32(2):238-244.
31. Malavolta EA, Assunção JH, Guglielmetti CL, de Souza FF, Gracitelli ME, Ferreira Neto AA. Accuracy of preoperative MRI in the diagnosis of disorders of the long head of the biceps tendon. Eur J Radiol. 2015;84(11):2250-2254.
32. Dubrow SA, Streit JJ, Shishani Y, Robbin MR, Gobezie R. Diagnostic accuracy in detecting tears in the proximal biceps tendon using standard nonenhancing shoulder MRI. Open Access J Sports Med. 2014;5:81-87.
33. Nourissat G, Tribot-Laspiere Q, Aim F, Radier C. Contribution of MRI and CT arthrography to the diagnosis of intra-articular tendinopathy of the long head of the biceps. Orthop Traumatol Surg Res. 2014;100(8 suppl):S391-S394.
34. De Maeseneer M, Boulet C, Pouliart N, et al. Assessment of the long head of the biceps tendon of the shoulder with 3T magnetic resonance arthrography and CT arthrography. Eur J Radiol. 2012;81(5):934-939.
35. Houtz CG, Schwartzberg RS, Barry JA, Reuss BL, Papa L. Shoulder MRI accuracy in the community setting. J Shoulder Elbow Surg. 2011;20(4):537-542.
36. Buck FM, Grehn H, Hilbe M, Pfirrmann CW, Manzanell S, Hodler J. Degeneration of the long biceps tendon: comparison of MRI with gross anatomy and histology. AJR Am J Roentgenol. 2009;193(5):1367-1375.
37. Mohtadi NG, Vellet AD, Clark ML, et al. A prospective, double-blind comparison of magnetic resonance imaging and arthroscopy in the evaluation of patients presenting with shoulder pain. J Shoulder Elbow Surg. 2004;13(3):258-265.
38. Sheridan K, Kreulen C, Kim S, Mak W, Lewis K, Marder R. Accuracy of magnetic resonance imaging to diagnose superior labrum anterior-posterior tears. Knee Surg Sports Traumatol Arthrosc. 2015;23(9):2645-2650.
39. Connolly KP, Schwartzberg RS, Reuss B, Crumbie D Jr, Homan BM. Sensitivity and specificity of noncontrast magnetic resonance imaging reports in the diagnosis of type-II superior labral anterior-posterior lesions in the community setting. J Bone Joint Surg Am. 2013;95(4):308-313.
40. Reuss BL, Schwartzberg R, Zlatkin MB, Cooperman A, Dixon JR. Magnetic resonance imaging accuracy for the diagnosis of superior labrum anterior-posterior lesions in the community setting: eighty-three arthroscopically confirmed cases. J Shoulder Elbow Surg. 2006;15(5):580-585.
41. Connell DA, Potter HG, Wickiewicz TL, Altchek DW, Warren RF. Noncontrast magnetic resonance imaging of superior labral lesions. 102 cases confirmed at arthroscopic surgery. Am J Sports Med. 1999;27(2):208-213.
42. Hashiuchi T, Sakurai G, Morimoto M, Komei T, Takakura Y, Tanaka Y. Accuracy of the biceps tendon sheath injection: ultrasound-guided or unguided injection? A randomized controlled trial. J Shoulder Elbow Surg. 2011;20(7):1069-1073.
43. Hsu AR, Ghodadra NS, Provencher MT, Lewis PB, Bach BR. Biceps tenotomy versus tenodesis: a review of clinical outcomes and biomechanical results. J Shoulder Elbow Surg. 2011;20(2):326-332.
44. Slenker NR, Lawson K, Ciccotti MG, Dodson CC, Cohen SB. Biceps tenotomy versus tenodesis: clinical outcomes. Arthroscopy. 2012;28(4):576-582.
45. Frost A, Zafar MS, Maffulli N. Tenotomy versus tenodesis in the management of pathologic lesions of the tendon of the long head of the biceps brachii. Am J Sports Med. 2009;37(4):828-833.
46. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213.
47. Berlemann U, Bayley I. Tenodesis of the long head of biceps brachii in the painful shoulder: improving results in the long term. J Shoulder Elbow Surg. 1995;4(6):429-435.
48. Gill TJ, McIrvin E, Mair SD, Hawkins RJ. Results of biceps tenotomy for treatment of pathology of the long head of the biceps brachii. J Shoulder Elbow Surg. 2001;10(3):247-249.
49. Sanders B, Lavery KP, Pennington S, Warner JJ. Clinical success of biceps tenodesis with and without release of the transverse humeral ligament. J Shoulder Elbow Surg. 2012;21(1):66-71.
50. Gartsman GM, Hammerman SM. Arthroscopic biceps tenodesis: operative technique. Arthroscopy. 2000;16(5):550-552.
51. Richards DP, Burkhart SS. Arthroscopic-assisted biceps tenodesis for ruptures of the long head of biceps brachii: the cobra procedure. Arthroscopy. 2004;20(suppl 2):201-207.
52. Klepps S, Hazrati Y, Flatow E. Arthroscopic biceps tenodesis. Arthroscopy. 2002;18(9):1040-1045.
53. Werner BC, Pehlivan HC, Hart JM, et al. Increased incidence of postoperative stiffness after arthroscopic compared with open biceps tenodesis. Arthroscopy. 2014;30(9):1075-1084.54. Werner BC, Lyons ML, Evans CL, et al. Arthroscopic suprapectoral and open subpectoral biceps tenodesis: a comparison of restoration of length-tension and mechanical strength between techniques. Arthroscopy. 2015;31(4):620-627.
55. Nho SJ, Reiff SN, Verma NN, Slabaugh MA, Mazzocca AD, Romeo AA. Complications associated with subpectoral biceps tenodesis: low rates of incidence following surgery. J Shoulder Elbow Surg. 2010;19(5):764-768.
56. Mazzocca AD, Cote MP, Arciero CL, Romeo AA, Arciero RA. Clinical outcomes after subpectoral biceps tenodesis with an interference screw. Am J Sports Med. 2008;36(10):1922-1929.
57. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc. 2008;16(3):170-176.
58. Taylor SA, Fabricant PD, Baret NJ, et al. Midterm clinical outcomes for arthroscopic subdeltoid transfer of the long head of the biceps tendon to the conjoint tendon. Arthroscopy. 2014;30(12):1574-1581.
59. Drakos MC, Verma NN, Gulotta LV, et al. Arthroscopic transfer of the long head of the biceps tendon: functional outcome and clinical results. Arthroscopy. 2008;24(2):217-223.
60. Ding DY, Gupta A, Snir N, Wolfson T, Meislin RJ. Nerve proximity during bicortical drilling for subpectoral biceps tenodesis: a cadaveric study. Arthroscopy. 2014;30(8):942-946.
61. Dickens JF, Kilcoyne KG, Tintle SM, Giuliani J, Schaefer RA, Rue JP. Subpectoral biceps tenodesis: an anatomic study and evaluation of at-risk structures. Am J Sports Med. 2012;40(10):2337-2341.
62. Ma H, Van Heest A, Glisson C, Patel S. Musculocutaneous nerve entrapment: an unusual complication after biceps tenodesis. Am J Sports Med. 2009;37(12):2467-2469.
63. Dein EJ, Huri G, Gordon JC, McFarland EG. A humerus fracture in a baseball pitcher after biceps tenodesis. Am J Sports Med. 2014;42(4):877-879.
64. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20(6):e7-e11.
65. O’Brien SJ, Taylor SA, DiPietro JR, Newman AM, Drakos MC, Voos JE. The arthroscopic “subdeltoid approach” to the anterior shoulder. J Shoulder Elbow Surg. 2013;22(4):e6-e10.
66. Urch E, Taylor SA, Ramkumar PN, et al. Biceps tenodesis: a comparison of tendon-to-bone and tendon-to-tendon healing in a rat model. Paper presented at: Closed Meeting of the American Shoulder and Elbow Surgeons; October 10, 2015; Asheville, NC. Paper 26.
67. Taylor SA, Ramkumar PN, Fabricant PD, et al. The clinical impact of bicipital tunnel decompression during long head of the biceps tendon surgery: a systematic review and meta-analysis. Arthroscopy. 2016;32(6):1155-1164.