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Comparison of Anterior and Posterior Cortico­steroid Injections for Pain Relief and Functional Improvement in Shoulder Impingement Syndrome

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Take-Home Points

  • When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.

  • Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months

  • CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used.

  • Clinical response to CSI may not depend on injection accuracy.

  • Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Shoulder pain, a common clinical problem, occurs in 7% to 34% of the general population and in 21% of people older than 70 years.1Subacromial impingement refers to shoulder pain resulting from mechanical impingement of the rotator cuff underneath the coracoacromial arch between the acromion and the humeral head.2,3 Subacromial impingement syndrome (SIS) is the most common cause of shoulder pain, resulting in significant functional deficits and disability.3

Treatment options for SIS include conservative modalities such as use of nonsteroidal anti-inflammatory drugs, physical therapy (PT), and subacromial corticosteroid injections (CSIs). Studies have found short- and long-term improvement in pain, function, and range of motion after CSI.4-8 Subacromial CSI can be administered through an anterior or a posterior route.4,9 There have been several studies of the accuracy of anterior and posterior CSIs,10-12 with 2 studies finding similar accuracy for these routes.10,11 However, there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12

Although the accuracy of anterior and posterior routes has been studied, their effect on clinical outcomes has not. We conducted a study to understand the effects of anterior and posterior CSIs on SIS. As one of the accuracy studies suggested anterior CSI is more accurate—the anterior route was theorized to provide easier access to the subacromial space12—we hypothesized patients treated with anterior CSI would have superior clinical outcomes 6 months after injection.12,13

Materials and Methods

Study Participants and Randomization

After this study received Institutional Review Board approval, patients with shoulder pain of more than 3 months’ duration and consistent with SIS were screened for inclusion. Eligible patients had pain in the anterior biceps and over the top of the shoulder with overhead activities as well as one or more clinical findings on physical examination: Hawkins-Kennedy sign, Neer sign, painful arc, and infraspinatus pain (pain with external rotation).

Patients were excluded if their history included prior subacromial CSI, adhesive capsulitis (inability to passively abduct shoulder to 90° with scapular stabilization), calcific tendonitis, radiographic evidence of os acromiale, cervical radiculopathy, Spurling sign, neck pain, radiating arm pain or numbness, sensory deficits, or neck and upper extremity motor dysfunction. Also excluded were patients with full-thickness rotator cuff tear, weakness on arm elevation, positive "drop arm sign," or high-riding humerus on standing shoulder radiograph. Patients who had work-related injuries or who were involved in worker compensation were excluded as well.

Enrolled patients were randomly assigned (with use of a computer-based random number generator) to receive either anterior CSI or posterior CSI.

Injection Procedures

All patients were administered 5 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone by 2 board-certified orthopedic surgeons using a 22-gauge 1½-inch needle. For patients who received their subacromial CSI by the anterior route, the arm was held in 0° of abduction and 20° of external rotation. The needle was inserted medial to the humeral head, lateral to the coracoid process, beginning 1 cm inferior to the clavicle with the needle directed posteriorly and laterally toward the acromion.10 For patients who received their CSI by the posterior route, the arm was held in 0° of abduction, the posterolateral corner of the acromion was identified by palpation, and the needle was inserted 1 cm inferior and medial to this point with the needle directed anteriorly and laterally toward the acromion.10,12 In both groups, the subacromial space was identified when a drop in pressure was felt during needle insertion. Accuracy was assessed post hoc by asking patients to grade their response to the injection on a visual analog scale (VAS); VAS score was used as a surrogate for improvement. All patients had a positive Neer test: Pain decreased with impingement maneuvers immediately after injection.

All patients were referred for PT provided according to an evidence-based rehabilitation protocol.14 This program emphasized range of motion with shoulder shrugs, scapular retraction, and pendulum exercises; flexibility with stretching exercises targeting the anterior and posterior aspects of the shoulder and cane stretching for forward elevation and external rotation; and strength with strengthening exercises involving the rotator cuff and scapular stabilizers.

Outcome Measures

Pain was measured with VAS scores and function with Single Assessment Numeric Evaluation (SANE) scores. The VAS is a validated outcome measure of pain intensity. A numeric version of the VAS was used: Patients selected the whole number, from 0 (no pain) to 10 (worst possible pain), that best reflected their pain intensity. On SANE, another validated outcome measure, patients rated their shoulder function as a percentage of normal, from 0% (no function possible) to 100% (perfect).15 Before injection, all patients were administered the VAS and SANE questionnaires to establish their baseline pain level and opinion of shoulder function. These measures were repeated 1, 3, and 6 months after injection. Telephone interviews were conducted at 1 month and 6 months. Patients were asked to return to clinic 3 months after injection as part of the standard of care. At 3 months, 47 (86%) of the 55 patients returned for follow-up and were administered the VAS and SANE questionnaires; the other 8 completed the questionnaires by telephone. At each time point, patients were asked to report on their participation in PT and/or adherence to their home exercise program.

Statistical Analysis

Power analysis performed with Student t test and a 2-sided level of P = .05 compared VAS pain scores between the anterior and posterior injection routes and found a mean (SD) difference of 1.4 (1.7).16 Power calculations made with nQuery Advisor Version 7.0 (Statistical Solutions) indicated a total sample size of 60 patients (30/group) would provide 80% power for detecting a significant difference assuming a 20% dropout rate.

Two-way mixed-model analysis of variance (ANOVA) was used to compare the anterior and posterior routes for statistical differences in both VAS pain scores and SANE function scores at baseline and 1, 3, and 6 months after injection. Likewise, time at baseline (just before injection)was compared with follow-up (1, 3, 6 months) with 2-way mixed-model ANOVA adjusting for anterior or posterior route. Multivariate analysis was performed to evaluate differences between baseline and 6-month follow-up with respect to anterior and posterior injection routes, controlling for age, sex, and body mass index (BMI) for VAS and SANE scores. Parametric testing methods were used for statistical analysis, which was performed with IBM SPSS Statistics Version 21.0 (IBM Corp). Significance was set at P < .05.

Results

Patient Characteristics

Of the 55 patients enrolled, 25 (46%) received anterior subacromial CSI and 30 (54%) received posterior CSI. All enrolled patients had a positive Neer impingement test immediately after injection. Mean (SD) age was 48 (9.3) years for anterior group patients and 48 (9.0) years for posterior group patients. There was no significant difference in age or BMI between the 2 groups (Table).

Table.

Five patients (9%) were excluded from the study after randomization and CSI: 2 for a full-thickness rotator cuff tear, 1 for a Bankart lesion, 1 for adhesive capsulitis, and 1 for a worker compensation claim.

One month after injection, 41 patients (75%) reported having engaged in PT as prescribed. Of the 47 patients (86%) who returned for the 3-month follow-up, 25 (46%) reported having engaged in PT between 1 month and 3 months after injection. Fourteen patients (26%) reported attending PT between 3 and 6 months post-injection.

Outcome Measures

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in VAS scores between the anterior and posterior groups at any time point (P = .45). Both groups had highly significant pain reductions (anterior, F = 9.71, P < .001; posterior, F = 13.46, P < .001). Figure 1 shows mean VAS scores and significant reductions in pain 1, 3, and 6 months after injection (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of pain reduction over time, as indicated by a nonsignificant (P = .50) difference in slopes. These pain score reductions were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 1.

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in SANE scores between the anterior and posterior groups, except for a higher mean score in the anterior group at 3 months
(P = .02). There were no other group differences (P > .10 for all). Both groups had highly significant improvements in function (anterior, F = 17.34,
P < .001; posterior, F = 13.57, P < .001). Figure 2 shows mean SANE scores and significant improvement at 1, 3, and 6 months (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of improved function over time, as indicated by a nonsignificant (P = .51) difference in slopes. These function score improvements were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 2.

From the results of this prospective randomized study, we concluded subacromial CSI significantly reduces pain and improves function regardless of route used. In addition, age, sex, and BMI do not significantly affect the efficacy of either anterior CSI or posterior CSI.

Discussion

In patients with SIS, anterior CSI and posterior CSI provided significant improvements in pain and function 1, 3, and 6 months after injection. These effects were independent of age, sex, BMI, and PT participation. There were no significant differences in outcomes between injection routes.

When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.4-8 Although clinical outcomes are inconsistent, CSI can be used to address SIS symptoms in appropriate patients. Specifically, Blair and colleagues6 found that, CSI consisting of 4 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone was effective in alleviating shoulder pain and improving shoulder range of motion. Other authors have similarly reported improved outcomes after subacromial injection and short-term follow-up with PT.4,7,8 Our findings are consistent with these reports: CSI coupled with a structured rehabilitation program is effective in alleviating symptoms associated with acute or subacute SIS.

Numerous studies have found improved clinical outcomes after anterior CSI and after posterior CSI,6-8 but no study has directly compared the clinical impact of anterior CSI with that of posterior CSI—which suggests injection route may not affect ultimate clinical outcomes.

CSI accuracy has been studied extensively.10-12,17-20 Although 2 studies found similar accuracy for anterior and posterior routes,10,11 there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12 Collectively, these studies expose the inherent difficulty in treating shoulder pain with localized subacromial injection. Therapy may fail because of errant needle positioning. Two prospective studies found improved clinical outcomes with successful delivery of medication into the subacromial space.17,18 Poor clinical outcomes may result from inaccurate CSI.

In contrast to other clinical studies, our study found that injection route was not associated with differences in clinical response. In a prospective randomized clinical trial in which 75 patients received a subacromial injection, Marder and colleagues12 found anterior routes 84% accurate and posterior routes 56% accurate; they concluded acromion anatomy and subacromial bursa anatomy make posterior injections more difficult. As theorized by Gruson and colleagues,13 with use of an anterior route, the needle enters inferior to the concavity of the acromion and provides easier access to the subacromial space. This idea is in line with Marder and colleagues’12 conclusion that subacromial bursa anatomy provides a favorable environment for accurate CSI.

If accuracy is positively correlated with clinical improvement and anterior routes are more accurate, there should be a difference in response to posterior injections. Our results provide evidence that clinical response to CSI may not depend on injection accuracy. Perhaps merely placing the corticosteroid near the bursa is adequate for improving symptoms or perhaps some of the clinical improvement is due to the systemic effect of corticosteroids. These possibilities require further analysis.

Establishing the efficacy of CSI in SIS is difficult. The literature includes various study designs, different CSI indications and medication formulations, and varying emphasis on the role of organized PT. Rehabilitation has been found to alleviate joint pain by reducing inflammation,14 but data do not universally support this finding.21,22 Nevertheless, use of PT might explain the divergence in clinical outcomes reported by Marder and colleagues,12 who found anterior CSI more accurate than posterior CSI. In our practice, PT is recommended for all SIS patients, not only those who have CSI. Thus, our findings are framed within the context of successful CSI but may include patients who improved with PT alone. This issue raises the question of whether subacromial CSI should be guided by ultrasound. Ultrasound guidance can improve CSI accuracy and clinical outcomes,23-25 though the value of this benefit is debated.26

This study had several limitations. First, pain relief was patient reported. Second, the treatment plan involved CSI with PT but did not control for CSI used alone. PT, which is part of the standard of care for patients with SIS, added another degree of complexity to the study. Third, there may have been some variability in SIS severity (stage 1, 2, or 3). Fourth, although the study design controlled for various shoulder pathologies, advanced imaging, which could have provided diagnosis confirmation, was not available for all patients. Therefore, concurrent conditions may have confounded results. However, randomization was used to try to minimize this effect. Fifth, although injection routes were randomly assigned, the trial was not blinded. Sixth, the study was underpowered by 1 patient, as there was an estimated 20% dropout rate over 3 and 6 months of follow-up. However, we do not think our results were significantly affected.

Although more research is needed to fully describe the role of subacromial CSI in SIS, our study findings suggested that CSI using either an anterior or a posterior route creates a window of symptomatic relief in which patients may be able to engage in PT.

Conclusion

Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months. No differences were found between anterior and posterior CSIs. In the context of this study, CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used. Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

References

1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev. 2003;(1):CD004016.

2. Bell AD, Conaway D. Corticosteroid injections for painful shoulders. Int J Clin Pract. 2005;59(10):1178-1186.

3. Michener LA, McClure PW, Karduna AR. Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech. 2003;18(5):369-379.

4. Akgün K, Birtane M, Akarirmak U. Is local subacromial corticosteroid injection beneficial in subacromial impingement syndrome? Clin Rheumatol. 2004;23(6):496-500.

5. Bhagra A, Syed H, Reed DA, et al. Efficacy of musculoskeletal injections by primary care providers in the office: a retrospective cohort study. Int J Gen Med. 2013;6:237-243.

6. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am. 1996;78(11):1685-1689.

7. Cummins CA, Sasso LM, Nicholson D. Impingement syndrome: temporal outcomes of nonoperative treatment.
J Shoulder Elbow Surg. 2009;18(2):172-177.

8. Yu C, Chen CH, Liu HT, Dai MH, Wang IC, Wang KC. Subacromial injections of corticosteroids and Xylocaine for painful subacromial impingement syndrome. Chang Gung Med J. 2006;29(5):474-478.

9. Codsi MJ. The painful shoulder: when to inject and when to refer. Cleve Clin J Med. 2007;74(7):473-474, 477-478, 480-482 passim.

10. Henkus HE, Cobben LP, Coerkamp EG, Nelissen RG, van Arkel ER. The accuracy of subacromial injections: a prospective randomized magnetic resonance imaging study. Arthroscopy. 2006;22(3):277-282.

11. Kang MN, Rizio L, Prybicien M, Middlemas DA, Blacksin MF. The accuracy of subacromial corticosteroid injections: a comparison of multiple methods. J Shoulder Elbow Surg. 2008;17(15):61S-66S.

12. Marder RA, Kim SH, Labson JD, Hunter JC. Injection of the subacromial bursa in patients with rotator cuff syndrome: a prospective, randomized study comparing the effectiveness of different routes. J Bone Joint Surg Am. 2012;94(16):
1442-1447.

13. Gruson, KI, Ruchelsman DE, Zuckerman JD. Subacromial corticosteroid injections. J Shoulder Elbow Surg. 2008;17(1 suppl):118S-130S.

14. Kuhn JE. Exercise in the treatment of rotator cuff impingement: a systematic review and a synthesized evidence-based rehabilitation protocol. J Shoulder Elbow Surg. 2009;18(1):138-160.

15. Williams GN, Gangel TJ, Arciero RA, Uhorchak JM, Taylor DC. Comparison of the Single Assessment Numeric Evaluation method and two shoulder rating scales. Outcomes measures after shoulder surgery. Am J Sports Med. 1999;27(2):214-221.

16. Tashjian RZ, Deloach J, Porucznik CA, Powell AP. Minimal clinically important differences (MCID) and patient acceptable symptomatic state (PASS) for visual analog scales (VAS) measuring pain in patients treated for rotator cuff disease.
J Shoulder Elbow Surg. 2009;88(6):927-932.

17. Eustace JA, Brophy DP, Gibney RP, Bresnihan B, FitzGerald O. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis. 1997;56(1):59-63.

18. Esenyel CZ, Esenyel M, Yeiltepe R, et al. The correlation between the accuracy of steroid injections and subsequent shoulder pain and function in subacromial impingement
syndrome [in Turkish]. Acta Orthop Traumatol Turc. 2003;37(1):
41-45.

19. Powell SE, Davis SM, Lee EH, et al. Accuracy of palpation-directed intra-articular glenohumeral injection confirmed by magnetic resonance arthrography. Arthroscopy. 2015;31(2):205-208.

20. Rutten MJ, Maresch BJ, Jager GJ, de Waal Malefijt MC. Injection of the subacromial-subdeltoid bursa: blind or ultrasound-guided? Acta Orthop. 2007;78(2):254-257.

21. Desmeules F, Côté CH, Frémont P. Therapeutic exercise and orthopedic manual therapy for impingement syndrome: a systematic review. Clin J Sport Med. 2003;13(3):176-182.

22. Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de Jong B. Comparison of physiotherapy, manipulation, and corticosteroid injection for treating shoulder complaints in general practice: randomised, single blind study. BMJ. 1997;314(7090):1320-1325.

23. Chen MJ, Lew HL, Hsu TC, et al. Ultrasound-guided shoulder injections in the treatment of subacromial bursitis. Am J Phys Med Rehabil. 2006;85(1):31-35.

24. Hsieh LF, Hsu WC, Lin YJ, Wu SH, Chang KC, Chang HL. Is ultrasound-guided injection more effective in chronic subacromial bursitis? Med Sci Sports Exerc. 2013;45(12):
2205-2213.

25. Naredo E, Cabero F, Beneyto P, et al. A randomized comparative study of short term response to blind injection versus sonographic-guided injection of local corticosteroids in patients with painful shoulder. J Rheumatol. 2004;31(2):308-314.

26. Hall S, Buchbinder R. Do imaging methods that guide needle placement improve outcome? Ann Rheum Dis. 2004;63(9):1007-1008.

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Take-Home Points

  • When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.

  • Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months

  • CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used.

  • Clinical response to CSI may not depend on injection accuracy.

  • Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Shoulder pain, a common clinical problem, occurs in 7% to 34% of the general population and in 21% of people older than 70 years.1Subacromial impingement refers to shoulder pain resulting from mechanical impingement of the rotator cuff underneath the coracoacromial arch between the acromion and the humeral head.2,3 Subacromial impingement syndrome (SIS) is the most common cause of shoulder pain, resulting in significant functional deficits and disability.3

Treatment options for SIS include conservative modalities such as use of nonsteroidal anti-inflammatory drugs, physical therapy (PT), and subacromial corticosteroid injections (CSIs). Studies have found short- and long-term improvement in pain, function, and range of motion after CSI.4-8 Subacromial CSI can be administered through an anterior or a posterior route.4,9 There have been several studies of the accuracy of anterior and posterior CSIs,10-12 with 2 studies finding similar accuracy for these routes.10,11 However, there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12

Although the accuracy of anterior and posterior routes has been studied, their effect on clinical outcomes has not. We conducted a study to understand the effects of anterior and posterior CSIs on SIS. As one of the accuracy studies suggested anterior CSI is more accurate—the anterior route was theorized to provide easier access to the subacromial space12—we hypothesized patients treated with anterior CSI would have superior clinical outcomes 6 months after injection.12,13

Materials and Methods

Study Participants and Randomization

After this study received Institutional Review Board approval, patients with shoulder pain of more than 3 months’ duration and consistent with SIS were screened for inclusion. Eligible patients had pain in the anterior biceps and over the top of the shoulder with overhead activities as well as one or more clinical findings on physical examination: Hawkins-Kennedy sign, Neer sign, painful arc, and infraspinatus pain (pain with external rotation).

Patients were excluded if their history included prior subacromial CSI, adhesive capsulitis (inability to passively abduct shoulder to 90° with scapular stabilization), calcific tendonitis, radiographic evidence of os acromiale, cervical radiculopathy, Spurling sign, neck pain, radiating arm pain or numbness, sensory deficits, or neck and upper extremity motor dysfunction. Also excluded were patients with full-thickness rotator cuff tear, weakness on arm elevation, positive "drop arm sign," or high-riding humerus on standing shoulder radiograph. Patients who had work-related injuries or who were involved in worker compensation were excluded as well.

Enrolled patients were randomly assigned (with use of a computer-based random number generator) to receive either anterior CSI or posterior CSI.

Injection Procedures

All patients were administered 5 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone by 2 board-certified orthopedic surgeons using a 22-gauge 1½-inch needle. For patients who received their subacromial CSI by the anterior route, the arm was held in 0° of abduction and 20° of external rotation. The needle was inserted medial to the humeral head, lateral to the coracoid process, beginning 1 cm inferior to the clavicle with the needle directed posteriorly and laterally toward the acromion.10 For patients who received their CSI by the posterior route, the arm was held in 0° of abduction, the posterolateral corner of the acromion was identified by palpation, and the needle was inserted 1 cm inferior and medial to this point with the needle directed anteriorly and laterally toward the acromion.10,12 In both groups, the subacromial space was identified when a drop in pressure was felt during needle insertion. Accuracy was assessed post hoc by asking patients to grade their response to the injection on a visual analog scale (VAS); VAS score was used as a surrogate for improvement. All patients had a positive Neer test: Pain decreased with impingement maneuvers immediately after injection.

All patients were referred for PT provided according to an evidence-based rehabilitation protocol.14 This program emphasized range of motion with shoulder shrugs, scapular retraction, and pendulum exercises; flexibility with stretching exercises targeting the anterior and posterior aspects of the shoulder and cane stretching for forward elevation and external rotation; and strength with strengthening exercises involving the rotator cuff and scapular stabilizers.

Outcome Measures

Pain was measured with VAS scores and function with Single Assessment Numeric Evaluation (SANE) scores. The VAS is a validated outcome measure of pain intensity. A numeric version of the VAS was used: Patients selected the whole number, from 0 (no pain) to 10 (worst possible pain), that best reflected their pain intensity. On SANE, another validated outcome measure, patients rated their shoulder function as a percentage of normal, from 0% (no function possible) to 100% (perfect).15 Before injection, all patients were administered the VAS and SANE questionnaires to establish their baseline pain level and opinion of shoulder function. These measures were repeated 1, 3, and 6 months after injection. Telephone interviews were conducted at 1 month and 6 months. Patients were asked to return to clinic 3 months after injection as part of the standard of care. At 3 months, 47 (86%) of the 55 patients returned for follow-up and were administered the VAS and SANE questionnaires; the other 8 completed the questionnaires by telephone. At each time point, patients were asked to report on their participation in PT and/or adherence to their home exercise program.

Statistical Analysis

Power analysis performed with Student t test and a 2-sided level of P = .05 compared VAS pain scores between the anterior and posterior injection routes and found a mean (SD) difference of 1.4 (1.7).16 Power calculations made with nQuery Advisor Version 7.0 (Statistical Solutions) indicated a total sample size of 60 patients (30/group) would provide 80% power for detecting a significant difference assuming a 20% dropout rate.

Two-way mixed-model analysis of variance (ANOVA) was used to compare the anterior and posterior routes for statistical differences in both VAS pain scores and SANE function scores at baseline and 1, 3, and 6 months after injection. Likewise, time at baseline (just before injection)was compared with follow-up (1, 3, 6 months) with 2-way mixed-model ANOVA adjusting for anterior or posterior route. Multivariate analysis was performed to evaluate differences between baseline and 6-month follow-up with respect to anterior and posterior injection routes, controlling for age, sex, and body mass index (BMI) for VAS and SANE scores. Parametric testing methods were used for statistical analysis, which was performed with IBM SPSS Statistics Version 21.0 (IBM Corp). Significance was set at P < .05.

Results

Patient Characteristics

Of the 55 patients enrolled, 25 (46%) received anterior subacromial CSI and 30 (54%) received posterior CSI. All enrolled patients had a positive Neer impingement test immediately after injection. Mean (SD) age was 48 (9.3) years for anterior group patients and 48 (9.0) years for posterior group patients. There was no significant difference in age or BMI between the 2 groups (Table).

Table.

Five patients (9%) were excluded from the study after randomization and CSI: 2 for a full-thickness rotator cuff tear, 1 for a Bankart lesion, 1 for adhesive capsulitis, and 1 for a worker compensation claim.

One month after injection, 41 patients (75%) reported having engaged in PT as prescribed. Of the 47 patients (86%) who returned for the 3-month follow-up, 25 (46%) reported having engaged in PT between 1 month and 3 months after injection. Fourteen patients (26%) reported attending PT between 3 and 6 months post-injection.

Outcome Measures

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in VAS scores between the anterior and posterior groups at any time point (P = .45). Both groups had highly significant pain reductions (anterior, F = 9.71, P < .001; posterior, F = 13.46, P < .001). Figure 1 shows mean VAS scores and significant reductions in pain 1, 3, and 6 months after injection (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of pain reduction over time, as indicated by a nonsignificant (P = .50) difference in slopes. These pain score reductions were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 1.

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in SANE scores between the anterior and posterior groups, except for a higher mean score in the anterior group at 3 months
(P = .02). There were no other group differences (P > .10 for all). Both groups had highly significant improvements in function (anterior, F = 17.34,
P < .001; posterior, F = 13.57, P < .001). Figure 2 shows mean SANE scores and significant improvement at 1, 3, and 6 months (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of improved function over time, as indicated by a nonsignificant (P = .51) difference in slopes. These function score improvements were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 2.

From the results of this prospective randomized study, we concluded subacromial CSI significantly reduces pain and improves function regardless of route used. In addition, age, sex, and BMI do not significantly affect the efficacy of either anterior CSI or posterior CSI.

Discussion

In patients with SIS, anterior CSI and posterior CSI provided significant improvements in pain and function 1, 3, and 6 months after injection. These effects were independent of age, sex, BMI, and PT participation. There were no significant differences in outcomes between injection routes.

When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.4-8 Although clinical outcomes are inconsistent, CSI can be used to address SIS symptoms in appropriate patients. Specifically, Blair and colleagues6 found that, CSI consisting of 4 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone was effective in alleviating shoulder pain and improving shoulder range of motion. Other authors have similarly reported improved outcomes after subacromial injection and short-term follow-up with PT.4,7,8 Our findings are consistent with these reports: CSI coupled with a structured rehabilitation program is effective in alleviating symptoms associated with acute or subacute SIS.

Numerous studies have found improved clinical outcomes after anterior CSI and after posterior CSI,6-8 but no study has directly compared the clinical impact of anterior CSI with that of posterior CSI—which suggests injection route may not affect ultimate clinical outcomes.

CSI accuracy has been studied extensively.10-12,17-20 Although 2 studies found similar accuracy for anterior and posterior routes,10,11 there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12 Collectively, these studies expose the inherent difficulty in treating shoulder pain with localized subacromial injection. Therapy may fail because of errant needle positioning. Two prospective studies found improved clinical outcomes with successful delivery of medication into the subacromial space.17,18 Poor clinical outcomes may result from inaccurate CSI.

In contrast to other clinical studies, our study found that injection route was not associated with differences in clinical response. In a prospective randomized clinical trial in which 75 patients received a subacromial injection, Marder and colleagues12 found anterior routes 84% accurate and posterior routes 56% accurate; they concluded acromion anatomy and subacromial bursa anatomy make posterior injections more difficult. As theorized by Gruson and colleagues,13 with use of an anterior route, the needle enters inferior to the concavity of the acromion and provides easier access to the subacromial space. This idea is in line with Marder and colleagues’12 conclusion that subacromial bursa anatomy provides a favorable environment for accurate CSI.

If accuracy is positively correlated with clinical improvement and anterior routes are more accurate, there should be a difference in response to posterior injections. Our results provide evidence that clinical response to CSI may not depend on injection accuracy. Perhaps merely placing the corticosteroid near the bursa is adequate for improving symptoms or perhaps some of the clinical improvement is due to the systemic effect of corticosteroids. These possibilities require further analysis.

Establishing the efficacy of CSI in SIS is difficult. The literature includes various study designs, different CSI indications and medication formulations, and varying emphasis on the role of organized PT. Rehabilitation has been found to alleviate joint pain by reducing inflammation,14 but data do not universally support this finding.21,22 Nevertheless, use of PT might explain the divergence in clinical outcomes reported by Marder and colleagues,12 who found anterior CSI more accurate than posterior CSI. In our practice, PT is recommended for all SIS patients, not only those who have CSI. Thus, our findings are framed within the context of successful CSI but may include patients who improved with PT alone. This issue raises the question of whether subacromial CSI should be guided by ultrasound. Ultrasound guidance can improve CSI accuracy and clinical outcomes,23-25 though the value of this benefit is debated.26

This study had several limitations. First, pain relief was patient reported. Second, the treatment plan involved CSI with PT but did not control for CSI used alone. PT, which is part of the standard of care for patients with SIS, added another degree of complexity to the study. Third, there may have been some variability in SIS severity (stage 1, 2, or 3). Fourth, although the study design controlled for various shoulder pathologies, advanced imaging, which could have provided diagnosis confirmation, was not available for all patients. Therefore, concurrent conditions may have confounded results. However, randomization was used to try to minimize this effect. Fifth, although injection routes were randomly assigned, the trial was not blinded. Sixth, the study was underpowered by 1 patient, as there was an estimated 20% dropout rate over 3 and 6 months of follow-up. However, we do not think our results were significantly affected.

Although more research is needed to fully describe the role of subacromial CSI in SIS, our study findings suggested that CSI using either an anterior or a posterior route creates a window of symptomatic relief in which patients may be able to engage in PT.

Conclusion

Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months. No differences were found between anterior and posterior CSIs. In the context of this study, CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used. Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Take-Home Points

  • When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.

  • Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months

  • CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used.

  • Clinical response to CSI may not depend on injection accuracy.

  • Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

Shoulder pain, a common clinical problem, occurs in 7% to 34% of the general population and in 21% of people older than 70 years.1Subacromial impingement refers to shoulder pain resulting from mechanical impingement of the rotator cuff underneath the coracoacromial arch between the acromion and the humeral head.2,3 Subacromial impingement syndrome (SIS) is the most common cause of shoulder pain, resulting in significant functional deficits and disability.3

Treatment options for SIS include conservative modalities such as use of nonsteroidal anti-inflammatory drugs, physical therapy (PT), and subacromial corticosteroid injections (CSIs). Studies have found short- and long-term improvement in pain, function, and range of motion after CSI.4-8 Subacromial CSI can be administered through an anterior or a posterior route.4,9 There have been several studies of the accuracy of anterior and posterior CSIs,10-12 with 2 studies finding similar accuracy for these routes.10,11 However, there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12

Although the accuracy of anterior and posterior routes has been studied, their effect on clinical outcomes has not. We conducted a study to understand the effects of anterior and posterior CSIs on SIS. As one of the accuracy studies suggested anterior CSI is more accurate—the anterior route was theorized to provide easier access to the subacromial space12—we hypothesized patients treated with anterior CSI would have superior clinical outcomes 6 months after injection.12,13

Materials and Methods

Study Participants and Randomization

After this study received Institutional Review Board approval, patients with shoulder pain of more than 3 months’ duration and consistent with SIS were screened for inclusion. Eligible patients had pain in the anterior biceps and over the top of the shoulder with overhead activities as well as one or more clinical findings on physical examination: Hawkins-Kennedy sign, Neer sign, painful arc, and infraspinatus pain (pain with external rotation).

Patients were excluded if their history included prior subacromial CSI, adhesive capsulitis (inability to passively abduct shoulder to 90° with scapular stabilization), calcific tendonitis, radiographic evidence of os acromiale, cervical radiculopathy, Spurling sign, neck pain, radiating arm pain or numbness, sensory deficits, or neck and upper extremity motor dysfunction. Also excluded were patients with full-thickness rotator cuff tear, weakness on arm elevation, positive "drop arm sign," or high-riding humerus on standing shoulder radiograph. Patients who had work-related injuries or who were involved in worker compensation were excluded as well.

Enrolled patients were randomly assigned (with use of a computer-based random number generator) to receive either anterior CSI or posterior CSI.

Injection Procedures

All patients were administered 5 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone by 2 board-certified orthopedic surgeons using a 22-gauge 1½-inch needle. For patients who received their subacromial CSI by the anterior route, the arm was held in 0° of abduction and 20° of external rotation. The needle was inserted medial to the humeral head, lateral to the coracoid process, beginning 1 cm inferior to the clavicle with the needle directed posteriorly and laterally toward the acromion.10 For patients who received their CSI by the posterior route, the arm was held in 0° of abduction, the posterolateral corner of the acromion was identified by palpation, and the needle was inserted 1 cm inferior and medial to this point with the needle directed anteriorly and laterally toward the acromion.10,12 In both groups, the subacromial space was identified when a drop in pressure was felt during needle insertion. Accuracy was assessed post hoc by asking patients to grade their response to the injection on a visual analog scale (VAS); VAS score was used as a surrogate for improvement. All patients had a positive Neer test: Pain decreased with impingement maneuvers immediately after injection.

All patients were referred for PT provided according to an evidence-based rehabilitation protocol.14 This program emphasized range of motion with shoulder shrugs, scapular retraction, and pendulum exercises; flexibility with stretching exercises targeting the anterior and posterior aspects of the shoulder and cane stretching for forward elevation and external rotation; and strength with strengthening exercises involving the rotator cuff and scapular stabilizers.

Outcome Measures

Pain was measured with VAS scores and function with Single Assessment Numeric Evaluation (SANE) scores. The VAS is a validated outcome measure of pain intensity. A numeric version of the VAS was used: Patients selected the whole number, from 0 (no pain) to 10 (worst possible pain), that best reflected their pain intensity. On SANE, another validated outcome measure, patients rated their shoulder function as a percentage of normal, from 0% (no function possible) to 100% (perfect).15 Before injection, all patients were administered the VAS and SANE questionnaires to establish their baseline pain level and opinion of shoulder function. These measures were repeated 1, 3, and 6 months after injection. Telephone interviews were conducted at 1 month and 6 months. Patients were asked to return to clinic 3 months after injection as part of the standard of care. At 3 months, 47 (86%) of the 55 patients returned for follow-up and were administered the VAS and SANE questionnaires; the other 8 completed the questionnaires by telephone. At each time point, patients were asked to report on their participation in PT and/or adherence to their home exercise program.

Statistical Analysis

Power analysis performed with Student t test and a 2-sided level of P = .05 compared VAS pain scores between the anterior and posterior injection routes and found a mean (SD) difference of 1.4 (1.7).16 Power calculations made with nQuery Advisor Version 7.0 (Statistical Solutions) indicated a total sample size of 60 patients (30/group) would provide 80% power for detecting a significant difference assuming a 20% dropout rate.

Two-way mixed-model analysis of variance (ANOVA) was used to compare the anterior and posterior routes for statistical differences in both VAS pain scores and SANE function scores at baseline and 1, 3, and 6 months after injection. Likewise, time at baseline (just before injection)was compared with follow-up (1, 3, 6 months) with 2-way mixed-model ANOVA adjusting for anterior or posterior route. Multivariate analysis was performed to evaluate differences between baseline and 6-month follow-up with respect to anterior and posterior injection routes, controlling for age, sex, and body mass index (BMI) for VAS and SANE scores. Parametric testing methods were used for statistical analysis, which was performed with IBM SPSS Statistics Version 21.0 (IBM Corp). Significance was set at P < .05.

Results

Patient Characteristics

Of the 55 patients enrolled, 25 (46%) received anterior subacromial CSI and 30 (54%) received posterior CSI. All enrolled patients had a positive Neer impingement test immediately after injection. Mean (SD) age was 48 (9.3) years for anterior group patients and 48 (9.0) years for posterior group patients. There was no significant difference in age or BMI between the 2 groups (Table).

Table.

Five patients (9%) were excluded from the study after randomization and CSI: 2 for a full-thickness rotator cuff tear, 1 for a Bankart lesion, 1 for adhesive capsulitis, and 1 for a worker compensation claim.

One month after injection, 41 patients (75%) reported having engaged in PT as prescribed. Of the 47 patients (86%) who returned for the 3-month follow-up, 25 (46%) reported having engaged in PT between 1 month and 3 months after injection. Fourteen patients (26%) reported attending PT between 3 and 6 months post-injection.

Outcome Measures

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in VAS scores between the anterior and posterior groups at any time point (P = .45). Both groups had highly significant pain reductions (anterior, F = 9.71, P < .001; posterior, F = 13.46, P < .001). Figure 1 shows mean VAS scores and significant reductions in pain 1, 3, and 6 months after injection (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of pain reduction over time, as indicated by a nonsignificant (P = .50) difference in slopes. These pain score reductions were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 1.

Two-way repeated-measures ANOVA with age, sex, and BMI included as covariates revealed no significant differences in SANE scores between the anterior and posterior groups, except for a higher mean score in the anterior group at 3 months
(P = .02). There were no other group differences (P > .10 for all). Both groups had highly significant improvements in function (anterior, F = 17.34,
P < .001; posterior, F = 13.57, P < .001). Figure 2 shows mean SANE scores and significant improvement at 1, 3, and 6 months (see asterisks for anterior and posterior groups; P < .001 for all). The groups had parallel rates of improved function over time, as indicated by a nonsignificant (P = .51) difference in slopes. These function score improvements were significant for both injection routes and were independent of age, sex, and BMI (P > .05 for all).

Figure 2.

From the results of this prospective randomized study, we concluded subacromial CSI significantly reduces pain and improves function regardless of route used. In addition, age, sex, and BMI do not significantly affect the efficacy of either anterior CSI or posterior CSI.

Discussion

In patients with SIS, anterior CSI and posterior CSI provided significant improvements in pain and function 1, 3, and 6 months after injection. These effects were independent of age, sex, BMI, and PT participation. There were no significant differences in outcomes between injection routes.

When conservative treatments for SIS do not resolve symptoms, inflammation and pain can be reduced with use of subacromial CSI.4-8 Although clinical outcomes are inconsistent, CSI can be used to address SIS symptoms in appropriate patients. Specifically, Blair and colleagues6 found that, CSI consisting of 4 mL of lidocaine 1% (without epinephrine) and 2 mL (80 mg) of triamcinolone was effective in alleviating shoulder pain and improving shoulder range of motion. Other authors have similarly reported improved outcomes after subacromial injection and short-term follow-up with PT.4,7,8 Our findings are consistent with these reports: CSI coupled with a structured rehabilitation program is effective in alleviating symptoms associated with acute or subacute SIS.

Numerous studies have found improved clinical outcomes after anterior CSI and after posterior CSI,6-8 but no study has directly compared the clinical impact of anterior CSI with that of posterior CSI—which suggests injection route may not affect ultimate clinical outcomes.

CSI accuracy has been studied extensively.10-12,17-20 Although 2 studies found similar accuracy for anterior and posterior routes,10,11 there may be a sex difference: In women, a posterior route may be less accurate than an anterior or a lateral route.12 Collectively, these studies expose the inherent difficulty in treating shoulder pain with localized subacromial injection. Therapy may fail because of errant needle positioning. Two prospective studies found improved clinical outcomes with successful delivery of medication into the subacromial space.17,18 Poor clinical outcomes may result from inaccurate CSI.

In contrast to other clinical studies, our study found that injection route was not associated with differences in clinical response. In a prospective randomized clinical trial in which 75 patients received a subacromial injection, Marder and colleagues12 found anterior routes 84% accurate and posterior routes 56% accurate; they concluded acromion anatomy and subacromial bursa anatomy make posterior injections more difficult. As theorized by Gruson and colleagues,13 with use of an anterior route, the needle enters inferior to the concavity of the acromion and provides easier access to the subacromial space. This idea is in line with Marder and colleagues’12 conclusion that subacromial bursa anatomy provides a favorable environment for accurate CSI.

If accuracy is positively correlated with clinical improvement and anterior routes are more accurate, there should be a difference in response to posterior injections. Our results provide evidence that clinical response to CSI may not depend on injection accuracy. Perhaps merely placing the corticosteroid near the bursa is adequate for improving symptoms or perhaps some of the clinical improvement is due to the systemic effect of corticosteroids. These possibilities require further analysis.

Establishing the efficacy of CSI in SIS is difficult. The literature includes various study designs, different CSI indications and medication formulations, and varying emphasis on the role of organized PT. Rehabilitation has been found to alleviate joint pain by reducing inflammation,14 but data do not universally support this finding.21,22 Nevertheless, use of PT might explain the divergence in clinical outcomes reported by Marder and colleagues,12 who found anterior CSI more accurate than posterior CSI. In our practice, PT is recommended for all SIS patients, not only those who have CSI. Thus, our findings are framed within the context of successful CSI but may include patients who improved with PT alone. This issue raises the question of whether subacromial CSI should be guided by ultrasound. Ultrasound guidance can improve CSI accuracy and clinical outcomes,23-25 though the value of this benefit is debated.26

This study had several limitations. First, pain relief was patient reported. Second, the treatment plan involved CSI with PT but did not control for CSI used alone. PT, which is part of the standard of care for patients with SIS, added another degree of complexity to the study. Third, there may have been some variability in SIS severity (stage 1, 2, or 3). Fourth, although the study design controlled for various shoulder pathologies, advanced imaging, which could have provided diagnosis confirmation, was not available for all patients. Therefore, concurrent conditions may have confounded results. However, randomization was used to try to minimize this effect. Fifth, although injection routes were randomly assigned, the trial was not blinded. Sixth, the study was underpowered by 1 patient, as there was an estimated 20% dropout rate over 3 and 6 months of follow-up. However, we do not think our results were significantly affected.

Although more research is needed to fully describe the role of subacromial CSI in SIS, our study findings suggested that CSI using either an anterior or a posterior route creates a window of symptomatic relief in which patients may be able to engage in PT.

Conclusion

Both anterior CSI and posterior CSI significantly improved pain and function for up to 6 months. No differences were found between anterior and posterior CSIs. In the context of this study, CSI combined with structured PT produced significant improvement in pain and function in patients with SIS, regardless of injection route used. Clinicians should rely on their clinical acumen when selecting injection routes, as anterior and posterior are both beneficial.

References

1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev. 2003;(1):CD004016.

2. Bell AD, Conaway D. Corticosteroid injections for painful shoulders. Int J Clin Pract. 2005;59(10):1178-1186.

3. Michener LA, McClure PW, Karduna AR. Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech. 2003;18(5):369-379.

4. Akgün K, Birtane M, Akarirmak U. Is local subacromial corticosteroid injection beneficial in subacromial impingement syndrome? Clin Rheumatol. 2004;23(6):496-500.

5. Bhagra A, Syed H, Reed DA, et al. Efficacy of musculoskeletal injections by primary care providers in the office: a retrospective cohort study. Int J Gen Med. 2013;6:237-243.

6. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am. 1996;78(11):1685-1689.

7. Cummins CA, Sasso LM, Nicholson D. Impingement syndrome: temporal outcomes of nonoperative treatment.
J Shoulder Elbow Surg. 2009;18(2):172-177.

8. Yu C, Chen CH, Liu HT, Dai MH, Wang IC, Wang KC. Subacromial injections of corticosteroids and Xylocaine for painful subacromial impingement syndrome. Chang Gung Med J. 2006;29(5):474-478.

9. Codsi MJ. The painful shoulder: when to inject and when to refer. Cleve Clin J Med. 2007;74(7):473-474, 477-478, 480-482 passim.

10. Henkus HE, Cobben LP, Coerkamp EG, Nelissen RG, van Arkel ER. The accuracy of subacromial injections: a prospective randomized magnetic resonance imaging study. Arthroscopy. 2006;22(3):277-282.

11. Kang MN, Rizio L, Prybicien M, Middlemas DA, Blacksin MF. The accuracy of subacromial corticosteroid injections: a comparison of multiple methods. J Shoulder Elbow Surg. 2008;17(15):61S-66S.

12. Marder RA, Kim SH, Labson JD, Hunter JC. Injection of the subacromial bursa in patients with rotator cuff syndrome: a prospective, randomized study comparing the effectiveness of different routes. J Bone Joint Surg Am. 2012;94(16):
1442-1447.

13. Gruson, KI, Ruchelsman DE, Zuckerman JD. Subacromial corticosteroid injections. J Shoulder Elbow Surg. 2008;17(1 suppl):118S-130S.

14. Kuhn JE. Exercise in the treatment of rotator cuff impingement: a systematic review and a synthesized evidence-based rehabilitation protocol. J Shoulder Elbow Surg. 2009;18(1):138-160.

15. Williams GN, Gangel TJ, Arciero RA, Uhorchak JM, Taylor DC. Comparison of the Single Assessment Numeric Evaluation method and two shoulder rating scales. Outcomes measures after shoulder surgery. Am J Sports Med. 1999;27(2):214-221.

16. Tashjian RZ, Deloach J, Porucznik CA, Powell AP. Minimal clinically important differences (MCID) and patient acceptable symptomatic state (PASS) for visual analog scales (VAS) measuring pain in patients treated for rotator cuff disease.
J Shoulder Elbow Surg. 2009;88(6):927-932.

17. Eustace JA, Brophy DP, Gibney RP, Bresnihan B, FitzGerald O. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis. 1997;56(1):59-63.

18. Esenyel CZ, Esenyel M, Yeiltepe R, et al. The correlation between the accuracy of steroid injections and subsequent shoulder pain and function in subacromial impingement
syndrome [in Turkish]. Acta Orthop Traumatol Turc. 2003;37(1):
41-45.

19. Powell SE, Davis SM, Lee EH, et al. Accuracy of palpation-directed intra-articular glenohumeral injection confirmed by magnetic resonance arthrography. Arthroscopy. 2015;31(2):205-208.

20. Rutten MJ, Maresch BJ, Jager GJ, de Waal Malefijt MC. Injection of the subacromial-subdeltoid bursa: blind or ultrasound-guided? Acta Orthop. 2007;78(2):254-257.

21. Desmeules F, Côté CH, Frémont P. Therapeutic exercise and orthopedic manual therapy for impingement syndrome: a systematic review. Clin J Sport Med. 2003;13(3):176-182.

22. Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de Jong B. Comparison of physiotherapy, manipulation, and corticosteroid injection for treating shoulder complaints in general practice: randomised, single blind study. BMJ. 1997;314(7090):1320-1325.

23. Chen MJ, Lew HL, Hsu TC, et al. Ultrasound-guided shoulder injections in the treatment of subacromial bursitis. Am J Phys Med Rehabil. 2006;85(1):31-35.

24. Hsieh LF, Hsu WC, Lin YJ, Wu SH, Chang KC, Chang HL. Is ultrasound-guided injection more effective in chronic subacromial bursitis? Med Sci Sports Exerc. 2013;45(12):
2205-2213.

25. Naredo E, Cabero F, Beneyto P, et al. A randomized comparative study of short term response to blind injection versus sonographic-guided injection of local corticosteroids in patients with painful shoulder. J Rheumatol. 2004;31(2):308-314.

26. Hall S, Buchbinder R. Do imaging methods that guide needle placement improve outcome? Ann Rheum Dis. 2004;63(9):1007-1008.

References

1. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev. 2003;(1):CD004016.

2. Bell AD, Conaway D. Corticosteroid injections for painful shoulders. Int J Clin Pract. 2005;59(10):1178-1186.

3. Michener LA, McClure PW, Karduna AR. Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech. 2003;18(5):369-379.

4. Akgün K, Birtane M, Akarirmak U. Is local subacromial corticosteroid injection beneficial in subacromial impingement syndrome? Clin Rheumatol. 2004;23(6):496-500.

5. Bhagra A, Syed H, Reed DA, et al. Efficacy of musculoskeletal injections by primary care providers in the office: a retrospective cohort study. Int J Gen Med. 2013;6:237-243.

6. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman JD. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am. 1996;78(11):1685-1689.

7. Cummins CA, Sasso LM, Nicholson D. Impingement syndrome: temporal outcomes of nonoperative treatment.
J Shoulder Elbow Surg. 2009;18(2):172-177.

8. Yu C, Chen CH, Liu HT, Dai MH, Wang IC, Wang KC. Subacromial injections of corticosteroids and Xylocaine for painful subacromial impingement syndrome. Chang Gung Med J. 2006;29(5):474-478.

9. Codsi MJ. The painful shoulder: when to inject and when to refer. Cleve Clin J Med. 2007;74(7):473-474, 477-478, 480-482 passim.

10. Henkus HE, Cobben LP, Coerkamp EG, Nelissen RG, van Arkel ER. The accuracy of subacromial injections: a prospective randomized magnetic resonance imaging study. Arthroscopy. 2006;22(3):277-282.

11. Kang MN, Rizio L, Prybicien M, Middlemas DA, Blacksin MF. The accuracy of subacromial corticosteroid injections: a comparison of multiple methods. J Shoulder Elbow Surg. 2008;17(15):61S-66S.

12. Marder RA, Kim SH, Labson JD, Hunter JC. Injection of the subacromial bursa in patients with rotator cuff syndrome: a prospective, randomized study comparing the effectiveness of different routes. J Bone Joint Surg Am. 2012;94(16):
1442-1447.

13. Gruson, KI, Ruchelsman DE, Zuckerman JD. Subacromial corticosteroid injections. J Shoulder Elbow Surg. 2008;17(1 suppl):118S-130S.

14. Kuhn JE. Exercise in the treatment of rotator cuff impingement: a systematic review and a synthesized evidence-based rehabilitation protocol. J Shoulder Elbow Surg. 2009;18(1):138-160.

15. Williams GN, Gangel TJ, Arciero RA, Uhorchak JM, Taylor DC. Comparison of the Single Assessment Numeric Evaluation method and two shoulder rating scales. Outcomes measures after shoulder surgery. Am J Sports Med. 1999;27(2):214-221.

16. Tashjian RZ, Deloach J, Porucznik CA, Powell AP. Minimal clinically important differences (MCID) and patient acceptable symptomatic state (PASS) for visual analog scales (VAS) measuring pain in patients treated for rotator cuff disease.
J Shoulder Elbow Surg. 2009;88(6):927-932.

17. Eustace JA, Brophy DP, Gibney RP, Bresnihan B, FitzGerald O. Comparison of the accuracy of steroid placement with clinical outcome in patients with shoulder symptoms. Ann Rheum Dis. 1997;56(1):59-63.

18. Esenyel CZ, Esenyel M, Yeiltepe R, et al. The correlation between the accuracy of steroid injections and subsequent shoulder pain and function in subacromial impingement
syndrome [in Turkish]. Acta Orthop Traumatol Turc. 2003;37(1):
41-45.

19. Powell SE, Davis SM, Lee EH, et al. Accuracy of palpation-directed intra-articular glenohumeral injection confirmed by magnetic resonance arthrography. Arthroscopy. 2015;31(2):205-208.

20. Rutten MJ, Maresch BJ, Jager GJ, de Waal Malefijt MC. Injection of the subacromial-subdeltoid bursa: blind or ultrasound-guided? Acta Orthop. 2007;78(2):254-257.

21. Desmeules F, Côté CH, Frémont P. Therapeutic exercise and orthopedic manual therapy for impingement syndrome: a systematic review. Clin J Sport Med. 2003;13(3):176-182.

22. Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de Jong B. Comparison of physiotherapy, manipulation, and corticosteroid injection for treating shoulder complaints in general practice: randomised, single blind study. BMJ. 1997;314(7090):1320-1325.

23. Chen MJ, Lew HL, Hsu TC, et al. Ultrasound-guided shoulder injections in the treatment of subacromial bursitis. Am J Phys Med Rehabil. 2006;85(1):31-35.

24. Hsieh LF, Hsu WC, Lin YJ, Wu SH, Chang KC, Chang HL. Is ultrasound-guided injection more effective in chronic subacromial bursitis? Med Sci Sports Exerc. 2013;45(12):
2205-2213.

25. Naredo E, Cabero F, Beneyto P, et al. A randomized comparative study of short term response to blind injection versus sonographic-guided injection of local corticosteroids in patients with painful shoulder. J Rheumatol. 2004;31(2):308-314.

26. Hall S, Buchbinder R. Do imaging methods that guide needle placement improve outcome? Ann Rheum Dis. 2004;63(9):1007-1008.

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The American Journal of Orthopedics - 46(4)
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Biceps Tenodesis: An Evolution of Treatment

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Biceps Tenodesis: An Evolution of Treatment

Take-Home Points

  • The LHB tendon has been shown to be a significant pain generator in the shoulder.
  • At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
  • The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
  • Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
  • Biceps tenodesis has become a more common procedure to treat shoulder pathology.

Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9

Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.

Methods

Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.

The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).

For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)

Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.

 

Results

Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).

Figure 1.
Mean (SD) age of the subgroup was 49.33 (13.2) years, and mean (SD) number of LHB tenodesis cases per year was 193.2 (130.5). Over time, mean age of patients who had these procedures did not change significantly (P = .934) (Figure 1), mean number of LHB tenodesis cases increased significantly (P = .0024) (Figure 2A), and percentage of LHB tenodesis cases increased significantly relative to percentage of all arthroscopic shoulder procedures (P = .0099) (Figure 2B).
Figure 2.
The concomitant procedures performed with LHB tenodesis during the study period are listed in the Table.

Discussion

Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.

Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15

Table.
Several fixation options have been used in open subpectoral biceps tenodesis. In this technique, which was used by all the surgeons in this study, the biceps tendon is fixed such that the musculotendinous junction of the biceps rests at the inferior border of the pectoralis major in the bicipital groove.16-19 Studies have found good, reliable outcomes with both the open and the arthroscopic surgical techniques.12,18 Comparing the LHB tenodesis trends in the present study with the SLAP repair trends we found at our institution in a previous study,20 we discovered that overall number of LHB tenodesis cases and percentage of LHB tenodesis cases relative to percentage of all arthroscopic shoulder procedures increased significantly more than for SLAP repairs.

Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.

One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.

Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. 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.

2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.

3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.

4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.

5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.

6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.

7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.

8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.

9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.

10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.

12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.

13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.

16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.

17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.

18. 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.

19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.

20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.

21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.

22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.

23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.

24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

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Take-Home Points

  • The LHB tendon has been shown to be a significant pain generator in the shoulder.
  • At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
  • The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
  • Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
  • Biceps tenodesis has become a more common procedure to treat shoulder pathology.

Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9

Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.

Methods

Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.

The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).

For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)

Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.

 

Results

Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).

Figure 1.
Mean (SD) age of the subgroup was 49.33 (13.2) years, and mean (SD) number of LHB tenodesis cases per year was 193.2 (130.5). Over time, mean age of patients who had these procedures did not change significantly (P = .934) (Figure 1), mean number of LHB tenodesis cases increased significantly (P = .0024) (Figure 2A), and percentage of LHB tenodesis cases increased significantly relative to percentage of all arthroscopic shoulder procedures (P = .0099) (Figure 2B).
Figure 2.
The concomitant procedures performed with LHB tenodesis during the study period are listed in the Table.

Discussion

Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.

Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15

Table.
Several fixation options have been used in open subpectoral biceps tenodesis. In this technique, which was used by all the surgeons in this study, the biceps tendon is fixed such that the musculotendinous junction of the biceps rests at the inferior border of the pectoralis major in the bicipital groove.16-19 Studies have found good, reliable outcomes with both the open and the arthroscopic surgical techniques.12,18 Comparing the LHB tenodesis trends in the present study with the SLAP repair trends we found at our institution in a previous study,20 we discovered that overall number of LHB tenodesis cases and percentage of LHB tenodesis cases relative to percentage of all arthroscopic shoulder procedures increased significantly more than for SLAP repairs.

Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.

One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.

Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • The LHB tendon has been shown to be a significant pain generator in the shoulder.
  • At our institution, the number of LHB tenodeses significantly increased from 2004 to 2014.
  • The age of patients who underwent a LHB tenodesis did not change significantly over the study period.
  • Furthermore, the percentage of shoulder procedures that involved a LHB tenodesis significantly increased over the study period.
  • Biceps tenodesis has become a more common procedure to treat shoulder pathology.

Although the exact function of the long head of the biceps (LHB) tendon is not completely understood, it is accepted that the LHB tendon can be a significant source of pain within the shoulder.1-4 Patients with symptoms related to biceps pathology often present with anterior shoulder pain that worsens with flexion and supination of the affected elbow and wrist.5 Although the sensitivity and specificity of physical examination maneuvers have been called into question, special tests have been developed to aid in the diagnosis of tendonitis of the LHB. These tests include the Speed, Yergason, bear hug, and uppercut tests as well as the O’Brien test (cross-body adduction).6,7 Recent studies have found LHB pathology in 45% of patients who undergo rotator cuff repair and in 63% of patients with a subscapularis tear.8,9

Pathology of the LHB tendon, including superior labrum anterior to posterior (SLAP) tears, can be treated in many ways.5,10,11 Options include SLAP repair, biceps tenodesis, débridement, and biceps tenotomy.11,12 Results of SLAP repairs have been less than optimal, but biceps tenodesis has been effective, and avoids the issue of cramping as can be seen with biceps tenotomy and débridement.10,12,13 Surgical methods for biceps tenodesis include open subpectoral and all-arthroscopic.11,12 Both methods have had good, reliable outcomes, but the all-arthroscopic technique is relatively new.11,12,14We conducted a study to determine LHB tenodesis trends, including patient age at time of surgery. We used surgical data from fellowship-trained sports or shoulder/elbow orthopedic surgeons at a busy subspecialty-based shoulder orthopedic practice. We hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis.

Methods

Our Institutional Review Board exempted this study. To determine the number of LHB tenodesis procedures performed at our institution, overall and in comparison with other common arthroscopic shoulder procedures, we queried the surgical database of 4 fellowship-trained orthopedic surgeons (shoulder/elbow, Drs. Nicholson and Cole; sports, Drs. Romeo and Verma) for the period January 1, 2004 to December 31, 2014. We used Current Procedural Terminology (CPT) code 23430 to determine the number of LHB tenodesis cases, as the surgeons primarily perform an open subpectoral biceps tenodesis. Patient age at time of surgery and the date of surgery were recorded. All patients who underwent LHB tenodesis between January 1, 2004 and December 31, 2014 were included. Number of procedures performed each year by each surgeon was recorded, as were concomitant procedures performed at the same time as the LHB tenodesis. To get the denominator (and reference point) for the number of arthroscopic shoulder surgeries performed by these 4 surgeons during the study period, and thereby determine the rate of LHB tenodesis, we selected the most common shoulder arthroscopy CPT codes used in our practice: 23430, 29806, 29807, 29822, 29823, 29825, 29826, and 29827. For a patient who underwent multiple procedures on the same day (multiple CPT codes entered on the same day), only one code was counted for that day. If 23430 was among the codes, it was included, and the case was placed in the numerator; if 23430 was not among the codes, the case was placed in the denominator.

The Arthroscopy Association of North America provides descriptions for the CPT codes: 23430 (tenodesis of long tendon of biceps), 29806 (arthroscopy, shoulder, surgical; capsulorrhaphy), 29807 (arthroscopy, shoulder, surgical; repair of SLAP lesion), 29822 (arthroscopy, shoulder, surgical; débridement, limited), 29823 (arthroscopy, shoulder, surgical; débridement, extensive), 29825 (arthroscopy, shoulder, surgical; with lysis and resection of adhesions, with or without manipulation), 29826 (arthroscopy, shoulder, surgical; decompression of subacromial space with partial acromioplasty, with or without coracoacromial release), and 29827 (arthroscopy, shoulder, surgical; with rotator cuff repair).

For analysis, we divided the data into total number of arthroscopic shoulder procedures performed by each surgeon each year and number of LHB tenodesis procedures performed by each surgeon each year. Total number of patients who had an arthroscopic procedure was used to create a denominator, and number of LHB tenodesis procedures showed the percentage of arthroscopic shoulder surgery patients who underwent LHB tenodesis. (All patients who undergo biceps tenodesis also have, at the least, diagnostic shoulder arthroscopy with or without tenotomy; if the tendon is ruptured, tenotomy is unnecessary.)

Descriptive statistics were calculated as means (SDs) for continuous variables and as frequencies with percentages for categorical variables. Linear regression analysis was used to determine whether the number of LHB tenodesis procedures changed during the study period and whether patient age changed over time. Significance was set at P < .05.

 

Results

Of the 7640 patients who underwent arthroscopic shoulder procedures between 2004 and 2014, 2125 had LHB tenodesis (CPT code 23430).

Figure 1.
Mean (SD) age of the subgroup was 49.33 (13.2) years, and mean (SD) number of LHB tenodesis cases per year was 193.2 (130.5). Over time, mean age of patients who had these procedures did not change significantly (P = .934) (Figure 1), mean number of LHB tenodesis cases increased significantly (P = .0024) (Figure 2A), and percentage of LHB tenodesis cases increased significantly relative to percentage of all arthroscopic shoulder procedures (P = .0099) (Figure 2B).
Figure 2.
The concomitant procedures performed with LHB tenodesis during the study period are listed in the Table.

Discussion

Tenodesis has become a common treatment option for several pathologic shoulder conditions involving the LHB tendon.5 We set out to determine trends in LHB tenodesis at a subspecialty-focused shoulder orthopedic practice and hypothesized that the rate of LHB tenodesis would increase significantly over time and that there would be no significant change in the age of patients who underwent LHB tenodesis. Our hypotheses were confirmed: The number of LHB tenodesis cases increased significantly without a significant change in patient age.

Treatment options for LHB pathology and SLAP tears include simple tenotomy, débridement, open biceps tenodesis, and arthroscopic tenodesis.11,12,15

Table.
Several fixation options have been used in open subpectoral biceps tenodesis. In this technique, which was used by all the surgeons in this study, the biceps tendon is fixed such that the musculotendinous junction of the biceps rests at the inferior border of the pectoralis major in the bicipital groove.16-19 Studies have found good, reliable outcomes with both the open and the arthroscopic surgical techniques.12,18 Comparing the LHB tenodesis trends in the present study with the SLAP repair trends we found at our institution in a previous study,20 we discovered that overall number of LHB tenodesis cases and percentage of LHB tenodesis cases relative to percentage of all arthroscopic shoulder procedures increased significantly more than for SLAP repairs.

Recent evidence has called into question the results of SLAP repairs and suggested biceps tenodesis may be a better treatment option for SLAP tears.10,13,21 Studies have found excellent outcomes with open subpectoral biceps tenodesis in the treatment of SLAP tears, and others have found better restoration of pitchers’ thoracic rotation with open subpectoral biceps tenodesis than with SLAP repair.13,14 Similarly, comparison studies have largely favored biceps tenodesis over SLAP repair, particularly in patients older than 35 years to 40 years.22 Given these results, it is not surprising that, querying the American Board of Orthopaedic Surgeons (ABOS) part II database for isolated SLAP lesions treated between 2002 and 2011, Patterson and colleagues23 found the percentage of SLAP repairs decreased from 69.3% to 44.8% (P < .0001), whereas the percentage of biceps tenodesis procedures increased from 1.9% to 18.8% (P < .0001), indicating the realization of improved outcomes with LHB tenodesis in the treatment of SLAP tears. On the other hand, in the ABOS part II database for the period 2003 to 2008, Weber and colleagues24 found that, despite a decrease in the percentage of SLAP repairs, total number of SLAP repairs increased from 9.4% to 10.1% (P = .0163). According to our study results, the number of SLAP repairs is decreasing over time, whereas the number of LHB tenodesis procedures is continuing to rise. The practice patterns seen in our study correlate with those in previous studies of the treatment of SLAP tears: good results in tenodesis groups and poor results in SLAP repair groups.10,13Werner and colleagues25 recently used the large PearlDiver database, which includes information from both private payers and Medicare, to determine overall LHB tenodesis trends in the United States for the period 2008 to 2011. Over those years, the incidence of LHB tenodesis increased 1.7-fold, and the rate of arthroscopic LHB tenodesis increased significantly more than the rate of open LHB tenodesis. These results are similar to ours in that the number of LHB tenodesis cases increased significantly over time. However, as the overwhelming majority of patients in our practice undergo open biceps tenodesis, the faster rate of growth in the arthroscopic cohort relative to the open cohort cannot be assessed. Additional randomized studies comparing biceps tenodesis, both open and arthroscopic, with SLAP repair are needed to properly determine the superiority of LHB tenodesis over SLAP repair.

One strength of this database study was the number of patients: more than 7000, 2125 of whom underwent biceps tenodesis performed by 1 of 4 fellowship-trained orthopedic surgeons. There were several study limitations. First, because the original diagnoses were not recorded, it was unclear exactly which pathologies were treated with tenodesis, limiting our ability to make recommendations regarding treatment trends for specific pathologies. Similarly, we did not assess outcome variables, which would have allowed us to draw conclusions about the effectiveness of the biceps tenodesis procedures. Furthermore, some procedures may have been coded incorrectly, and therefore some patients may have been erroneously included or excluded. In addition, using data from only one institution may have introduced bias into our conclusions, though the results are consistent with national trends. Finally, there was some variability among the 4 surgeons in the number of LHB tenodesis procedures performed, and this variability may have confounded results, though these surgeons treat biceps pathology in similar ways.

Am J Orthop. 2017;46(4):E219-E223. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. 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.

2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.

3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.

4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.

5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.

6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.

7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.

8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.

9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.

10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.

12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.

13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.

16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.

17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.

18. 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.

19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.

20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.

21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.

22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.

23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.

24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

References

1. 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.

2. Ejnisman B, Monteiro GC, Andreoli CV, de Castro Pochini A. Disorder of the long head of the biceps tendon. Br J Sports Med. 2010;44(5):347-354.

3. Mellano CR, Shin JJ, Yanke AB, Verma NN. Disorders of the long head of the biceps tendon. Instr Course Lect. 2015;64:567-576.

4. Szabo I, Boileau P, Walch G. The proximal biceps as a pain generator and results of tenotomy. Sports Med Arthrosc Rev. 2008;16(3):180-186.

5. Harwin SF, Birns ME, Mbabuike JJ, Porter DA, Galano GJ. Arthroscopic tenodesis of the long head of the biceps. Orthopedics. 2014;37(11):743-747.

6. Holtby R, Razmjou H. Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy. 2004;20(3):231-236.

7. Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840-1847.

8. Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy. 2007;23(1):73-80.

9. Adams CR, Schoolfield JD, Burkhart SS. The results of arthroscopic subscapularis tendon repairs. Arthroscopy. 2008;24(12):1381-1389.

10. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

11. Gombera MM, Kahlenberg CA, Nair R, Saltzman MD, Terry MA. All-arthroscopic suprapectoral versus open subpectoral tenodesis of the long head of the biceps brachii. Am J Sports Med. 2015;43(5):1077-1083.

12. Delle Rose G, Borroni M, Silvestro A, et al. The long head of biceps as a source of pain in active population: tenotomy or tenodesis? A comparison of 2 case series with isolated lesions. Musculoskelet Surg. 2012;96(suppl 1):S47-S52.

13. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

14. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

15. Ge H, Zhang Q, Sun Y, Li J, Sun L, Cheng B. Tenotomy or tenodesis for the long head of biceps lesions in shoulders: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0121286.

16. Kaback LA, Gowda AL, Paller D, Green A, Blaine T. Long head biceps tenodesis with a knotless cinch suture anchor: a biomechanical analysis. Arthroscopy. 2015;31(5):831-835.

17. Kany J, Guinand R, Amaravathi RS, Alassaf I. The keyhole technique for arthroscopic tenodesis of the long head of the biceps tendon. In vivo prospective study with a radio-opaque marker. Orthop Traumatol Surg Res. 2015;101(1):31-34.

18. 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.

19. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc Rev. 2008;16(3):170-176.

20. Erickson BJ, Jain A, Abrams GD, et al. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976-981.

21. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.

22. Denard PJ, Ladermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37(3):e292-e297.

23. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42(8):1904-1910.

24. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

25. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

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A New Option for Glenoid Reconstruction in Recurrent Anterior Shoulder Instability

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A New Option for Glenoid Reconstruction in Recurrent Anterior Shoulder Instability

Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

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Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Repair anterior bone defect on the glenoid related to recurrent anterior instability with preshaped, predrilled allograft.
  • Avoid graft harvest complications related to coracoid (Latarjet) or iliac crest autograft.
  • Simple guide system to allow for appropriate graft and screw placement.
  • Soft tissues can be repaired to the allograft in predrilled suture holes either inside or outside of the graft
  • Position the graft without step at the anterior glenoid.

Anteroinferior glenoid bone loss plays a significant role in recurrent glenohumeral instability. Arthroscopic capsulolabral reconstruction has been associated with a recurrence rate of 4% in the absence of significant glenoid bone loss but 67% in patients with either bone loss of more than 25% of the inferior glenoid diameter or an engaging Hill-Sachs lesion.1,2 Anteroinferior glenoid rim deficiency has been reported in up to 90% of cases of recurrent instability.3 Glenoid reconstruction is therefore recommended in patients with bone loss of more than 25% and in certain revision cases.4 Surgical strategies in these cases include coracoid transfer, iliac crest autograft, and allograft (osteochondral and iliac crest). These procedures all successfully restore stability of the glenohumeral joint. However, they carry the drawbacks of technical complexity with increased operative time or risk of neurovascular damage, or they create a nonanatomical reconstruction, which may contribute to subsequent instability arthropathy. In this article, we introduce a technique in which a preshaped allograft (Glenojet; Arthrosurface, Inc.) is used to match the contour of the glenoid defect. The graft is simple to insert and can reduce operative time.

Graft Preparation

The shaped human tissue cortical bone allograft is usually prepared from proximal or distal tibia or femur. There is no cartilage on the graft. It can be ordered in 2 sizes, 10 mm × 29 mm and 13 mm × 34 mm, for different amounts of bone loss. The more commonly used smaller graft reconstructs defects of 20% to 30% of the glenoid.

Figure 1.
The graft has a flat surface that abuts the glenoid and a concave surface that repairs to the capsule. The graft has predrilled holes for cortical screw placement as well as smaller holes for threading suture for capsule repair. It is shaped to match the contour of the glenoid (Figure 1).

The sutures through this allograft can be prepared on the back table while the rest of the equipment is set up. Start by tying a No. 2 FiberWire (or equivalent) over a small thin object, such as a Freer elevator. Once the knot is secure, remove the Freer and trim the knot tails short. Thread another suture through the loop that has been created and pull to make the 2 tails even. Then thread these tails through one of the small holes of the graft, going from the flat side to the concave side. Pull the suture tails all the way through, including through the loop of the prior suture. The knot of the loop prevents the entire construct from pulling through. The suture tails are then able to slide as if attached to an anchor. Repeat these steps for the other 2 small holes to get a total of 3 sutures exiting the concave side of the graft (Figure 1). Alternatively, pass the suture the opposite way, if tying the capsule inside the graft is preferred.

Surgical Technique

A standard deltopectoral approach is used to expose the anterior glenoid. The subscapularis can either be split in line with its fibers or tenotomized with 1 cm to 2 cm attached to the tuberosity for later repair. In either instance, it is important to separate the muscle from the underlying capsule layer, as the capsule is what is directly repaired to the graft.

The capsule is carefully peeled off the anterior glenoid. A Fukuda or similar retractor may be used on the humerus, and a glenoid retractor is placed on the anterior glenoid, under the capsule and subscapularis, for optimal exposure. Once the anterior glenoid surface is exposed, the drill guide is placed flush against the surface of the glenoid.

Figure 2.
It is important to confirm the guide is seated flush on the glenoid, as this ensures correct positioning, angulation, and alignment of the graft. The laser mark on the guide is positioned in line with the anterior glenoid fracture plane. The guide is securely held while 2 guide pins are drilled in place, until just past the posterior cortex of the glenoid (Figure 2).

The guide is removed. The cannulated reamer is introduced and advanced until the guide pin appears in the viewing window of the reamer and hits the stop—approximating the correct amount of bone to remove. This step is repeated for the second guide pin. Reaming flattens the anterior glenoid and allows for maximal stable apposition of the graft to the glenoid. The allograft is then inserted onto the pins in the correct orientation to match the surface of the native glenoid.

The length of the superior guide pin is measured with the depth gauge device. It is then removed, and the appropriate-length 3.5-mm cortical bone screw is inserted (alternatively, the guide pin is removed, and a standard depth gauge is used to measure screw length). Once the superior guide pin is secure, the process is repeated for the inferior guide pin (Figure 3).
Figure 3.
The screws should have excellent bicortical fixation. Although we have not had any intraoperative graft fractures, overtensioning of the screws could cause the graft to fail at the screw site at follow-up. Therefore, we recommend not overtightening the screws.

Once the graft is secure, the capsule is attached to the graft with the use of a free needle on the suture of the graft (Figure 4).
Figure 4.
The capsule is advanced as necessary for appropriate anterior soft-tissue tensioning. Once the capsular repair is complete, the subscapularis is repaired as necessary.

 

 

Outcomes

Coracoid bone transfer or the Bristow-Latarjet technique has become more popular since bone loss was recognized as an important cause of failure of soft-tissue repair for anterior instability. This procedure, however, is not without complications. In a recent systematic review of 45 studies (1904 shoulders), Griesser and colleagues5 found an overall complication rate of 30% and a reoperation rate of 7%.

Given the potential complications of coracoid bone transfer, allograft reconstruction of the anteroinferior glenoid has become increasingly popular and proved successful at short- and medium-term follow-up. Allograft reconstruction avoids the drawbacks of traditional coracoid bone transfer—namely, high rates of neurovascular injury, and nonanatomical reconstruction with high rates of graft resorption and arthritis.5,6 At average 45-month follow-up after fresh distal tibia allograft reconstruction, Provencher and colleagues7 found an 89% radiographic union rate (average lysis, 3%), significantly improved patient-reported outcomes, and no recurrent instability. Similarly, in a study of iliac crest allograft reconstruction in 10 patients with an average 4-year follow-up, Mascarenhas and colleagues8 found an 80% radiographic union rate at 6 months, significantly improved patient-reported outcomes, and no recurrent shoulder instability.

The advantage of Glenojet over other allografts is that it is preshaped and predrilled and saves the surgeon the time and effort of preparing graft in the operating room. The surgical technologist can place the sutures before the patient enters the room. The 2 allograft sizes (10 mm × 29 mm, 13 mm × 34 mm) accommodate the spectrum of bone loss in glenoid deficiency, and graft contour fits the native glenoid well. So far we have implanted this allograft in 15 patients, and at short-term follow-up there are no known cases of recurrent instability.

The potential disadvantages of Glenojet are similar to those of other allografts. Care must be taken with retractor placement to avoid damaging the axillary and musculocutaneous nerves. There are concerns about graft union and subsequent resorption, but this will require long-term follow-up to determine. At 9-month follow-up, we had 1 fracture at the superior corner of the graft, which may have resulted from overtightening the screws in the graft, creating a stress concentration. After removal of this fragment arthroscopically, the patient has done very well clinically with no pain, instability and has returned to all activities. Although the graft does not have an articular surface, the capsular repair covers much of the articular side of the graft, and therefore we do not anticipate that the absence of articular cartilage will contribute to glenohumeral arthritis, though long-term follow-up is lacking. The other question many have is related to the lack of the sling effect since there is no conjoined tendon on the graft. Yamamoto and colleagues9 have reported that the conjoined tendon is the major stabilizing force at time zero in a cadaver model. However, other authors7,8 have successfully reconstructed glenoid defects in these difficult cases without the “sling effect” of the conjoined tendon with excellent clinical results. Our experience has been similar. It is likely that long-term studies will be necessary to answer this question. We have also done some cases with the tendon attached after releasing it from the coracoid, but the series is too small to make any comment about whether this is important or not.

The main limitation of this allograft technique is the lack of long-term outcome studies. However, short-term results are promising, and the ease of the procedure makes it an attractive option for either glenoid reconstruction of bony Bankart lesions or failed bone reconstruction, such as Bristow-Latarjet reconstruction.

Glenojetallograft is a new glenoid reconstruction option that is technically easy and simple to perform in cases of glenoid bone loss, while still creating an anatomical buttress with less surgical dissection than traditional coracoid bone transfer. Short-term outcomes are reassuring, though more research is needed for long-term graft follow-up and recurrent instability.

Am J Orthop. 2017;46(4):199-202. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

References

1. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.

2. Rowe CR, Sakellarides HT. Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop. 1961;(20):40-48.

3. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

4. Sayegh ET, Mascarenhas R, Chalmers PN, Cole BJ, Verma NN, Romeo AA. Allograft reconstruction for glenoid bone loss in glenohumeral instability: a systematic review. Arthroscopy. 2014;30(12):1642-1649.

5. Griesser MJ, Harris JD, McCoy BW, et al. Complications and re-operati ons after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292.

6. Young DC, Rockwood CA Jr. Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am. 1991;73(7):969-981.

7. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

8. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132.

9. Yamamoto N, Muraki T, An KN, et al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397.

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Traumatic Anterior Shoulder Instability: The US Military Experience

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Traumatic Anterior Shoulder Instability: The US Military Experience

Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

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Authors’ Disclosure Statement: Dr. Provencher reports that he receives support from Arthrex and is a consultant to JRF Ortho, patent numbers (issued): 9226743, 20150164498, 20150150594, 20110040339, and receives publishing royalties from Arthrex and SLACK. Dr. Mannava reports that he receives support from the Arthroscopy Association of North America as a board member. Dr. Tokish reports that he receives support from the Arthroscopy Association of North America, the Journal of Shoulder and Elbow Surgery, Orthopedics Today, and the Hawkins Foundation as a board member; is a paid consultant to Arthrex, Mitek, and DePuy Synthes; and is a paid presenter for Arthrex. Dr. Rogers reports no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Provencher reports that he receives support from Arthrex and is a consultant to JRF Ortho, patent numbers (issued): 9226743, 20150164498, 20150150594, 20110040339, and receives publishing royalties from Arthrex and SLACK. Dr. Mannava reports that he receives support from the Arthroscopy Association of North America as a board member. Dr. Tokish reports that he receives support from the Arthroscopy Association of North America, the Journal of Shoulder and Elbow Surgery, Orthopedics Today, and the Hawkins Foundation as a board member; is a paid consultant to Arthrex, Mitek, and DePuy Synthes; and is a paid presenter for Arthrex. Dr. Rogers reports no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Provencher reports that he receives support from Arthrex and is a consultant to JRF Ortho, patent numbers (issued): 9226743, 20150164498, 20150150594, 20110040339, and receives publishing royalties from Arthrex and SLACK. Dr. Mannava reports that he receives support from the Arthroscopy Association of North America as a board member. Dr. Tokish reports that he receives support from the Arthroscopy Association of North America, the Journal of Shoulder and Elbow Surgery, Orthopedics Today, and the Hawkins Foundation as a board member; is a paid consultant to Arthrex, Mitek, and DePuy Synthes; and is a paid presenter for Arthrex. Dr. Rogers reports no actual or potential conflict of interest in relation to this article.

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Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Arthroscopic stabilization performed early results in better outcomes in patients with Bankart lesions.
  • A subcritical level of bone loss of 13.5% has been shown to have a significant effect on outcomes, in addition to the established “critical amount”.
  • Bone loss is a bipolar issue. Both sides must be considered in order to properly address shoulder instability.
  • Off-track measurement has been shown to be even more positively predictive of outcomes than glenoid bone loss assessment.
  • There are several bone loss management options including, the most common coracoid transfer, as well as distal tibial allograft and distal clavicular autograft.

Given its relatively young age, high activity level, and centralized medical care system, the US military population is ideal for studying traumatic anterior shoulder instability. There is a long history of military surgeons who have made significant contributions that have advanced our understanding of this pathology and its treatment and results. In this article, we describe the scope, treatment, and results of this pathology in the US military population.

Incidence and Pathology

At the United States Military Academy (USMA), Owens and colleagues1 studied the incidence of shoulder instability, including dislocation and subluxation, and found anterior instability events were far more common than in civilian populations. The incidence of shoulder instability was 0.08 per 1000 person-years in the general US population vs 1.69 per 1000 person-years in US military personnel. The factors associated with increased risk of shoulder instability injury in the military population were male sex, white race, junior enlisted rank, and age under 30 years. Owens and colleagues2 noted that subluxation accounted for almost 85% of the total anterior instability events. Owens and colleagues3 found the pathology in subluxation events was similar to that in full dislocations, with a soft-tissue anterior Bankart lesion and a Hill-Sachs lesion detected on magnetic resonance imaging in more than 90% of patients. In another study at the USMA, DeBerardino and colleagues4 noted that 97% of arthroscopically assessed shoulders in first-time dislocators involved complete detachment of the capsuloligamentous complex from the anterior glenoid rim and neck—a so-called Bankart lesion. Thus, in a military population, anterior instability resulting from subluxation or dislocation is a common finding that is often represented by a soft-tissue Bankart lesion and a Hill-Sachs defect.

Natural History of Traumatic Anterior Shoulder Instability in the Military

Several studies have evaluated the outcomes of nonoperative and operative treatment of shoulder instability. Although most have found better outcomes with operative intervention, Aronen and Regan5 reported good results (25% recurrence at nearly 3-year follow-up) with nonoperative treatment and adherence to a strict rehabilitation program. Most other comparative studies in this population have published contrary results. Wheeler and colleagues6 studied the natural history of anterior shoulder dislocations in a USMA cadet cohort and found recurrent instability after shoulder dislocation in 92% of cadets who had nonoperative treatment. Similarly, DeBerardino and colleagues4 found that, in the USMA, 90% of first-time traumatic anterior shoulder dislocations managed nonoperatively experienced recurrent instability. In a series of Army soldiers with shoulder instability, Bottoni and colleagues7 reported that 75% of nonoperatively managed patients had recurrent instability, and, of these, 67% progressed to surgical intervention. Nonoperative treatment for a first-time dislocation is still reasonable if a cadet or soldier needs to quickly return to functional duties. Athletes who develop shoulder instability during their playing season have been studied in a military population as well. In a multicenter study of service academy athletes with anterior instability, Dickens and colleagues8 found that, with conservative management and accelerated rehabilitation of in-season shoulder instability, 73% of athletes returned to sport by a mean of 5 days. However, the durability of this treatment should be questioned, as 64% later experienced recurrence.

Arthroscopic Stabilization of Acute Anterior Shoulder Dislocations

In an early series of cases of traumatic anterior shoulder instability in USMA cadets, Wheeler and colleagues6 found that, at 14 months, 78% of arthroscopically stabilized cases and 92% of nonoperatively treated cases were successful. Then, in the 1990s, DeBerardino and colleagues4 studied a series of young, active patients in the USMA and noted significantly better results with arthroscopic treatment, vs nonoperative treatment, at 2- to 5-year follow-up. Of the arthroscopically treated shoulders, 88% remained stable during the study and returned to preinjury activity levels, and 12% experienced recurrent instability (risk factors included 2+ sulcus sign, poor capsular labral tissue, and history of bilateral shoulder instability). In a long-term follow-up (mean, 11.7 years; range, 9.1-13.9 years) of the same cohort, Owens and colleagues9 found that 14% of patients available for follow-up had undergone revision stabilization surgery, and, of these, 21% reported experiencing subluxation events. The authors concluded that, in first-time dislocators in this active military population, acute arthroscopic Bankart repair resulted in excellent return to athletics and subjective function, and had acceptable recurrence and reoperation rates. Bottoni and colleagues,7 in a prospective, randomized evaluation of arthroscopic stabilization of acute, traumatic, first-time shoulder dislocations in the Army, noted an 89% success rate for arthroscopic treatment at an average follow-up of 36 months, with no recurrent instability. DeBerardino and colleagues10 compared West Point patients treated nonoperatively with those arthroscopically treated with staples, transglenoid sutures, or bioabsorbable anchors. Recurrence rates were 85% for nonoperative treatment, 22% for staples, 14% for transglenoid sutures, and 10% for bioabsorbable anchors.

Arthroscopic Versus Open Stabilization of Anterior Shoulder Instability

In a prospective, randomized clinical trial comparing open and arthroscopic shoulder stabilization for recurrent anterior instability in active-duty Army personnel, Bottoni and colleagues11 found comparable clinical outcomes. Stabilization surgery failed clinically in only 3 cases, 2 open and 1 arthroscopic. The authors concluded that arthroscopic stabilization can be safely performed for recurrent shoulder instability and that arthroscopic outcomes are similar to open outcomes. In a series of anterior shoulder subluxations in young athletes with Bankart lesions, Owens and colleagues12 found that open and arthroscopic stabilization performed early resulted in better outcomes, regardless of technique used. Recurrent subluxation occurred at a mean of 17 months in 3 of the 10 patients in the open group and 3 of the 9 patients in the arthroscopic group, for an overall recurrence rate of 31%. The authors concluded that, in this patient population with Bankart lesions caused by anterior subluxation events, surgery should be performed early.

Bone Lesions

Burkhart and De Beer13 first noted that bone loss has emerged as one of the most important considerations in the setting of shoulder instability in active patients. Other authors have found this to be true in military populations.14,15

The diagnosis of bone loss may include historical findings, such as increased number and ease of dislocations, as well as dislocation in lower positions of abduction. Physical examination findings may include apprehension in the midrange of motion. Advanced imaging, such as magnetic resonance arthrography, has since been validated as equivalent to 3-dimensional computed tomography (3-D CT) in determining glenoid bone loss.16 In 2007, Mologne and colleagues15 studied the amount of glenoid bone loss and the presence of fragmented bone or attritional bone loss and its effect on outcomes. They evaluated 21 patients who had arthroscopic treatment for anterior instability with anteroinferior glenoid bone loss between 20% and 30%. Average follow-up was 34 months. All patients received 3 or 4 anterior anchors. No patient with a bone fragment incorporated into the repair experienced recurrence or subluxation, whereas 30% of patients with attritional bone loss had recurrent instability.15

 

 

Classifying Bone Loss and Recognizing Its Effects

Burkhart and De Beer13 helped define the role and significance of bone loss in the setting of shoulder instability. They defined significant bone loss as an engaging Hill-Sachs lesion of the humerus in an abducted and externally rotated position or an “inverted pear” lesion of the glenoid. Overall analysis revealed recurrence in 4% of cases without significant bone loss and 65% of cases with significant bone loss. In a subanalysis of contact-sport athletes in the setting of bone loss, the failure rate increased to 89%, from 6.5%. Aiding in the quantitative assessment of glenoid bone loss, Itoi and colleagues17 showed that 21% glenoid bone loss resulted in instability that would not be corrected by a soft-tissue procedure alone. Bone loss of 20% to 25% has since been considered a “critical amount,” above which an arthroscopic Bankart has been questioned. More recently, several authors have shown that even less bone loss can have a significant effect on outcomes. Shaha and colleagues18 established that a subcritical level of bone loss (13.5%) on the anteroinferior glenoid resulted in clinical failure (as determined with the Western Ontario Shoulder Instability Index) even in cases in which frank recurrence or subluxation was avoided. It is thought that, in recurrent instability, glenoid bone loss incident rate is as high as 90%, and the corresponding percentage of patients with Hill-Sachs lesions is almost 100%.19,20 Thus, it is increasingly understood that bone loss is a bipolar issue and that both sides must be considered in order to properly address shoulder instability in this setting. In 2007, Yamamoto and colleagues21 introduced the glenoid track, a method for predicting whether a Hill-Sachs lesion will engage. Di Giacomo and colleagues22 refined the track concept to quantitatively determine which lesions will engage in the setting of both glenoid and humeral bone loss. Metzger and colleagues,23 confirming the track concept arthroscopically, found that manipulation with anesthesia and arthroscopic visualization was well predicted by preoperative track measurements, and thus these measurements can be a good guide for surgical management (Figures 1A, 1B).

Figure 1.
At Tripler Army Medical Center, Shaha and colleagues14 clinically validated the concept in a series of arthroscopic stabilization cases. They found that the recurrence rate was 8% for “on-track” patients’ and 75% for “off-track” patients treated with the same intervention. In addition, positive predictive value was 75% for the off-track measurement and 44% for the glenoid bone loss assessment alone. The authors recommended the preoperative off-track measurement over the glenoid bone loss assessment.
Figure 2.
In an analysis of computer modeling of 3-D CT of patients who underwent Bankart repair, Arciero and colleagues24 found that bipolar bone defects (glenoid bone loss combined with humeral head Hill-Sachs lesion) had an additive and combined negative effect on soft-tissue Bankart repair. In particular, soft-tissue Bankart repair could be compromised by a 2-mm glenoid defect combined with a medium-size Hill-Sachs lesion or, conversely, by a 4-mm glenoid defect combined with a small Hill-Sachs lesion (Figures 2A, 2B).

Strategies for Addressing Bone Loss in Anterior Shoulder Instability

Several approaches for managing bone loss in shoulder instability have been described—the most common being coracoid transfer (Latarjet procedure). Waterman and colleagues25 recently studied the effects of coracoid transfer, distal tibial allograft, and iliac crest augmentation on anterior shoulder instability in US military patients treated between 2006 and 2012. Of 64 patients who underwent a bone block procedure, 16 (25%) had a complication during short-term follow-up. Complications included neurologic injury, pain, infection, hardware failure, and recurrent instability.

Figure 3.
After undergoing 1 of the 3 procedures, 33% of patients had persistent pain, and 23% had recurrent instability. In an older, long-term study of Naval Academy midshipmen, patients who underwent a modified Bristow procedure between 1975 and 1979 demonstrated 70% good to excellent results at an average follow-up of 26.4 years.26
Figure 4.
The recurrent instability rate was 15%, with 9% of the cohort dislocating again and 6% of the cohort experiencing recurrent subluxation. Direct bone grafting to the glenoid has also been described. Provencher and colleagues27 introduced use of distal tibial allograft in addressing bony deficiency, and clinical results were promising (Figures 3A-3C). Tokish and colleagues28 introduced use of distal clavicular autograft in addressing these deficiencies but did not report clinical outcomes (Figures 4A-4C).

Conclusion

Traumatic anterior shoulder instability is a common pathology that continues to significantly challenge the readiness of the US military. Military surgeon-researchers have a long history of investigating approaches to the treatment of this pathology—applying good science to a large controlled population, using a single medical record, and demonstrating a commitment to return service members to the ready defense of the nation.

Am J Orthop. 2017;46(4):184-189. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

References

1. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791-796.

2. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.

3. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611.

4. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM. Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med. 2001;29(5):586-592.

5. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291.

6. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217.

7. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580.

8. Dickens JF, Owens BD, Cameron KL, et al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850.

9. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673.

10. DeBerardino TM, Arciero RA, Taylor DC. Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc. 1996;5(4):263-271.

11. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737.

12. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084.

13. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694.14. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923.

15. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283.

16. Markenstein JE, Jaspars KC, van der Hulst VP, Willems WJ. The quantification of glenoid bone loss in anterior shoulder instability; MR-arthro compared to 3D-CT. Skeletal Radiol. 2014;43(4):475-483.

17. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46.

18. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725.

19. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493.

20. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252.

21. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656.

22. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98.

23. Metzger PD, Barlow B, Leonardelli D, Peace W, Solomon DJ, Provencher MT. Clinical application of the “glenoid track” concept for defining humeral head engagement in anterior shoulder instability: a preliminary report. Orthop J Sports Med. 2013;1(2):2325967113496213.

24. Arciero RA, Parrino A, Bernhardson AS, et al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429.

25. Waterman BR, Chandler PJ, Teague E, Provencher MT, Tokish JM, Pallis MP. Short-term outcomes of glenoid bone block augmentation for complex anterior shoulder instability in a high-risk population. Arthroscopy. 2016;32(9):1784-1790.

26. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786.

27. Provencher MT, Frank RM, Golijanin P, et al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891-897.

28. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481.

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Head, Neck, and Shoulder Injuries in Ice Hockey: Current Concepts

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Head, Neck, and Shoulder Injuries in Ice Hockey: Current Concepts

Take-Home Points

  • Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
  • Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
  • Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
  • A player with unresolved concussion symptoms should not be allowed to return to the ice.
  • Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.

On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2

Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4

Table 1.
In the United States, an estimated 20,000 hockey players present to the emergency department (ED) with injuries each year.5 In some leagues, game-related injury rates can be as high as 96 per 1000 player-hours (Table 1).

Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.

In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.

Evaluation and Management of Common Hockey Injuries

Eye Injuries

Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10

Table 2.
Some of these injuries have the potential to cause permanent ocular damage and loss of sight. A clear understanding of how to correctly evaluate, triage, and manage ocular trauma is therefore essential for any physician providing primary medical care for hockey players and teams.

As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.

Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.

Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10

 

 

Dental Injuries

The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19

In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11

Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).

Figure 1.
If reimplantation is not possible, the avulsed tooth should be transported in saline, saliva, or milk for emergent dental care.16 If the tooth is driven into the alveolar socket, it should not be repositioned acutely but referred for dental evaluation.11A player with a dental injury should be immediately evaluated for airway obstruction, and the injured area should be washed with sterile water and dabbed with gauze.23 Dental injuries are often permanent and can cause complications later in life.19 Therefore, it is imperative to manage dental injuries appropriately, especially as reimplanting a tooth within 30 minutes results in 90% probability of tooth survival, whereas a 2-hour delay reduces tooth survival to <5%.12 Return to play should be individualized. For completely avulsed teeth that cannot be reimplanted, the player can return to play (with mouth guard protection) within 48 hours as long as there are no bone fractures.24 Players who undergo reimplantation and splinting of avulsed teeth should wait 2 to 4 weeks before returning to play.23 Use of mouth guards and face protection is directly associated with prevention of dental injuries; these protective devices should be worn in practice and competition.16,19,23

Concussions

A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3

Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28

Table 3.
Physicians caring for hockey players should be aware of common symptoms and signs of concussion (Table 3). Concussions can result in abnormalities of balance, cognition, and vision.29

As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.

Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
Table 4.
After being asymptomatic at rest, a player usually takes at least 1 week to progress through the protocol.25 In the event of a setback during the stepwise program, the player must return to the previous asymptomatic level after 24 hours of rest. Most concussions resolve quickly, without sequelae. Players with persisting symptoms may require medication, vestibular therapy, or other treatment. A player with unresolved symptoms should not be allowed to return to play.

On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.

 

 

Cervical Spine Injuries

Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40

Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37

The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.

Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46

Table 5.
Although the literature lacks a standardized protocol, 4 fundamental criteria can be applied to a hockey player returning to the ice: The player should be pain-free and have full cervical neck motion, return of full strength, and no evidence of residual neurologic injury47 (Table 5).

Shoulder Injuries

For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50

In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).

Figure 2.
Physical examination reveals swelling and tenderness at the joint. Skin tenting can occur with type III and type V injuries, and posterior deformity with type IV. We recommend initially obtaining anteroposterior (AP), scapular-Y, and axillary radiographs in cases of suspected AC joint injury. Weighted views are unnecessary and can exacerbate pain in acutely injured players.

Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Figure 3.
Some authors recommend drilling only 1 hole in order to minimize the risk, but doing so may come at the price of mild anteriorization of the clavicle with this nonanatomical technique. As the optimal surgical treatment for AC joints remains controversial, there is no consensus at this time.

Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.

Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
Figure 4.
All athletes younger than 25 years carry a risk for this injury pattern, as that age is when the medial clavicle physis closes (Figures 4A-4C). Posterior sternoclavicular injuries should be taken to the operating room for closed versus possible open reduction with a cardiothoracic surgeon on standby (Figure 4D).

The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.

CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.

After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Figure 5.
We usually recommend focusing initial physical therapy on joint rehabilitation with an emphasis on ROM and strength. We typically recommend players use a Sully brace when players return to the ice59 (Figure 5).

Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.

Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Figure 6.
In some cases, RCCs that alter shoulder function can result in missed games and practices. RCC, an acute shoulder injury in an athlete with prior normal RC function, is followed by recovery of RC function—in contrast to tears, which can cause prolonged loss of function and strength.64 RCCs can involve the enthesis, the tendon, the myotendinous junction, or the muscle belly (Figures 6A, 6B). On examination, a hockey player with RCC has decreased active ROM with weakness in external rotation with the arm in 90° of abduction and with scapular plane elevation.
Table 6.
We recommend the treatment protocol outlined by Cohen and colleagues64 (Table 6). Return to ice is allowed after full shoulder ROM and strength have returned. Average time missed is usually about 1 week.

 

 

Summary

Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.

Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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Take-Home Points

  • Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
  • Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
  • Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
  • A player with unresolved concussion symptoms should not be allowed to return to the ice.
  • Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.

On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2

Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4

Table 1.
In the United States, an estimated 20,000 hockey players present to the emergency department (ED) with injuries each year.5 In some leagues, game-related injury rates can be as high as 96 per 1000 player-hours (Table 1).

Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.

In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.

Evaluation and Management of Common Hockey Injuries

Eye Injuries

Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10

Table 2.
Some of these injuries have the potential to cause permanent ocular damage and loss of sight. A clear understanding of how to correctly evaluate, triage, and manage ocular trauma is therefore essential for any physician providing primary medical care for hockey players and teams.

As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.

Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.

Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10

 

 

Dental Injuries

The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19

In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11

Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).

Figure 1.
If reimplantation is not possible, the avulsed tooth should be transported in saline, saliva, or milk for emergent dental care.16 If the tooth is driven into the alveolar socket, it should not be repositioned acutely but referred for dental evaluation.11A player with a dental injury should be immediately evaluated for airway obstruction, and the injured area should be washed with sterile water and dabbed with gauze.23 Dental injuries are often permanent and can cause complications later in life.19 Therefore, it is imperative to manage dental injuries appropriately, especially as reimplanting a tooth within 30 minutes results in 90% probability of tooth survival, whereas a 2-hour delay reduces tooth survival to <5%.12 Return to play should be individualized. For completely avulsed teeth that cannot be reimplanted, the player can return to play (with mouth guard protection) within 48 hours as long as there are no bone fractures.24 Players who undergo reimplantation and splinting of avulsed teeth should wait 2 to 4 weeks before returning to play.23 Use of mouth guards and face protection is directly associated with prevention of dental injuries; these protective devices should be worn in practice and competition.16,19,23

Concussions

A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3

Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28

Table 3.
Physicians caring for hockey players should be aware of common symptoms and signs of concussion (Table 3). Concussions can result in abnormalities of balance, cognition, and vision.29

As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.

Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
Table 4.
After being asymptomatic at rest, a player usually takes at least 1 week to progress through the protocol.25 In the event of a setback during the stepwise program, the player must return to the previous asymptomatic level after 24 hours of rest. Most concussions resolve quickly, without sequelae. Players with persisting symptoms may require medication, vestibular therapy, or other treatment. A player with unresolved symptoms should not be allowed to return to play.

On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.

 

 

Cervical Spine Injuries

Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40

Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37

The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.

Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46

Table 5.
Although the literature lacks a standardized protocol, 4 fundamental criteria can be applied to a hockey player returning to the ice: The player should be pain-free and have full cervical neck motion, return of full strength, and no evidence of residual neurologic injury47 (Table 5).

Shoulder Injuries

For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50

In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).

Figure 2.
Physical examination reveals swelling and tenderness at the joint. Skin tenting can occur with type III and type V injuries, and posterior deformity with type IV. We recommend initially obtaining anteroposterior (AP), scapular-Y, and axillary radiographs in cases of suspected AC joint injury. Weighted views are unnecessary and can exacerbate pain in acutely injured players.

Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Figure 3.
Some authors recommend drilling only 1 hole in order to minimize the risk, but doing so may come at the price of mild anteriorization of the clavicle with this nonanatomical technique. As the optimal surgical treatment for AC joints remains controversial, there is no consensus at this time.

Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.

Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
Figure 4.
All athletes younger than 25 years carry a risk for this injury pattern, as that age is when the medial clavicle physis closes (Figures 4A-4C). Posterior sternoclavicular injuries should be taken to the operating room for closed versus possible open reduction with a cardiothoracic surgeon on standby (Figure 4D).

The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.

CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.

After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Figure 5.
We usually recommend focusing initial physical therapy on joint rehabilitation with an emphasis on ROM and strength. We typically recommend players use a Sully brace when players return to the ice59 (Figure 5).

Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.

Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Figure 6.
In some cases, RCCs that alter shoulder function can result in missed games and practices. RCC, an acute shoulder injury in an athlete with prior normal RC function, is followed by recovery of RC function—in contrast to tears, which can cause prolonged loss of function and strength.64 RCCs can involve the enthesis, the tendon, the myotendinous junction, or the muscle belly (Figures 6A, 6B). On examination, a hockey player with RCC has decreased active ROM with weakness in external rotation with the arm in 90° of abduction and with scapular plane elevation.
Table 6.
We recommend the treatment protocol outlined by Cohen and colleagues64 (Table 6). Return to ice is allowed after full shoulder ROM and strength have returned. Average time missed is usually about 1 week.

 

 

Summary

Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.

Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Hockey is a high-speed collision sport with one of the highest injury rates among all sports.
  • Use of a helmet with visors or full-face shields significantly reduces the risk for eye injury.
  • Broken portions of teeth should be found and placed in a protective medium such as saline, saliva, or milk for transport.
  • A player with unresolved concussion symptoms should not be allowed to return to the ice.
  • Shoulder dominance, which determines stick grip, is an important consideration in the treatment of shoulder instability in an ice hockey player.

On a surface of ice in Windsor, Nova Scotia in the middle of the 19th century, the modern game of ice hockey evolved.1 A blend of hurley, a Gaelic sport, and lacrosse, from the native Mi’kmaq culture, the sport of ice hockey gained rapidly in popularity throughout Canada and is now the country’s national sport. Hockey quickly spread to the United States and then Europe. It is presently played in 77 countries across the world.2

Hockey players can reach speeds of up to 48 km (~30 miles) per hour on razor-sharp skates on an ice surface surrounded by rigid plastic composite boards topped with plexiglass.3 They use sticks made of wood, aluminum, or a composite material to advance a 6-ounce vulcanized rubber puck on the opposing goal, and this puck sometimes reaches speeds over 160 km (~100 miles) per hour. Older, male players are allowed to make physical contact with their opposing counterparts to separate them from the puck (body-checking). Not surprisingly, the potential risk for injury in hockey is high. At the 2010 Winter Olympics, men’s ice hockey players had the highest rate of injury of any other competitors there—more than 30% were affected.4

Table 1.
In the United States, an estimated 20,000 hockey players present to the emergency department (ED) with injuries each year.5 In some leagues, game-related injury rates can be as high as 96 per 1000 player-hours (Table 1).

Hockey is played and enjoyed by athletes ranging widely in age. Youth hockey leagues accept players as young as 5 years. Hockey can become a lifelong recreational activity. In North America, old timers’ leagues have many players up to age 70 years.6 According to International Ice Hockey Federation data for 2016, more than 543,000 and 639,500 people play hockey in the United States and Canada, respectively.2 Most of the rules, protective equipment, skates, ice surfaces, and goal sizes are the same in men’s and women’s hockey.7 The major difference is in body-checking—this practice is not allowed at any age in women’s ice hockey.

In this article, we review the evaluation and management of common head, neck, and shoulder hockey injuries for physicians who provide medical support and coverage for youth, amateur, and senior hockey teams.

Evaluation and Management of Common Hockey Injuries

Eye Injuries

Although eye injuries are less common than musculoskeletal injuries and concussions in hockey, they are a serious risk for recreational and competitive players alike. Furthermore, recovery may be difficult, and eye injuries can have serious lifelong consequences.8 In hockey, the most commonly reported eye injuries are periorbital contusions and lacerations, hyphema, corneal and conjunctival abrasions, orbital fractures, and ruptured globes (Table 2).9,10

Table 2.
Some of these injuries have the potential to cause permanent ocular damage and loss of sight. A clear understanding of how to correctly evaluate, triage, and manage ocular trauma is therefore essential for any physician providing primary medical care for hockey players and teams.

As a contact sport, hockey often involves high-impact, blunt-force trauma. The trauma in hockey results from collisions with other players, the boards, hockey sticks, and pucks. It is therefore not surprising that the most common ocular injuries in this sport are periorbital contusions. Although most contusions cause only mild swelling and ecchymosis of the soft tissues around the eye, there is potential for serious consequences. In a Scandinavia study, Leivo and colleagues10 found that 9% of patients who sustained a periocular contusion also had a clinically significant secondary diagnosis, such as retinal tear or hemorrhage, eyelid laceration, vitreous hemorrhage, or retinal detachment. Although the study was hospital-based, and therefore biased toward more severe cases, its findings highlight the potential severity of eye injuries in hockey. Furthermore, the study found that the majority of players who sustained blunt trauma to the eye itself required lifelong follow-up because of increased risk for glaucoma. This is particularly true for hyphema, as this finding indicates significant damage to intraocular tissues.10Players can also sustain fractures of the orbital bones, including orbital blowout fractures. Typical signs and symptoms of blowout fractures include diplopia, proptosis or enophthalmos, infraorbital hypoesthesia, painful and decreased extraocular movement (particularly upgaze), and palpable crepitance caused by sinus air entering the lower eyelid.11 If orbital fracture is suspected, as it should be in any case in which the injured player experiences pain with eye movement or diplopia, the player should be referred to the ED for computed tomography (CT) and ophthalmologic evaluation.12 Continued participation seriously risks making the injury much worse, particularly should another impact occur. In addition, given the impact needed to cause orbital fractures, consideration must be given to the potential for a coexisting concussion injury.

Severe direct trauma to the eye—from a puck, a stick, or a fist—can result in a ruptured globe, a particularly serious injury that requires immediate surgical attention. Signs and symptoms of a ruptured globe are rarely subtle, but associated eyelid swelling or laceration may obscure the injury, delaying proper diagnosis and treatment. More obvious signs include severely reduced vision, hemorrhagic chemosis (swelling) of the conjunctiva, and an irregular or peaked pupil. If a rupture or any significant intraocular injury is suspected, it is crucial to avoid applying any pressure to the globe, as this can significantly worsen the damage to the intraocular tissues. Use of a helmet with protective shields and cages attached markedly reduces the risk for such injuries.13All eye injuries require prompt assessment, which allows for appropriate management and prevention of secondary damage.14 Initial evaluation of a patient with ocular trauma should begin with external examination for lacerations, swelling, or orbital rim step-off deformity. The physician should also check visual acuity in order to assess for significant vision impairment (counting fingers or reading a sign in the arena; confrontation visual fields). This should be done before attending to any periocular injuries, with the uninjured side serving as a control. Next, the physician should assess the extraocular eye movements as well as the size, shape, and reactivity of the pupils. Particular attention should be paid to detecting any deficit in extraocular movement or irregularity in pupil size, shape, or reactivity, as such findings are highly suggestive of serious injury to the globe.13 Hyphema (blood in anterior chamber of eye anterior to pupil) should be suspected if vision is reduced and the pupil cannot be clearly visualized. However, a bright red clot is not always apparent at time of injury or if the amount of blood is small. An irregular pupil, or a pupil that does not constrict well to light, is also a red flag for serious contusion injury to the eye, and requires ophthalmologic evaluation. It is important to keep in mind that blunt trauma severe enough to produce hyphema or an irregular and poorly reactive pupil is often associated with retinal damage as well, including retinal edema or detachment.

Minor injuries (eg, small foreign bodies, minor periocular contusions and lacerations) can often be managed rink-side. Foreign bodies not embedded in the cornea, but lodged under the upper eyelid, can sometimes be removed by everting the eyelid and sweeping with a moistened cotton swab or using diffuse, sterile saline irrigation.11 Corneal abrasions generally cause severe pain, photophobia, and tearing and are easily diagnosed with use of topical fluorescein and a blue light. A topical anesthetic can be extremely helpful in this setting, as it allows for proper pain-free evaluation, but should never be used in an ongoing manner for pain relief. Small lacerations of the brow can be sutured with 5-0 or 6-0 nylon or closed with 2-Octyl cyanoacrylate tissue adhesive (Dermabond). Eyelid lacerations, unless very small, are best managed by an ophthalmologist; care must be taken to rule out injury to the deeper orbital tissues and eye. If serious injury is suspected, or the eye cannot be appropriately evaluated, it should be stabilized and protected with a protective shield or plastic cup, and the player should be transferred to an ED for appropriate ophthalmologic evaluation.13Most eye injuries are accidental, caused by sticks or deflected pucks, but 18% are acquired in fights.8 Use of visors or full-face cages effectively minimizes the rate of eye injuries.8,13,15,16 In a cohort study of 282 elite amateur ice hockey players, the risk of eye injury was 4.7 times higher in players without face protection than in players who used half-face shields; there were no eye injuries in players who used full-face protection.13 For visors to prevent eye injury, they must be positioned to cover the eyes and the lower edge of the nose in all projections.10

 

 

Dental Injuries

The incidence and type of facial and dental injuries depend directly on the type of face protection used.11,17,18 In a study of face, head, and neck injuries in elite amateur ice hockey players, Stuart and colleagues13 found game-related injury rates of 158.9 per 1000 player-hours in players without face protection, 73.5 in players who used half-face shields, and 23.2 in players who used full-face shields. Players who wore full-face shields had facial, head, and neck injury rates of only 23.2 per 1000 player-game hours.13 Other studies clearly support the important role face shields play in lowering injury risk in hockey. Face and head injuries account for 20% to 40% of all hockey-related injuries,3,16,19 and dental injuries up to 11.5%.20 In a study from Finland, Lahti and colleagues19 found that over a 2-year period, 479 hockey players sustained injuries, including 650 separate dental injuries. The most commonly diagnosed dental injury was an uncomplicated crown fracture, and the most common cause was a hit with a hockey stick, which accounted for 52.7% and 40.3% of dental injuries in games and practices, respectively.19

In the management of dental fractures, the broken portions of teeth should be found and placed in a transportation-protective medium, such as saline, saliva, or milk,16 which can improve functional and esthetic replacement outcomes.21,22 Loose pieces of teeth should not be left in the player’s mouth. The residual tooth should be stabilized and exposure to air and occlusion limited. Dental fractures can affect the enamel, the enamel and dentin structures (uncomplicated fracture), or enamel, dentin, and pulp (complicated).23 Fractures involving only the enamel do not require urgent dental evaluation. Dentin or pulp involvement may cause temperature and air sensitivity.23 If a tooth is air-sensitive, the player should be referred to a specialist immediately.11

Direct trauma can cause instability without displacement (subluxation) or complete displacement of the tooth from its alveolar socket (avulsion).23 An avulsed tooth should be handled by the crown to avoid further damage to the root and periodontal ligament.16,24 The tooth should be rinsed gently with saline and reimplanted in its socket, ideally within 5 to 10 minutes,23with the athlete biting down gently on gauze to hold the tooth in place. A 1-mL supraperiosteal infiltration of 1% or 2% lidocaine hydrochloride (1:100,000 epinephrine) can be given into the apex of the tooth being anesthetized (Figure 1).

Figure 1.
If reimplantation is not possible, the avulsed tooth should be transported in saline, saliva, or milk for emergent dental care.16 If the tooth is driven into the alveolar socket, it should not be repositioned acutely but referred for dental evaluation.11A player with a dental injury should be immediately evaluated for airway obstruction, and the injured area should be washed with sterile water and dabbed with gauze.23 Dental injuries are often permanent and can cause complications later in life.19 Therefore, it is imperative to manage dental injuries appropriately, especially as reimplanting a tooth within 30 minutes results in 90% probability of tooth survival, whereas a 2-hour delay reduces tooth survival to <5%.12 Return to play should be individualized. For completely avulsed teeth that cannot be reimplanted, the player can return to play (with mouth guard protection) within 48 hours as long as there are no bone fractures.24 Players who undergo reimplantation and splinting of avulsed teeth should wait 2 to 4 weeks before returning to play.23 Use of mouth guards and face protection is directly associated with prevention of dental injuries; these protective devices should be worn in practice and competition.16,19,23

Concussions

A concussion is a “complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”25 Concussion is largely a functional disturbance instead of a structural injury, owing to the rotational and/or shearing forces involved. Many studies have identified concussion as the most common type of injury in all of youth hockey.26 Concussions account for up to 19% of all injuries in men’s collegiate hockey.3

Concussion can be challenging to diagnose on the ice. The most important factor in concussion management is symptom reporting by the athlete.27 Despite significant efforts in education and awareness, student athletes, especially hockey players, withhold reporting a possible concussion.28 Reasons for underreporting include fear of letting down other players and coaches, thinking the injury is not severe enough to warrant evaluation, and fear of losing standing with the current team or future teams.28

Table 3.
Physicians caring for hockey players should be aware of common symptoms and signs of concussion (Table 3). Concussions can result in abnormalities of balance, cognition, and vision.29

As postinjury concussion assessments are ideal when comparisons can be made with preseason (baseline) scores, preseason testing is becoming standard in professional, college, junior, and high school hockey. This testing involves the Sport Concussion Assessment Tool, 3rd edition (SCAT3), and the King-Devick (K-D) test.30,31 Some youth leagues have baseline testing as well, though the frequency of baseline testing in their players is controversial,32 as the adolescent mind’s processing speed and memory increase exponentially.33 For these younger athletes, it may be necessary to perform baseline testing more frequently than annually.32 A physician can use baseline test results to help diagnose a concussion at the rink and then track the athlete’s recovery and help with return-to-play decisions.29 Vision involves almost half of the brain’s circuits,34 including areas vulnerable to head impact. A neuro-ophthalmologic test can assess for irregularities in accommodation, convergence, ocular muscle balance, pursuit, and saccades.29 The K-D test is a visual performance examination that allows easy and objective assessment of eye movements. Use of both the K-D test and the SCAT3 at the rink may increase the number of concussions detected.29,35 We recommend that physicians use both tests to assess for concussion at the hockey rink.

Initial treatment involves a period of physical rest and relative cognitive rest. Acute worsening of symptoms warrants urgent imaging to rule out a subdural or subarachnoid bleed. Once a player is symptom-free, a graded return-to-play protocol should be followed (Table 4).
Table 4.
After being asymptomatic at rest, a player usually takes at least 1 week to progress through the protocol.25 In the event of a setback during the stepwise program, the player must return to the previous asymptomatic level after 24 hours of rest. Most concussions resolve quickly, without sequelae. Players with persisting symptoms may require medication, vestibular therapy, or other treatment. A player with unresolved symptoms should not be allowed to return to play.

On the prevention side, great efforts have been made to improve hockey helmets. (Some manufacturers claim to have made concussion-proof helmets, but there is no evidence supporting this claim.6) Numerous investigators have reported a lower overall injury rate in players who wear a helmet and a full-face shield.6,13 In addition, rule changes aimed at decreasing head contact have been implemented to decrease the incidence of sport-related concussions.36 Moreover, education on proper helmet use and wear should be emphasized. A study of the effects of hockey helmet fit on cervical motion found that 7 (39%) of 18 players wore a game or competition helmet so loosely that it could be removed without unbuttoning its chinstrap.37 Improperly worn helmets cannot prevent injury as well as properly worn helmets can.

 

 

Cervical Spine Injuries

Whereas American football is associated with a higher annual number of nonfatal catastrophic neck injuries, hockey has a 3 to 6 times higher incidence of cervical spine injuries and spinal cord damage.38,39 A Canadian Ice Hockey Spinal Injuries Registry review of the period 2006 to 2011 identified 44 cervical spine injuries, 7.3 per year on average.40 Severe injury, defined as complete motor and sensory loss, complete motor loss and incomplete sensory, or complete motor loss, occurred in 4 (9.1%) of the 44 injured players. In hockey, a major mechanism of cervical spine injury is an axial load to the slightly flexed spine.39 Of 355 hockey-related cervical spine injuries in a Canada study, 95 (35.5%) were caused by a check from behind.40,41 The Canadian neurosurgeons’ work led to rule changes prohibiting checks from behind, and this prohibition has reduced the incidence of cervical spine injuries in ice hockey.38,40

Team physicians should be comfortable managing serious neck and spine injuries on the ice. Initial evaluation should follow the standard ABCs (airway, breathing, circulation). The physician places a hand on each side of the head to stabilize the neck until the initial examination is complete. The goal is to minimize cervical spine motion until transportation to the hospital for advanced imaging and definitive treatment.37 The decision to remove or leave on the helmet is now controversial. Hockey helmets differ from football helmets in that their chinstraps do not afford significant cervical stabilization, and the helmets have less padding and cover less of the head; in addition, a shockingly high percentage of hockey players do not wear properly fitting helmets.37 In one study, 3-dimensional motion analysis of a hockey player during the logroll technique showed less transverse and sagittal cervical plane motion with the helmet removed than with the helmet (properly fitting or not) in place; the authors recommended removing the helmet to limit extraneous cervical spine motion during the technique.37 However, 2 other studies found that helmet removal can result in significantly increased cervical spine motion of the immobilized hockey player.42,43Recommendation 4 of the recently released interassociation consensus statement of the National Athletic Trainers’ Association reads, “Protective athletic equipment should be removed before transport to an emergency facility for an athlete-patient with suspected cervical spine instability.”44 This represents a shift from leaving the helmet and shoulder pads in place. For ice hockey players with suspected cervical spine injury, more research is needed on cervical motion during the entire sequence—partial logrolls, spine-boarding, placement of cervical collar before or after logroll, and different immobilization techniques for transport.37

The athlete must be carefully transferred to a spine board with either logroll or lift-and-slide. Although an extrication cervical collar can be placed before the spine board is placed, the effectiveness of this collar in executing the spine-board transfer is not proven.45 When the player is on the spine board, the head can be secured with pads and straps en route to the hospital.

Return-to-Play Criteria for Cervical Spine Injuries There is no clear consensus on return-to-play guidelines for cervical spine injuries in athletes.46

Table 5.
Although the literature lacks a standardized protocol, 4 fundamental criteria can be applied to a hockey player returning to the ice: The player should be pain-free and have full cervical neck motion, return of full strength, and no evidence of residual neurologic injury47 (Table 5).

Shoulder Injuries

For hockey players, the upper extremity traditionally has been considered a well-protected area.48 However, shoulder pads are considerably more flexible in hockey than in football and other collision sports. In addition, hockey gloves allow a fair amount of motion for stick handling, and the wrist may be in maximal flexion or extension when a hit against the boards or the ice occurs. Open-ice checking, board collisions, and hockey stick use have been postulated as reasons for the high incidence of upper extremity injuries in hockey. Researchers in Finland found that upper extremity injuries accounted for up to 31% of all hockey injuries.49 More than 50% of these injuries resulted from checking or board collisions. Furthermore, study findings highlighted a low rate of injury in younger players and indicated the rate increases with age.49,50

In hockey players, the acromioclavicular (AC) joint is the most commonly injured shoulder structure.51 The mechanism of injury can be a board collision or an open-ice hit, but most often is a direct blow to the shoulder. The collision disrupts the AC joint and can sprain or tear the coracoclavicular ligaments. The Rockwood classification is used to categorize AC joint injuries (Figure 2).

Figure 2.
Physical examination reveals swelling and tenderness at the joint. Skin tenting can occur with type III and type V injuries, and posterior deformity with type IV. We recommend initially obtaining anteroposterior (AP), scapular-Y, and axillary radiographs in cases of suspected AC joint injury. Weighted views are unnecessary and can exacerbate pain in acutely injured players.

Initial management involves icing the AC joint and placing a sling for comfort. Type I and type II injuries can be managed with progressive range-of-motion (ROM) exercises, strengthening, cryotherapy, and a period of rest. Treatment of type III injuries remains controversial,52 but in hockey players these injuries are almost always treated nonoperatively. Return to play requires full motion, normal strength, and minimal discomfort. Players return a few days to 2 weeks after a grade I injury; recovery from grade II injuries may take 2 to 3 weeks, and recovery from grade III injuries, 6 to 12 weeks. Surgical treatment is usually required in type IV and type V injuries, but we have had experience treating these injuries nonoperatively in high-level players. AC joint reinjury in hockey players is common, and surgical treatment should be approached cautiously, as delayed fracture after return to sport has been reported.53 Special precautions should be taken in collision athletes who undergo AC joint reconstruction. In the anatomical reconstruction described by Carofino and Mazzocca,54 2 holes are drilled in the clavicle; these holes are a potential source of fracture when the collision athlete returns to sport (Figure 3).
Figure 3.
Some authors recommend drilling only 1 hole in order to minimize the risk, but doing so may come at the price of mild anteriorization of the clavicle with this nonanatomical technique. As the optimal surgical treatment for AC joints remains controversial, there is no consensus at this time.

Clavicle fracture is another common hockey injury.55 Studies have shown clavicle fractures proportionally occur most often in people 15 to 19 years old.49 The injury presents with pain and deformity over the clavicle; in more severe fractures, skin tenting is identified. Initial management of suspected clavicle fracture includes cryotherapy, sling, and radiographs. Radiographs should include an AP view and then a 45° cephalad view, which eliminates overshadowing from the ribs. Most clavicle fractures are successfully managed nonoperatively, though there is evidence that significantly displaced or comminuted fractures have better union rates and shoulder function when treated with open reduction and internal fixation.56 After a clavicle fracture, return to skating and noncontact practice usually takes 8 weeks, with return to full contact occurring around 12 weeks.

Sternoclavicular injuries are relatively uncommon, but potentially serious. Special attention should also be given to adolescent athletes with sternoclavicular pain. Although sternoclavicular dislocations have been reported in hockey players, instead these likely are fractures involving the medial clavicle physis.57
Figure 4.
All athletes younger than 25 years carry a risk for this injury pattern, as that age is when the medial clavicle physis closes (Figures 4A-4C). Posterior sternoclavicular injuries should be taken to the operating room for closed versus possible open reduction with a cardiothoracic surgeon on standby (Figure 4D).

The shoulder is the most commonly dislocated major joint, and the incidence of shoulder dislocation in elite hockey players is 8% to 21%.50,58 Anterior shoulder instability occurs from a fall with the shoulder in an abducted, externally rotated and extended position or from a direct anteriorly placed impact to the posterior shoulder. We recommend taking players off the ice for evaluation. Depending on physician comfort, the shoulder can be reduced in the training room, and the athlete sent for radiographs after reduction. If resources or support for closed reduction is not available at the rink, the athlete should be sent to the ED. Initial radiographic evaluation of a player with shoulder injury begins with plain radiographs, including a true AP (Grashey) view with the humerus in neutral, internal, and external rotation and an axillary view. The axillary radiograph is crucial in determining anterior or posterior dislocation. If the patient cannot tolerate the pain associated with having an axillary radiograph taken, a Velpeau radiograph can be used. This radiograph is taken with the patient’s arm in a sling and with the patient leaning back 30° while the x-ray beam is directed superior to inferior.

CT is performed for a suspected osseous injury. CT is more accurate than plain radiographs in showing glenoid and humeral fractures in the acute setting as well as the amount of bone loss in the case of chronic instability. Magnetic resonance arthrography is the imaging modality of choice for the diagnoses of capsulolabral injury.

After shoulder reduction, treatment with a sling, cryotherapy, and a nonsteroidal anti-inflammatory drug is initiated. In a Minnesota study of nonoperative management of shoulder instability, 9 of 10 hockey players were able to return to play the same season, and 6 of the 10 required surgery at the end of the season.59
Figure 5.
We usually recommend focusing initial physical therapy on joint rehabilitation with an emphasis on ROM and strength. We typically recommend players use a Sully brace when players return to the ice59 (Figure 5).

Compared with noncontact athletes, hockey players and other collision athletes are at increased risk for recurrence.60-62 For collision athletes who want to continue playing their sport after recurrent instability, surgery is recommended. A shoulder instability study in Toronto found that more than 54% of 24 professional hockey players had associated Hill-Sachs lesions, but only 3 shoulders (12.5%) had glenoid defects.50 Arthroscopic and open techniques both demonstrate good results, and identification of bone loss can help determine which surgery to recommend.63 Hockey players can usually return to sport 6 months after shoulder stabilization.

Another important consideration in managing shoulder instability in hockey players is shoulder dominance, which determines stick grip. A left-handed player places the right hand on top of the stick for support, but most of the motion associated with shooting the puck—including abduction and external rotation—occurs with the left shoulder. Thus, a left-handed player with a history of previous left-side shoulder dislocation may dislocate with each shot, but a right-handed player with left shoulder instability may have considerably less trouble on the ice.58Shoulder and rotator cuff contusions (RCCs) occur in hockey and other collision sports.49,64 RCCs almost always result from a direct blow to the shoulder, and present with shoulder function loss, weakness, and pain.
Figure 6.
In some cases, RCCs that alter shoulder function can result in missed games and practices. RCC, an acute shoulder injury in an athlete with prior normal RC function, is followed by recovery of RC function—in contrast to tears, which can cause prolonged loss of function and strength.64 RCCs can involve the enthesis, the tendon, the myotendinous junction, or the muscle belly (Figures 6A, 6B). On examination, a hockey player with RCC has decreased active ROM with weakness in external rotation with the arm in 90° of abduction and with scapular plane elevation.
Table 6.
We recommend the treatment protocol outlined by Cohen and colleagues64 (Table 6). Return to ice is allowed after full shoulder ROM and strength have returned. Average time missed is usually about 1 week.

 

 

Summary

Hockey is a high-speed collision sport with one of the highest injury rates among all sports. Physicians caring for youth, amateur, and senior hockey teams see a range of acute head, neck, and shoulder injuries. Although treatment of eye injuries, dental injuries, and concussions is not always considered orthopedic care, an orthopedic surgeon who is covering hockey needs to be comfortable managing these injuries acutely. Quality rink-side care minimizes the impact of the injury, maximizes the functional result, and expedites the safe return of the injured player back to the ice.

Am J Orthop. 2017;46(3):123-134. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

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4. Engebretsen L, Steffen K, Alonso JM, et al. Sports injuries and illnesses during the Winter Olympic Games 2010. Br J Sports Med. 2010;44(11):772-780.

5. Deits J, Yard EE, Collins CL, Fields SK, Comstock RD. Patients with ice hockey injuries presenting to US emergency departments, 1990-2006. J Athl Train. 2010;45(5):467-474.

6. Brooks A, Loud KJ, Brenner JS, et al. Reducing injury risk from body checking in boys’ youth ice hockey. Pediatrics. 2014;133(6):1151-1157.

7. Agel J, Harvey EJ. A 7-year review of men’s and women’s ice hockey injuries in the NCAA. Can J Surg. 2010;53(5):319-323.

8. Micieli JA, Zurakowski D, Ahmed, II. Impact of visors on eye and orbital injuries in the National Hockey League. Can J Ophthalmol. 2014;49(3):243-248.

9. Pashby TJ. Ocular injuries in hockey. Int Ophthalmol Clin. 1988;28(3):228-231.

10. Leivo T, Haavisto AK, Sahraravand A. Sports-related eye injuries: the current picture. Acta Ophthalmol. 2015;93(3):224-231.

11. Cohn RM, Alaia MJ, Strauss EJ, Feldman AF. Rink-side management of ice hockey related injuries to the face, neck, and chest. Bull Hosp Jt Dis. 2013;71(4):253-256.

12. Reehal P. Facial injury in sport. Curr Sports Med Rep. 2010;9(1):27-34.

13. Stuart MJ, Smith AM, Malo-Ortiguera SA, Fischer TL, Larson DR. A comparison of facial protection and the incidence of head, neck, and facial injuries in Junior A hockey players. A function of individual playing time. Am J Sports Med. 2002;30(1):39-44.

14. MacEwen CJ, McLatchie GR. Eye injuries in sport. Scott Med J. 2010;55(2):22-24.

15. Stevens ST, Lassonde M, de Beaumont L, Keenan JP. The effect of visors on head and facial injury in National Hockey League players. J Sci Med Sport. 2006;9(3):238-242.

16. Moslener MD, Wadsworth LT. Ice hockey: a team physician’s perspective. Curr Sports Med Rep. 2010;9(3):134-138.

17. LaPrade RF, Burnett QM, Zarzour R, Moss R. The effect of the mandatory use of face masks on facial lacerations and head and neck injuries in ice hockey. A prospective study. Am J Sports Med. 1995;23(6):773-775.

18. Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. Head and neck injuries among ice hockey players wearing full face shields vs half face shields. JAMA. 1999;282(24):2328-2332.

19. Lahti H, Sane J, Ylipaavalniemi P. Dental injuries in ice hockey games and training. Med Sci Sports Exerc. 2002;34(3):400-402.

20. Sane J, Ylipaavalniemi P, Leppanen H. Maxillofacial and dental ice hockey injuries. Med Sci Sports Exerc. 1988;20(2):202-207.

21. Emerich K, Kaczmarek J. First aid for dental trauma caused by sports activities: state of knowledge, treatment and prevention. Sports Med. 2010;40(5):361-366.

22. Rosenberg H, Rosenberg H, Hickey M. Emergency management of a traumatic tooth avulsion. Ann Emerg Med. 2011;57(4):375-377.

23. Young EJ, Macias CR, Stephens L. Common dental injury management in athletes. Sports Health. 2015;7(3):250-255.

24. Andersson L, Andreasen JO, Day P, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 2. Avulsion of permanent teeth. Dent Traumatol. 2012;28(2):88-96.

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46. Morganti C, Sweeney CA, Albanese SA, Burak C, Hosea T, Connolly PJ. Return to play after cervical spine injury. Spine. 2001;26(10):1131-1136.

47. Huang P, Anissipour A, McGee W, Lemak L. Return-to-play recommendations after cervical, thoracic, and lumbar spine injuries: a comprehensive review. Sports Health. 2016;8(1):19-25.

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49. Molsa J, Kujala U, Myllynen P, Torstila I, Airaksinen O. Injuries to the upper extremity in ice hockey: analysis of a series of 760 injuries. Am J Sports Med. 2003;31(5):751-757.

50. Dwyer T, Petrera M, Bleakney R, Theodoropoulos JS. Shoulder instability in ice hockey players: incidence, mechanism, and MRI findings. Clin Sports Med. 2013;32(4):803-813.

51. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. Br J Sports Med. 2009;43(13):1000-1005.

52. Willimon SC, Gaskill TR, Millett PJ. Acromioclavicular joint injuries: anatomy, diagnosis, and treatment. Phys Sportsmed. 2011;39(1):116-122.

53. Martetschlager F, Horan MP, Warth RJ, Millett PJ. Complications after anatomic fixation and reconstruction of the coracoclavicular ligaments. Am J Sports Med. 2013;41(12):2896-2903.

54. Carofino BC, Mazzocca AD. The anatomic coracoclavicular ligament reconstruction: surgical technique and indications. J Shoulder Elbow Surg. 2010;19(2 suppl):37-46.

55. Laprade RF, Surowiec RK, Sochanska AN, et al. Epidemiology, identification, treatment and return to play of musculoskeletal-based ice hockey injuries. Br J Sports Med. 2014;48(1):4-10.

56. Canadian Orthopaedic Trauma Society. Nonoperative treatment compared with plate fixation of displaced midshaft clavicular fractures. A multicenter, randomized clinical trial. J Bone Joint Surg Am. 2007;89(1):1-10.

57. Lee JT, Nasreddine AY, Black EM, Bae DS, Kocher MS. Posterior sternoclavicular joint injuries in skeletally immature patients. J Pediatr Orthop. 2014;34(4):369-375.

58. Hovelius L. Shoulder dislocation in Swedish ice hockey players. Am J Sports Med. 1978;6(6):373-377.

59. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433.

60. Mazzocca AD, Brown FM Jr, Carreira DS, Hayden J, Romeo AA. Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med. 2005;33(1):52-60.

61. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.

62. Cho NS, Hwang JC, Rhee YG. Arthroscopic stabilization in anterior shoulder instability: collision athletes versus noncollision athletes. Arthroscopy. 2006;22(9):947-953.

63. Griffin JW, Brockmeier SF. Shoulder instability with concomitant bone loss in the athlete. Orthop Clin North Am. 2015;46(1):89-103.

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References

1. Vaughan G. The Puck Starts Here: The Origin of Canada’s Great Winter Game, Ice Hockey. Fredericton, Canada: Goose Lane Editions; 1996.

2. IIHF member national associations. International Ice Hockey Federation website. http://www.iihf.com/iihf-home/the-iihf/members. Accessed April 6, 2017.

3. Flik K, Lyman S, Marx RG. American collegiate men’s ice hockey: an analysis of injuries. Am J Sports Med. 2005;33(2):183-187.

4. Engebretsen L, Steffen K, Alonso JM, et al. Sports injuries and illnesses during the Winter Olympic Games 2010. Br J Sports Med. 2010;44(11):772-780.

5. Deits J, Yard EE, Collins CL, Fields SK, Comstock RD. Patients with ice hockey injuries presenting to US emergency departments, 1990-2006. J Athl Train. 2010;45(5):467-474.

6. Brooks A, Loud KJ, Brenner JS, et al. Reducing injury risk from body checking in boys’ youth ice hockey. Pediatrics. 2014;133(6):1151-1157.

7. Agel J, Harvey EJ. A 7-year review of men’s and women’s ice hockey injuries in the NCAA. Can J Surg. 2010;53(5):319-323.

8. Micieli JA, Zurakowski D, Ahmed, II. Impact of visors on eye and orbital injuries in the National Hockey League. Can J Ophthalmol. 2014;49(3):243-248.

9. Pashby TJ. Ocular injuries in hockey. Int Ophthalmol Clin. 1988;28(3):228-231.

10. Leivo T, Haavisto AK, Sahraravand A. Sports-related eye injuries: the current picture. Acta Ophthalmol. 2015;93(3):224-231.

11. Cohn RM, Alaia MJ, Strauss EJ, Feldman AF. Rink-side management of ice hockey related injuries to the face, neck, and chest. Bull Hosp Jt Dis. 2013;71(4):253-256.

12. Reehal P. Facial injury in sport. Curr Sports Med Rep. 2010;9(1):27-34.

13. Stuart MJ, Smith AM, Malo-Ortiguera SA, Fischer TL, Larson DR. A comparison of facial protection and the incidence of head, neck, and facial injuries in Junior A hockey players. A function of individual playing time. Am J Sports Med. 2002;30(1):39-44.

14. MacEwen CJ, McLatchie GR. Eye injuries in sport. Scott Med J. 2010;55(2):22-24.

15. Stevens ST, Lassonde M, de Beaumont L, Keenan JP. The effect of visors on head and facial injury in National Hockey League players. J Sci Med Sport. 2006;9(3):238-242.

16. Moslener MD, Wadsworth LT. Ice hockey: a team physician’s perspective. Curr Sports Med Rep. 2010;9(3):134-138.

17. LaPrade RF, Burnett QM, Zarzour R, Moss R. The effect of the mandatory use of face masks on facial lacerations and head and neck injuries in ice hockey. A prospective study. Am J Sports Med. 1995;23(6):773-775.

18. Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. Head and neck injuries among ice hockey players wearing full face shields vs half face shields. JAMA. 1999;282(24):2328-2332.

19. Lahti H, Sane J, Ylipaavalniemi P. Dental injuries in ice hockey games and training. Med Sci Sports Exerc. 2002;34(3):400-402.

20. Sane J, Ylipaavalniemi P, Leppanen H. Maxillofacial and dental ice hockey injuries. Med Sci Sports Exerc. 1988;20(2):202-207.

21. Emerich K, Kaczmarek J. First aid for dental trauma caused by sports activities: state of knowledge, treatment and prevention. Sports Med. 2010;40(5):361-366.

22. Rosenberg H, Rosenberg H, Hickey M. Emergency management of a traumatic tooth avulsion. Ann Emerg Med. 2011;57(4):375-377.

23. Young EJ, Macias CR, Stephens L. Common dental injury management in athletes. Sports Health. 2015;7(3):250-255.

24. Andersson L, Andreasen JO, Day P, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 2. Avulsion of permanent teeth. Dent Traumatol. 2012;28(2):88-96.

25. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Clin J Sport Med. 2009;19(3):185-200.

26. Schneider KJ, Meeuwisse WH, Kang J, Schneider GM, Emery CA. Preseason reports of neck pain, dizziness, and headache as risk factors for concussion in male youth ice hockey players. Clin J Sport Med. 2013;23(4):267-272.

27. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med. 2013;47(5):250-258.

28. Delaney JS, Lamfookon C, Bloom GA, Al-Kashmiri A, Correa JA. Why university athletes choose not to reveal their concussion symptoms during a practice or game. Clin J Sport Med. 2015;25(2):113-125.

29. Ventura RE, Balcer LJ, Galetta SL. The concussion toolbox: the role of vision in the assessment of concussion. Semin Neurol. 2015;35(5):599-606.

30. Vartiainen MV, Holm A, Peltonen K, Luoto TM, Iverson GL, Hokkanen L. King-Devick test normative reference values for professional male ice hockey players. Scand J Med Sci Sports. 2015;25(3):e327-e330.

31. Galetta MS, Galetta KM, McCrossin J, et al. Saccades and memory: baseline associations of the King-Devick and SCAT2 SAC tests in professional ice hockey players. J Neurol Sci. 2013;328(1-2):28-31.

32. Vernau BT, Grady MF, Goodman A, et al. Oculomotor and neurocognitive assessment of youth ice hockey players: baseline associations and observations after concussion. Dev Neuropsychol. 2015;40(1):7-11.

 

 

33. Fry AF, Hale S. Relationships among processing speed, working memory, and fluid intelligence in children. Biol Psychol. 2000;54(1-3):1-34.

34. Felleman DJ, Van Essen DC. Distributed hierarchical processing in the primate cerebral cortex. Cereb Cortex. 1991;1(1):1-47.

35. Guskiewicz KM, Register-Mihalik J, McCrory P, et al. Evidence-based approach to revising the SCAT2: introducing the SCAT3. Br J Sports Med. 2013;47(5):289-293.

36. Smith AM, Stuart MJ, Dodick DW, et al. Ice Hockey Summit II: zero tolerance for head hits and fighting. Curr Sports Med Rep. 2015;14(2):135-144.

37. Mihalik JP, Beard JR, Petschauer MA, Prentice WE, Guskiewicz KM. Effect of ice hockey helmet fit on cervical spine motion during an emergency log roll procedure. Clin J Sport Med. 2008;18(5):394-398.

38. Banerjee R, Palumbo MA, Fadale PD. Catastrophic cervical spine injuries in the collision sport athlete, part 1: epidemiology, functional anatomy, and diagnosis. Am J Sports Med. 2004;32(4):1077-1087.

39. Reynen PD, Clancy WG Jr. Cervical spine injury, hockey helmets, and face masks. Am J Sports Med. 1994;22(2):167-170.

40. Tator CH, Provvidenza C, Cassidy JD. Update and overview of spinal injuries in Canadian ice hockey, 1943 to 2011: the continuing need for injury prevention and education. Clin J Sport Med. 2016;26(3):232-238.

41. Tator CH, Edmonds VE, Lapczak L, Tator IB. Spinal injuries in ice hockey players, 1966-1987. Can J Surg. 1991;34(1):63-69.

42. Laprade RF, Schnetzler KA, Broxterman RJ, Wentorf F, Gilbert TJ. Cervical spine alignment in the immobilized ice hockey player. A computed tomographic analysis of the effects of helmet removal. Am J Sports Med. 2000;28(6):800-803.

43. Metz CM, Kuhn JE, Greenfield ML. Cervical spine alignment in immobilized hockey players: radiographic analysis with and without helmets and shoulder pads. Clin J Sport Med. 1998;8(2):92-95.

44. National Athletic Trainers’ Association. Appropriate prehospital management of the spine-injured athlete: updated from 1998 document. http://www.nata.org/sites/default/files/Executive-Summary-Spine-Injury-updated.pdf. Updated August 5, 2015. Accessed April 6, 2017.

45. Del Rossi G, Heffernan TP, Horodyski M, Rechtine GR. The effectiveness of extrication collars tested during the execution of spine-board transfer techniques. Spine J. 2004;4(6):619-623.

46. Morganti C, Sweeney CA, Albanese SA, Burak C, Hosea T, Connolly PJ. Return to play after cervical spine injury. Spine. 2001;26(10):1131-1136.

47. Huang P, Anissipour A, McGee W, Lemak L. Return-to-play recommendations after cervical, thoracic, and lumbar spine injuries: a comprehensive review. Sports Health. 2016;8(1):19-25.

48. Shindle MK, Marx RG, Kelly BT, Bisson L, Burke CJ 3rd. Hockey injuries: a pediatric sport update. Curr Opin Pediatr. 2010;22(1):54-60.

49. Molsa J, Kujala U, Myllynen P, Torstila I, Airaksinen O. Injuries to the upper extremity in ice hockey: analysis of a series of 760 injuries. Am J Sports Med. 2003;31(5):751-757.

50. Dwyer T, Petrera M, Bleakney R, Theodoropoulos JS. Shoulder instability in ice hockey players: incidence, mechanism, and MRI findings. Clin Sports Med. 2013;32(4):803-813.

51. LaPrade RF, Wijdicks CA, Griffith CJ. Division I intercollegiate ice hockey team coverage. Br J Sports Med. 2009;43(13):1000-1005.

52. Willimon SC, Gaskill TR, Millett PJ. Acromioclavicular joint injuries: anatomy, diagnosis, and treatment. Phys Sportsmed. 2011;39(1):116-122.

53. Martetschlager F, Horan MP, Warth RJ, Millett PJ. Complications after anatomic fixation and reconstruction of the coracoclavicular ligaments. Am J Sports Med. 2013;41(12):2896-2903.

54. Carofino BC, Mazzocca AD. The anatomic coracoclavicular ligament reconstruction: surgical technique and indications. J Shoulder Elbow Surg. 2010;19(2 suppl):37-46.

55. Laprade RF, Surowiec RK, Sochanska AN, et al. Epidemiology, identification, treatment and return to play of musculoskeletal-based ice hockey injuries. Br J Sports Med. 2014;48(1):4-10.

56. Canadian Orthopaedic Trauma Society. Nonoperative treatment compared with plate fixation of displaced midshaft clavicular fractures. A multicenter, randomized clinical trial. J Bone Joint Surg Am. 2007;89(1):1-10.

57. Lee JT, Nasreddine AY, Black EM, Bae DS, Kocher MS. Posterior sternoclavicular joint injuries in skeletally immature patients. J Pediatr Orthop. 2014;34(4):369-375.

58. Hovelius L. Shoulder dislocation in Swedish ice hockey players. Am J Sports Med. 1978;6(6):373-377.

59. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433.

60. Mazzocca AD, Brown FM Jr, Carreira DS, Hayden J, Romeo AA. Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med. 2005;33(1):52-60.

61. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.

62. Cho NS, Hwang JC, Rhee YG. Arthroscopic stabilization in anterior shoulder instability: collision athletes versus noncollision athletes. Arthroscopy. 2006;22(9):947-953.

63. Griffin JW, Brockmeier SF. Shoulder instability with concomitant bone loss in the athlete. Orthop Clin North Am. 2015;46(1):89-103.

64. Cohen SB, Towers JD, Bradley JP. Rotator cuff contusions of the shoulder in professional football players: epidemiology and magnetic resonance imaging findings. Am J Sports Med. 2007;35(3):442-447.

65. Lorentzon R, Wedrèn H, Pietilä T. Incidence, nature, and causes of ice hockey injuries. A three-year prospective study of a Swedish elite ice hockey team. Am J Sports Med. 1988;16(4):392-396.

66. Stuart MJ, Smith A. Injuries in Junior A ice hockey. A three-year prospective study. Am J Sports Med. 1995;23(4):458-461.

67. Voaklander DC, Saunders LD, Quinney HA, Macnab RB. Epidemiology of recreational and old-timer ice hockey injuries. Clin J Sport Med. 1996;6(1):15-21.

68. Mölsä J, Airaksinen O, Näsman O, Torstila I. Ice hockey injuries in Finland. A prospective epidemiologic study. Am J Sports Med. 1997;25(4):495-499.

69. Ferrara MS, Schurr KT. Intercollegiate ice hockey injuries: a casual analysis. Clin J Sport Med. 1999;9(1):30-33.

70. Pinto M, Kuhn JE, Greenfield ML, Hawkins RJ. Prospective analysis of ice hockey injuries at the Junior A level over the course of one season. Clin J Sport Med. 1999;9(2):70-74.

71. Emery CA, Meeuwisse WH. Injury rates, risk factors, and mechanisms of injury in minor hockey. Am J Sports Med. 2006;34(12):1960-1969.

72. Kuzuhara K, Shimamoto H, Mase Y. Ice hockey injuries in a Japanese elite team: a 3-year prospective study. J Athl Train. 2009;44(2):208-214.

73. Rishiraj N, Lloyd-Smith R, Lorenz T, Niven B, Michel M. University men’s ice hockey: rates and risk of injuries over 6-years. J Sports Med Phys Fitness. 2009;49(2):159-166.

74. Tuominen M, Stuart MJ, Aubry M, Kannus P, Parkkari J. Injuries in men’s international ice hockey: a 7-year study of the International Ice Hockey Federation Adult World Championship Tournaments and Olympic Winter Games. Br J Sports Med. 2015;49(1):30-36.

75. Heckman JD, Bucholz RW. In: Rockwood CA, Green DP, Heckman JD, Bucholz RW, eds. Rockwood and Green’s Fractures in Adults, Volume 1. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.

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Subscapularis Tenotomy Versus Lesser Tuberosity Osteotomy for Total Shoulder Arthroplasty: A Systematic Review

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Subscapularis Tenotomy Versus Lesser Tuberosity Osteotomy for Total Shoulder Arthroplasty: A Systematic Review

Take-Home Points

  • According to the orthopedic literature, ST and LTO for a TSA produce excellent clinical outcomes, and technique selection should be based on surgeon discretion and expertise.
  • Compared with the LTO approach, the ST approach produced significantly more forward elevation improvement and trended toward more external rotation and abduction and fewer revisions.
  • ST and LTO approaches for a TSA result in similar Constant scores, pain scores, radiographic outcomes, and complication rates.

During total shoulder arthroplasty (TSA) exposure, the subscapularis muscle must be mobilized; its repair is crucial to the stability of the arthroplasty. The subscapularis is the largest rotator cuff muscle and has a contractile force equal to that of the other 3 muscles combined.1,2 Traditionally it is mobilized with a tenotomy just medial to the tendon’s insertion onto the lesser tuberosity. Over the past 15 years, however, numerous authors have reported dysfunction after subscapularis tenotomy (ST). In 2003, Miller and colleagues3 reported that, at 2-year follow-up, almost 70% of patients had abnormal belly-press and liftoff tests, surrogate markers of subscapularis function. Other authors have found increased rates of anterior instability after subscapularis rupture.4,5

In 2005, Gerber and colleagues6 introduced a technique for circumventing surgical division of the subscapularis. They described a lesser tuberosity osteotomy (LTO), in which the subscapularis tendon is detached with a bone fragment 5 mm to 10 mm in thickness and 3 cm to 4 cm in length. This approach was based on the premise that bone-to-bone healing is more reliable than tendon-to-tendon healing. Initial studies reported successful osteotomy healing, improved clinical outcome scores, and fewer abnormalities with belly-press and liftoff tests.2,6 More recent literature, however, has questioned the necessity of LTO.2,4,7-9We performed a systematic review to evaluate the literature, describe ST and LTO, and summarize the radiographic and clinical outcomes of both techniques. We hypothesized there would be no significant clinical differences between these approaches.

Methods

Search Strategy and Study Selection

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we systematically reviewed the literature.10 Searches were completed in September 2014 using the PubMed Medline database and the Cochrane Central Register of Clinical Trials. Two reviewers (Dr. Louie, Dr. Levy) independently performed the search and assessed eligibility of all relevant studies based on predetermined inclusion criteria. Disagreements between reviewers were resolved by discussion. Key word selection was designed to capture all English-language studies with clinical and/or radiographic outcomes and level I to IV evidence. We used an electronic search algorithm with key words and a series of NOT phrases to match certain exclusion criteria:

(((((((((((((((((((((((((((((((((((((total[Text Word]) AND shoulder[Title]) AND arthroplasty[Title] AND (English[lang]))) NOT reverse[Title/Abstract]) NOT hemiarthroplasty[Title]) NOT nonoperative[Title]) NOT nonsurgical[Title] AND (English[lang]))) NOT rheumatoid[Title/Abstract]) NOT inflammatory[Title/Abstract]) NOT elbow[Title/Abstract]) NOT wrist[Title/Abstract]) NOT hip[Title/Abstract]) NOT knee[Title/Abstract]) NOT ankle[Title/Abstract] AND (English[lang]))) NOT biomechanic[Title/Abstract]) NOT biomechanics[Title/Abstract]) NOT biomechanical [Title/Abstract]) NOT cadaveric[Title/Abstract]) NOT revision[Title]) NOT resurfacing[Title/Abstract]) NOT surface[Title/Abstract]) NOT interphalangeal[Title/Abstract] AND (English[lang]))) NOT radiostereometric[Title/Abstract] AND (English[lang]))) NOT cmc[Title/Abstract]) NOT carpometacarpal[Title/Abstract]) NOT cervical[Title/Abstract]) NOT histology[Title/Abstract]) NOT histological[Title/Abstract]) NOT collagen[Title/Abstract] AND (English[lang]))) NOT kinematic[Title/Abstract]) NOT kinematics[Title/Abstract] AND (English[lang]))) NOT vitro[Title/Abstract] AND (English[lang]))) NOT inverted[Title/Abstract]) NOT grammont[Title/Abstract]) NOT arthrodesis[Title/Abstract]) NOT fusion[Title/Abstract]) NOT reverse[Title/Abstract] AND (English[lang]))

Study exclusion criteria consisted of cadaveric, biomechanical, histologic, and kinematic results as well as analyses of nonoperative management, hemiarthroplasty, or reverse TSA. Studies were excluded if they did not report clinical and/or radiographic data. Minimum mean follow-up was 2 years. To discount the effect of other TSA technical innovations, we evaluated the same period for the 2 surgical approaches. The first study with clinical outcomes after LTO was published in early 2005,6 so all studies published before 2005 were excluded.

We reviewed all references within the studies included by the initial search algorithm: randomized control trials, retrospective and prospective cohort designs, case series, and treatment studies. Technical notes, review papers, letters to the editor, and level V evidence reviews were excluded. To avoid counting patients twice, we compared each study’s authors and data collection period with those of the other studies. If there was overlap in authorship, period, and place, only the study with the longer follow-up or more comprehensive data was included. All trials comparing ST and LTO were included. If the authors of a TSA study did not describe the approach used, that study was excluded from our review.

Data Extraction

We collected details of study design, sample size, and patient demographics (sex, age, hand dominance, primary diagnosis). We also abstracted surgical factors about the glenoid component (cemented vs uncemented; pegged vs keeled; all-polyethylene vs metal-backed) and the humeral component (cemented vs press-fit; stemmed vs stemless). Clinical outcomes included pain scores, functional scores, number of revisions, range of motion (ROM), and subscapularis-specific tests (eg, belly-press, liftoff). As pain scales varied between studies, all values were converted to a 10-point scoring scale (0 = no pain; 10 = maximum pain) for comparisons. Numerous functional outcome scores were reported, but the Constant score was the only one consistently used across studies, making it a good choice for comparisons. One study used Penn Shoulder Scores (PSSs) and directly compared ST and LTO groups, so its data were included. In addition, radiographic data were compiled: radiolucencies around the humeral stem and glenoid component, humeral head subluxation/migration, and osteotomy healing. The only consistent radiographic parameter available for comparisons between groups was the presence of radiolucencies.

 

 

The Modified Coleman Methodology Score (MCMS), described by Cowan and colleagues,11 was used to evaluate the methodologic quality of each study. The MCMS is a 15-item instrument that has been used to assess both randomized and nonrandomized trials.12,13 It has a scaled score ranging from 0 to 100 (85-100, excellent; 70-84, good; 55-69, fair; <55, poor). Study quality was not factored into the data synthesis analysis.

Statistical Analysis

Data are reported as weighted means and standard deviations. A mean was calculated for each study reporting on a respective data point and was then weighed according to the study sample size. The result was that the nonweighted means from studies with smaller samples did not carry as much weight as those from studies with larger samples. Student t tests and 2-way analysis of variance were used to compare the ST and LTO groups and assess differences over time (SPSS Version 18; IBM). An α of 0.05 was set as statistically significant.

Results

Twenty studies (1420 shoulders, 1392 patients) were included in the final dataset (Figure).2,6,8,14-30 

Figure.
Table 1 lists the demographic characteristics of included patients. Of the 20 studies, 12 reported level IV evidence, 6 reported level III, 1 reported level II, and 1 reported level I. Mean (SD) MCMS was 51.9 (11.2) for ST studies and 46.3 (8.1) for LTO studies.

The youngest patients in the ST and LTO groups were 22 years and 19 years of age, respectively.

Table 1.
The oldest patient in each group was 92 years of age. On average, the ST study populations (mean age, 66.6 years; SD, 2.0 years) were older (P = .04) than the LTO populations (mean age, 62.1 years; SD, 4.2 years). The ST group had a higher percentage of patients with osteoarthritis (P = .03) and fewer patients with posttraumatic arthritis (P = .04). There were no significant differences in sex, shoulder side, or shoulder dominance between the 2 groups.

Table 2 lists the details regarding the surgical components. For glenoid components, the ST and LTO groups’ fixation types and material used were not significantly different.
Table 2.
There was a significant (P < .01) difference in use of pegged (vs keeled) glenoid components (all LTO components were pegged). There was also a significant (P = .04) difference in use of cement for humeral components (the ST group had a larger percentage of cemented humeral components). There were no other significant differences in components between the groups. When subgroup analysis was applied to keeled glenoid components and uncemented humeral components in the ST study populations, there were no significant changes in the radiographic or clinical trends.

Table 3 lists the clinical and radiographic outcomes most consistently reported in the literature. Physical examination data were reported in 18 ST populations8,14-16,21-30 and 11 LTO populations.2,6,14-20
Table 3.
Mean (SD) forward elevation improvements were significantly (P < .01) larger for the ST group, +50.9° (17.5°), than for the LTO group, +31.3° (0.9°). There were no significant differences in preoperative/postoperative shoulder external rotation or abduction. In a common method of testing internal rotation, the patient is asked to internally rotate the surgical arm as high as possible behind the back. Internal rotation improved from L4–S1 (before surgery) to T5–T12 (after surgery) in the ST group8,16,24,26,28,29 and from S1 to T7–T12 in the LTO group.16,31 There were isolated improvements in other subscapularis-specific tests, such as belly-press resistance (lb),14 belly-press force (N),15 bear hug resistance (lb),14,23 liftoff,2,8,16 and ability to tuck in one’s shirt,2,16,23 but data were insufficient for comparisons between the 2 groups.

Constant scores were reported in 4 ST studies14,22,24,27 and 3 LTO studies14,17,18 (Table 3). There was no significant difference (P = .37) in post-TSA Constant score improvement between the 2 groups. In the one study that performed direct comparisons, PSS improved on average from 29 to 81 in the ST group and from 29 to 92 in the LTO group.15 Several ST studies reported improved scores on various indices: WOOS (Western Ontario Osteoarthritis of the Shoulder), ASES (American Shoulder and Elbow Surgeons), SST (Simple Shoulder Test), DASH (Disabilities of the Arm, Shoulder, and Hand), SF-12 (Short Form 12-Item Health Survey), MACTAR (McMaster Toronto Arthritis Patient Preference Disability Questionnaire), and Neer shoulder impingement test.8,14,15,21,23-25,27-30 However, these outcomes were not reported in LTO cohorts for comparison. Similarly, 2 LTO cohorts reported improvements in SSV (subjective shoulder value) scores, but this measure was not used in the ST cohorts.6,17 Five ST studies recorded patients’ subjective satisfaction: 58% of patients indicated an excellent outcome, 35% a satisfactory outcome, and 7% a less than satisfactory outcome.21,23,25,26,29 Only 1 LTO study reported patient satisfaction: 69% excellent, 31% satisfactory, 0% dissatisfied.17

Complications were reported in 16 ST studies8,15,21-30 and 6 LTO studies.15,17-19 There were 117 complications (17.8%) and 58 revisions (10.0%) in the ST group and 52 complications (17.2%) and 49 revisions (16.2%) in the LTO group. In the ST group, aseptic loosening (6.2%) was the most common complication, followed by subscapularis tear or attenuation (5.2%), dislocation (2.1%), and deep infection (0.5%). In the LTO group, aseptic loosening was again the most common (9.0%), followed by dislocation (4.0%), subscapularis tear or attenuation (2.2%), and deep infection (0.7%). There were no significant differences in the incidence of individual complications between groups. The difference in revision rates was not statistically significant (P = .31).

Radiolucency data were reported in 12 ST studies19,21-26,28,30 and 2 LTO studies.17,18 There were no discussions of humeral component radiolucencies in the LTO studies. At final follow-up, radiolucencies of the glenoid component were detected in 42.3% of patients in the ST group and 40.7% of patients in the LTO group (P = .76).

 

 

Discussion

Our goal in this systematic review was to analyze outcomes associated with ST and LTO in a heterogenous TSA population. We hypothesized TSA with ST or LTO would produce similar clinical and radiographic outcomes. There were no significant differences in Constant scores, pain scores, radiolucencies, or complications between the 2 groups. The ST group showed trends toward wider ROM improvements and fewer revisions, but only the change in forward elevation was significant. The components used in the 2 groups were similar with the exception of a lack of keeled glenoids and cemented humeral stems in the LTO group; data stratification controlling for these differences revealed no change in outcomes.

The optimal method of subscapularis mobilization for TSA remains a source of debate. Jackson and colleagues23 found significant improvements in Neer and DASH scores after ST. However, 7 of 15 patients ruptured the subscapularis after 6 months and had significantly lower DASH scores. In 2005, Gerber and colleagues6 first described the LTO technique as an alternative to ST. After a mean of 39 months, 89% of their patients had a negative belly-press test, and 75% had a normal liftoff test. Radiographic evaluation revealed that the osteotomized fragment had healed in an anatomical position in all shoulders. In a large case series, Small and colleagues20 used radiographs and computed tomography to further investigate LTO healing rates and found that 89% of patients had bony union by 6 months and that smoking was a significant risk factor for nonunion.

Biomechanical studies comparing ST and LTO approaches have shown mixed results. Ponce and colleagues2 found decreased cyclic displacement and increased maximum load to failure with LTO, but Giuseffi and colleagues32 showed less cyclic displacement with ST and no difference in load to failure. Others authors have found no significant differences in stiffness or maximum load to failure.33 Van den Berghe and colleagues7 reported a higher failure rate in bone-to-bone repairs compared with tendon-to-tendon constructs. Moreover, they found that suture cut-out through bone tunnels is the primary mode of LTO failure, so many LTO surgeons now pass sutures around the humeral stem instead.

Three TSA studies directly compared ST and LTO approaches. Buckley and colleagues14 analyzed 60 TSAs and found no significant differences in WOOS, DASH, or Constant scores between groups. The authors described an ST subgroup with subscapularis attenuation on ultrasound but did not report the group as having any inferior functional outcome. Scalise and colleagues15 showed improved strength and PSSs in both groups after 2 years. However, the LTO group had a lower rate of subscapularis tears and significantly higher PSSs. Finally, Jandhyala and colleagues16 reported more favorable outcomes with LTO, which trended toward wider ROM and significantly higher belly-press test grades. Lapner and colleagues34 conducted a randomized, controlled trial (often referenced) and found no significant differences between the 2 groups in terms of strength or functional outcome at 2-year follow-up. Their study, however, included hemiarthroplasties and did not substratify the TSA population, so we did not include it in our review.

Our systematic review found significantly more forward elevation improvement for the ST group than the LTO group, which may suggest improved ROM with a soft-tissue approach than a bony approach. At the same time, the ST group trended toward better passive external rotation relative to the LTO group. This trend indicates fewer constraints to external rotation in the ST group, possibly attributable to a more attenuated subscapularis after tenotomy. Subscapularis tear or attenuation was more commonly reported in the ST group than in the LTO group, though not significantly so. This may indicate that more ST studies than LTO studies specially emphasized postoperative subscapularis function, but these data also highlight some authors’ concerns regarding subscapularis dysfunction after tenotomy.6,15,16The study populations’ complication rates were similar, just over 17%. The LTO group trended toward a higher revision rate, but it was not statistically significant. The LTO group also had significantly fewer patients with osteoarthritis and more patients with posttraumatic arthritis, so this group may have had more complex patients predisposed to a higher likelihood of revision surgery. Revisions were most commonly performed for aseptic loosening; theoretically, if osteotomies heal less effectively than tenotomies, the LTO approach could produce component instability and aseptic loosening. However, no prior studies or other clinical findings from this review suggest LTO predisposes to aseptic loosening. Overall, the uneven revision rates represent a clinical concern that should be monitored as larger samples of patients undergo ST and LTO procedures.

Glenoid radiolucencies were the only radiographic parameter consistently reported in the included studies. Twelve ST studies had radiolucency data—compared with only 2 LTO studies. Thus, our ability to compare radiographic outcomes was limited. Our data revealed similar rates of glenoid radiolucencies between the 2 approaches. The clinical relevance of radiolucencies is questioned by some authors, and, indeed, Razmjou and colleagues25 found no correlation of radiolucencies with patient satisfaction. Nevertheless, early presence of radiolucencies may raise concerns about progressive loss of fixation,35,36 so this should be monitored.

Limitations of this systematic review reflect the studies analyzed. We minimized selection bias by including level I to IV evidence, but most studies were level IV, and only 1 was level I. As such, there was a relative paucity of consistent clinical and radiographic data. For instance, although many ST studies reported patient satisfaction as an outcomes measure, only 1 LTO study commented on it. Perhaps the relative novelty of the LTO approach has prompted some authors to focus more on technical details and less on reporting a variety of outcome measures. As mentioned earlier, the significance of radiolucency data is controversial, and determination of their presence or absence depends on the observer. A radiolucency found in one study may not qualify as one in a study that uses different criteria. However, lucency data were the most frequently and reliably reported radiographic parameter, so we deemed it the most appropriate method for comparing radiographic outcomes. Finally, the baseline differences in diagnosis between the ST and LTO groups complicated comparisons. We stratified the groups by component design because use of keeled or pegged implants or humeral cemented or press-fit stems was usually a uniform feature of each study—enabling removal of certain studies for data stratification. However, we were unable to stratify by original diagnosis because these groups were not stratified within the individual studies.

 

 

Conclusion

Our systematic review found similar Constant scores, pain scores, radiographic outcomes, and complication rates for the ST and LTO approaches. Compared with the LTO approach, the ST approach produced significantly more forward elevation improvement and trended toward more external rotation and abduction and fewer revisions. Although not definitive, these data suggest the ST approach may provide more stability over the long term, but additional comprehensive studies are needed to increase the sample size and the power of the trends elucidated in this review. According to the orthopedic literature, both techniques produce excellent clinical outcomes, and technique selection should be based on surgeon discretion and expertise.

Am J Orthop. 2017;46(2):E131-E138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

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2. Ponce BA, Ahluwalia RS, Mazzocca AD, Gobezie RG, Warner JJ, Millett PJ. Biomechanical and clinical evaluation of a novel lesser tuberosity repair technique in total shoulder arthroplasty. J Bone Joint Surg Am. 2005;87(suppl 2):1-8.

3. Miller SL, Hazrati Y, Klepps S, Chiang A, Flatow EL. Loss of subscapularis function after total shoulder replacement: a seldom recognized problem. J Shoulder Elbow Surg. 2003;12(1):29-34.

4. Gerber A, Ghalambor N, Warner JJ. Instability of shoulder arthroplasty: balancing mobility and stability. Orthop Clin North Am. 2001;32(4):661-670, ix.

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6. Gerber C, Yian EH, Pfirrmann CA, Zumstein MA, Werner CM. Subscapularis muscle function and structure after total shoulder replacement with lesser tuberosity osteotomy and repair. J Bone Joint Surg Am. 2005;87(8):1739-1745.

7. Van den Berghe GR, Nguyen B, Patil S, et al. A biomechanical evaluation of three surgical techniques for subscapularis repair. J Shoulder Elbow Surg. 2008;17(1):156-161.

8. Caplan JL, Whitfield B, Neviaser RJ. Subscapularis function after primary tendon to tendon repair in patients after replacement arthroplasty of the shoulder. J Shoulder Elbow Surg. 2009;18(2):193-196.

9. Armstrong A, Lashgari C, Teefey S, Menendez J, Yamaguchi K, Galatz LM. Ultrasound evaluation and clinical correlation of subscapularis repair after total shoulder arthroplasty. J Shoulder Elbow Surg. 2006;15(5):541-548.

10. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred Reporting Items for Systematic Reviews and Meta-Analyses: the PRISMA statement. Int J Surg. 2010;8(5):336-341.

11. Cowan J, Lozano-Calderón S, Ring D. Quality of prospective controlled randomized trials. Analysis of trials of treatment for lateral epicondylitis as an example. J Bone Joint Surg Am. 2007;89(8):1693-1699.

12. Harris JD, Siston RA, Pan X, Flanigan DC. Autologous chondrocyte implantation: a systematic review. J Bone Joint Surg Am. 2010;92(12):2220-2233.

13. Harris JD, Siston RA, Brophy RH, Lattermann C, Carey JL, Flanigan DC. Failures, re-operations, and complications after autologous chondrocyte implantation—a systematic review. Osteoarthritis Cartilage. 2011;19(7):779-791.

14. Buckley T, Miller R, Nicandri G, Lewis R, Voloshin I. Analysis of subscapularis integrity and function after lesser tuberosity osteotomy versus subscapularis tenotomy in total shoulder arthroplasty using ultrasound and validated clinical outcome measures. J Shoulder Elbow Surg. 2014;23(9):1309-1317.

15. Scalise JJ, Ciccone J, Iannotti JP. Clinical, radiographic, and ultrasonographic comparison of subscapularis tenotomy and lesser tuberosity osteotomy for total shoulder arthroplasty. J Bone Joint Surg Am. 2010;92(7):1627-1634.

16. Jandhyala S, Unnithan A, Hughes S, Hong T. Subscapularis tenotomy versus lesser tuberosity osteotomy during total shoulder replacement: a comparison of patient outcomes. J Shoulder Elbow Surg. 2011;20(7):1102-1107.

17. Fucentese SF, Costouros JG, Kühnel SP, Gerber C. Total shoulder arthroplasty with an uncemented soft-metal-backed glenoid component. J Shoulder Elbow Surg. 2010;19(4):624-631.

18. Clement ND, Duckworth AD, Colling RC, Stirrat AN. An uncemented metal-backed glenoid component in total shoulder arthroplasty for osteoarthritis: factors affecting survival and outcome. J Orthop Sci. 2013;18(1):22-28.

19. Rosenberg N, Neumann L, Modi A, Mersich IJ, Wallace AW. Improvements in survival of the uncemented Nottingham Total Shoulder prosthesis: a prospective comparative study. BMC Musculoskelet Disord. 2007;8(1):76.

20. Small KM, Siegel EJ, Miller LR, Higgins LD. Imaging characteristics of lesser tuberosity osteotomy after total shoulder replacement: a study of 220 patients. J Shoulder Elbow Surg. 2014;23(9):1318-1326.

21. Mileti J, Sperling JW, Cofield RH, Harrington JR, Hoskin TL. Monoblock and modular total shoulder arthroplasty for osteoarthritis. J Bone Joint Surg Br. 2005;87(4):496-500.

22. Merolla G, Paladini P, Campi F, Porcellini G. Efficacy of anatomical prostheses in primary glenohumeral osteoarthritis. Chir Organi Mov. 2008;91(2):109-115.

23. Jackson JD, Cil A, Smith J, Steinmann SP. Integrity and function of the subscapularis after total shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(7):1085-1090.

24. Jost PW, Dines JS, Griffith MH, Angel M, Altchek DW, Dines DM. Total shoulder arthroplasty utilizing mini-stem humeral components: technique and short-term results. HSS J. 2011;7(3):213-217.

25. Razmjou H, Holtby R, Christakis M, Axelrod T, Richards R. Impact of prosthetic design on clinical and radiologic outcomes of total shoulder arthroplasty: a prospective study. J Shoulder Elbow Surg. 2013;22(2):206-214.

26. Raiss P, Schmitt M, Bruckner T, et al. Results of cemented total shoulder replacement with a minimum follow-up of ten years. J Bone Joint Surg Am. 2012;94(23):e1711-1710.

27. Litchfied RB, McKee MD, Balyk R, et al. Cemented versus uncemented fixation of humeral components in total shoulder arthroplasty for osteoarthritis of the shoulder: a prospective, randomized, double-blind clinical trial—a JOINTs Canada Project. J Shoulder Elbow Surg. 2011;20(4):529-536.

28. Martin SD, Zurakowski D, Thornhill TS. Uncemented glenoid component in total shoulder arthroplasty. Survivorship and outcomes. J Bone Joint Surg Am. 2005;87(6):1284-1292.

29. Taunton MJ, McIntosh AL, Sperling JW, Cofield RH. Total shoulder arthroplasty with a metal-backed, bone-ingrowth glenoid component. Medium to long-term results. J Bone Joint Surg Am. 2008;90(10):2180-2188.

30. Budge MD, Nolan EM, Heisey MH, Baker K, Wiater JM. Results of total shoulder arthroplasty with a monoblock porous tantalum glenoid component: a prospective minimum 2-year follow-up study. J Shoulder Elbow Surg. 2013;22(4):535-541.

31. Gerber C, Costouros JG, Sukthankar A, Fucentese SF. Static posterior humeral head subluxation and total shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(4):505-510.

32. Giuseffi SA, Wongtriratanachai P, Omae H, et al. Biomechanical comparison of lesser tuberosity osteotomy versus subscapularis tenotomy in total shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(8):1087-1095.

 

 

33. Van Thiel GS, Wang VM, Wang FC, et al. Biomechanical similarities among subscapularis repairs after shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(5):657-663.

34. Lapner PL, Sabri E, Rakhra K, Bell K, Athwal GS. Comparison of lesser tuberosity osteotomy to subscapularis peel in shoulder arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2012;94(24):2239-2246.

35. Cofield RH. Total shoulder arthroplasty with the Neer prosthesis. J Bone Joint Surg Am. 1984;66(6):899-906.

36. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.

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Authors’ Disclosure Statement: Dr. Bach reports that he has received research support from Arthrex, Conmed Linvatec, DJ Orthopaedics, Ossur, Slack, Smith & Nephew, and Tornier. Dr. Nicholson reports that he has received publishing royalties and financial or material support from Slack, intellectual property royalties from Innomed, research support and consultant fees from Tornier, and stock or stock options from Zimmer Biomet. Dr. Romeo reports that he
has received research support from Arthrex, DJO Surgical, Ossur, and Smith & Nephew; consultant, presenter, or speaker fees from Arthrex; and royalties or other financial or material support from Arthrex and Slack. The other authors report no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Bach reports that he has received research support from Arthrex, Conmed Linvatec, DJ Orthopaedics, Ossur, Slack, Smith & Nephew, and Tornier. Dr. Nicholson reports that he has received publishing royalties and financial or material support from Slack, intellectual property royalties from Innomed, research support and consultant fees from Tornier, and stock or stock options from Zimmer Biomet. Dr. Romeo reports that he
has received research support from Arthrex, DJO Surgical, Ossur, and Smith & Nephew; consultant, presenter, or speaker fees from Arthrex; and royalties or other financial or material support from Arthrex and Slack. The other authors report no actual or potential conflict of interest in relation to this article.

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Authors’ Disclosure Statement: Dr. Bach reports that he has received research support from Arthrex, Conmed Linvatec, DJ Orthopaedics, Ossur, Slack, Smith & Nephew, and Tornier. Dr. Nicholson reports that he has received publishing royalties and financial or material support from Slack, intellectual property royalties from Innomed, research support and consultant fees from Tornier, and stock or stock options from Zimmer Biomet. Dr. Romeo reports that he
has received research support from Arthrex, DJO Surgical, Ossur, and Smith & Nephew; consultant, presenter, or speaker fees from Arthrex; and royalties or other financial or material support from Arthrex and Slack. The other authors report no actual or potential conflict of interest in relation to this article.

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Take-Home Points

  • According to the orthopedic literature, ST and LTO for a TSA produce excellent clinical outcomes, and technique selection should be based on surgeon discretion and expertise.
  • Compared with the LTO approach, the ST approach produced significantly more forward elevation improvement and trended toward more external rotation and abduction and fewer revisions.
  • ST and LTO approaches for a TSA result in similar Constant scores, pain scores, radiographic outcomes, and complication rates.

During total shoulder arthroplasty (TSA) exposure, the subscapularis muscle must be mobilized; its repair is crucial to the stability of the arthroplasty. The subscapularis is the largest rotator cuff muscle and has a contractile force equal to that of the other 3 muscles combined.1,2 Traditionally it is mobilized with a tenotomy just medial to the tendon’s insertion onto the lesser tuberosity. Over the past 15 years, however, numerous authors have reported dysfunction after subscapularis tenotomy (ST). In 2003, Miller and colleagues3 reported that, at 2-year follow-up, almost 70% of patients had abnormal belly-press and liftoff tests, surrogate markers of subscapularis function. Other authors have found increased rates of anterior instability after subscapularis rupture.4,5

In 2005, Gerber and colleagues6 introduced a technique for circumventing surgical division of the subscapularis. They described a lesser tuberosity osteotomy (LTO), in which the subscapularis tendon is detached with a bone fragment 5 mm to 10 mm in thickness and 3 cm to 4 cm in length. This approach was based on the premise that bone-to-bone healing is more reliable than tendon-to-tendon healing. Initial studies reported successful osteotomy healing, improved clinical outcome scores, and fewer abnormalities with belly-press and liftoff tests.2,6 More recent literature, however, has questioned the necessity of LTO.2,4,7-9We performed a systematic review to evaluate the literature, describe ST and LTO, and summarize the radiographic and clinical outcomes of both techniques. We hypothesized there would be no significant clinical differences between these approaches.

Methods

Search Strategy and Study Selection

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we systematically reviewed the literature.10 Searches were completed in September 2014 using the PubMed Medline database and the Cochrane Central Register of Clinical Trials. Two reviewers (Dr. Louie, Dr. Levy) independently performed the search and assessed eligibility of all relevant studies based on predetermined inclusion criteria. Disagreements between reviewers were resolved by discussion. Key word selection was designed to capture all English-language studies with clinical and/or radiographic outcomes and level I to IV evidence. We used an electronic search algorithm with key words and a series of NOT phrases to match certain exclusion criteria:

(((((((((((((((((((((((((((((((((((((total[Text Word]) AND shoulder[Title]) AND arthroplasty[Title] AND (English[lang]))) NOT reverse[Title/Abstract]) NOT hemiarthroplasty[Title]) NOT nonoperative[Title]) NOT nonsurgical[Title] AND (English[lang]))) NOT rheumatoid[Title/Abstract]) NOT inflammatory[Title/Abstract]) NOT elbow[Title/Abstract]) NOT wrist[Title/Abstract]) NOT hip[Title/Abstract]) NOT knee[Title/Abstract]) NOT ankle[Title/Abstract] AND (English[lang]))) NOT biomechanic[Title/Abstract]) NOT biomechanics[Title/Abstract]) NOT biomechanical [Title/Abstract]) NOT cadaveric[Title/Abstract]) NOT revision[Title]) NOT resurfacing[Title/Abstract]) NOT surface[Title/Abstract]) NOT interphalangeal[Title/Abstract] AND (English[lang]))) NOT radiostereometric[Title/Abstract] AND (English[lang]))) NOT cmc[Title/Abstract]) NOT carpometacarpal[Title/Abstract]) NOT cervical[Title/Abstract]) NOT histology[Title/Abstract]) NOT histological[Title/Abstract]) NOT collagen[Title/Abstract] AND (English[lang]))) NOT kinematic[Title/Abstract]) NOT kinematics[Title/Abstract] AND (English[lang]))) NOT vitro[Title/Abstract] AND (English[lang]))) NOT inverted[Title/Abstract]) NOT grammont[Title/Abstract]) NOT arthrodesis[Title/Abstract]) NOT fusion[Title/Abstract]) NOT reverse[Title/Abstract] AND (English[lang]))

Study exclusion criteria consisted of cadaveric, biomechanical, histologic, and kinematic results as well as analyses of nonoperative management, hemiarthroplasty, or reverse TSA. Studies were excluded if they did not report clinical and/or radiographic data. Minimum mean follow-up was 2 years. To discount the effect of other TSA technical innovations, we evaluated the same period for the 2 surgical approaches. The first study with clinical outcomes after LTO was published in early 2005,6 so all studies published before 2005 were excluded.

We reviewed all references within the studies included by the initial search algorithm: randomized control trials, retrospective and prospective cohort designs, case series, and treatment studies. Technical notes, review papers, letters to the editor, and level V evidence reviews were excluded. To avoid counting patients twice, we compared each study’s authors and data collection period with those of the other studies. If there was overlap in authorship, period, and place, only the study with the longer follow-up or more comprehensive data was included. All trials comparing ST and LTO were included. If the authors of a TSA study did not describe the approach used, that study was excluded from our review.

Data Extraction

We collected details of study design, sample size, and patient demographics (sex, age, hand dominance, primary diagnosis). We also abstracted surgical factors about the glenoid component (cemented vs uncemented; pegged vs keeled; all-polyethylene vs metal-backed) and the humeral component (cemented vs press-fit; stemmed vs stemless). Clinical outcomes included pain scores, functional scores, number of revisions, range of motion (ROM), and subscapularis-specific tests (eg, belly-press, liftoff). As pain scales varied between studies, all values were converted to a 10-point scoring scale (0 = no pain; 10 = maximum pain) for comparisons. Numerous functional outcome scores were reported, but the Constant score was the only one consistently used across studies, making it a good choice for comparisons. One study used Penn Shoulder Scores (PSSs) and directly compared ST and LTO groups, so its data were included. In addition, radiographic data were compiled: radiolucencies around the humeral stem and glenoid component, humeral head subluxation/migration, and osteotomy healing. The only consistent radiographic parameter available for comparisons between groups was the presence of radiolucencies.

 

 

The Modified Coleman Methodology Score (MCMS), described by Cowan and colleagues,11 was used to evaluate the methodologic quality of each study. The MCMS is a 15-item instrument that has been used to assess both randomized and nonrandomized trials.12,13 It has a scaled score ranging from 0 to 100 (85-100, excellent; 70-84, good; 55-69, fair; <55, poor). Study quality was not factored into the data synthesis analysis.

Statistical Analysis

Data are reported as weighted means and standard deviations. A mean was calculated for each study reporting on a respective data point and was then weighed according to the study sample size. The result was that the nonweighted means from studies with smaller samples did not carry as much weight as those from studies with larger samples. Student t tests and 2-way analysis of variance were used to compare the ST and LTO groups and assess differences over time (SPSS Version 18; IBM). An α of 0.05 was set as statistically significant.

Results

Twenty studies (1420 shoulders, 1392 patients) were included in the final dataset (Figure).2,6,8,14-30 

Figure.
Table 1 lists the demographic characteristics of included patients. Of the 20 studies, 12 reported level IV evidence, 6 reported level III, 1 reported level II, and 1 reported level I. Mean (SD) MCMS was 51.9 (11.2) for ST studies and 46.3 (8.1) for LTO studies.

The youngest patients in the ST and LTO groups were 22 years and 19 years of age, respectively.

Table 1.
The oldest patient in each group was 92 years of age. On average, the ST study populations (mean age, 66.6 years; SD, 2.0 years) were older (P = .04) than the LTO populations (mean age, 62.1 years; SD, 4.2 years). The ST group had a higher percentage of patients with osteoarthritis (P = .03) and fewer patients with posttraumatic arthritis (P = .04). There were no significant differences in sex, shoulder side, or shoulder dominance between the 2 groups.

Table 2 lists the details regarding the surgical components. For glenoid components, the ST and LTO groups’ fixation types and material used were not significantly different.
Table 2.
There was a significant (P < .01) difference in use of pegged (vs keeled) glenoid components (all LTO components were pegged). There was also a significant (P = .04) difference in use of cement for humeral components (the ST group had a larger percentage of cemented humeral components). There were no other significant differences in components between the groups. When subgroup analysis was applied to keeled glenoid components and uncemented humeral components in the ST study populations, there were no significant changes in the radiographic or clinical trends.

Table 3 lists the clinical and radiographic outcomes most consistently reported in the literature. Physical examination data were reported in 18 ST populations8,14-16,21-30 and 11 LTO populations.2,6,14-20
Table 3.
Mean (SD) forward elevation improvements were significantly (P < .01) larger for the ST group, +50.9° (17.5°), than for the LTO group, +31.3° (0.9°). There were no significant differences in preoperative/postoperative shoulder external rotation or abduction. In a common method of testing internal rotation, the patient is asked to internally rotate the surgical arm as high as possible behind the back. Internal rotation improved from L4–S1 (before surgery) to T5–T12 (after surgery) in the ST group8,16,24,26,28,29 and from S1 to T7–T12 in the LTO group.16,31 There were isolated improvements in other subscapularis-specific tests, such as belly-press resistance (lb),14 belly-press force (N),15 bear hug resistance (lb),14,23 liftoff,2,8,16 and ability to tuck in one’s shirt,2,16,23 but data were insufficient for comparisons between the 2 groups.

Constant scores were reported in 4 ST studies14,22,24,27 and 3 LTO studies14,17,18 (Table 3). There was no significant difference (P = .37) in post-TSA Constant score improvement between the 2 groups. In the one study that performed direct comparisons, PSS improved on average from 29 to 81 in the ST group and from 29 to 92 in the LTO group.15 Several ST studies reported improved scores on various indices: WOOS (Western Ontario Osteoarthritis of the Shoulder), ASES (American Shoulder and Elbow Surgeons), SST (Simple Shoulder Test), DASH (Disabilities of the Arm, Shoulder, and Hand), SF-12 (Short Form 12-Item Health Survey), MACTAR (McMaster Toronto Arthritis Patient Preference Disability Questionnaire), and Neer shoulder impingement test.8,14,15,21,23-25,27-30 However, these outcomes were not reported in LTO cohorts for comparison. Similarly, 2 LTO cohorts reported improvements in SSV (subjective shoulder value) scores, but this measure was not used in the ST cohorts.6,17 Five ST studies recorded patients’ subjective satisfaction: 58% of patients indicated an excellent outcome, 35% a satisfactory outcome, and 7% a less than satisfactory outcome.21,23,25,26,29 Only 1 LTO study reported patient satisfaction: 69% excellent, 31% satisfactory, 0% dissatisfied.17

Complications were reported in 16 ST studies8,15,21-30 and 6 LTO studies.15,17-19 There were 117 complications (17.8%) and 58 revisions (10.0%) in the ST group and 52 complications (17.2%) and 49 revisions (16.2%) in the LTO group. In the ST group, aseptic loosening (6.2%) was the most common complication, followed by subscapularis tear or attenuation (5.2%), dislocation (2.1%), and deep infection (0.5%). In the LTO group, aseptic loosening was again the most common (9.0%), followed by dislocation (4.0%), subscapularis tear or attenuation (2.2%), and deep infection (0.7%). There were no significant differences in the incidence of individual complications between groups. The difference in revision rates was not statistically significant (P = .31).

Radiolucency data were reported in 12 ST studies19,21-26,28,30 and 2 LTO studies.17,18 There were no discussions of humeral component radiolucencies in the LTO studies. At final follow-up, radiolucencies of the glenoid component were detected in 42.3% of patients in the ST group and 40.7% of patients in the LTO group (P = .76).

 

 

Discussion

Our goal in this systematic review was to analyze outcomes associated with ST and LTO in a heterogenous TSA population. We hypothesized TSA with ST or LTO would produce similar clinical and radiographic outcomes. There were no significant differences in Constant scores, pain scores, radiolucencies, or complications between the 2 groups. The ST group showed trends toward wider ROM improvements and fewer revisions, but only the change in forward elevation was significant. The components used in the 2 groups were similar with the exception of a lack of keeled glenoids and cemented humeral stems in the LTO group; data stratification controlling for these differences revealed no change in outcomes.

The optimal method of subscapularis mobilization for TSA remains a source of debate. Jackson and colleagues23 found significant improvements in Neer and DASH scores after ST. However, 7 of 15 patients ruptured the subscapularis after 6 months and had significantly lower DASH scores. In 2005, Gerber and colleagues6 first described the LTO technique as an alternative to ST. After a mean of 39 months, 89% of their patients had a negative belly-press test, and 75% had a normal liftoff test. Radiographic evaluation revealed that the osteotomized fragment had healed in an anatomical position in all shoulders. In a large case series, Small and colleagues20 used radiographs and computed tomography to further investigate LTO healing rates and found that 89% of patients had bony union by 6 months and that smoking was a significant risk factor for nonunion.

Biomechanical studies comparing ST and LTO approaches have shown mixed results. Ponce and colleagues2 found decreased cyclic displacement and increased maximum load to failure with LTO, but Giuseffi and colleagues32 showed less cyclic displacement with ST and no difference in load to failure. Others authors have found no significant differences in stiffness or maximum load to failure.33 Van den Berghe and colleagues7 reported a higher failure rate in bone-to-bone repairs compared with tendon-to-tendon constructs. Moreover, they found that suture cut-out through bone tunnels is the primary mode of LTO failure, so many LTO surgeons now pass sutures around the humeral stem instead.

Three TSA studies directly compared ST and LTO approaches. Buckley and colleagues14 analyzed 60 TSAs and found no significant differences in WOOS, DASH, or Constant scores between groups. The authors described an ST subgroup with subscapularis attenuation on ultrasound but did not report the group as having any inferior functional outcome. Scalise and colleagues15 showed improved strength and PSSs in both groups after 2 years. However, the LTO group had a lower rate of subscapularis tears and significantly higher PSSs. Finally, Jandhyala and colleagues16 reported more favorable outcomes with LTO, which trended toward wider ROM and significantly higher belly-press test grades. Lapner and colleagues34 conducted a randomized, controlled trial (often referenced) and found no significant differences between the 2 groups in terms of strength or functional outcome at 2-year follow-up. Their study, however, included hemiarthroplasties and did not substratify the TSA population, so we did not include it in our review.

Our systematic review found significantly more forward elevation improvement for the ST group than the LTO group, which may suggest improved ROM with a soft-tissue approach than a bony approach. At the same time, the ST group trended toward better passive external rotation relative to the LTO group. This trend indicates fewer constraints to external rotation in the ST group, possibly attributable to a more attenuated subscapularis after tenotomy. Subscapularis tear or attenuation was more commonly reported in the ST group than in the LTO group, though not significantly so. This may indicate that more ST studies than LTO studies specially emphasized postoperative subscapularis function, but these data also highlight some authors’ concerns regarding subscapularis dysfunction after tenotomy.6,15,16The study populations’ complication rates were similar, just over 17%. The LTO group trended toward a higher revision rate, but it was not statistically significant. The LTO group also had significantly fewer patients with osteoarthritis and more patients with posttraumatic arthritis, so this group may have had more complex patients predisposed to a higher likelihood of revision surgery. Revisions were most commonly performed for aseptic loosening; theoretically, if osteotomies heal less effectively than tenotomies, the LTO approach could produce component instability and aseptic loosening. However, no prior studies or other clinical findings from this review suggest LTO predisposes to aseptic loosening. Overall, the uneven revision rates represent a clinical concern that should be monitored as larger samples of patients undergo ST and LTO procedures.

Glenoid radiolucencies were the only radiographic parameter consistently reported in the included studies. Twelve ST studies had radiolucency data—compared with only 2 LTO studies. Thus, our ability to compare radiographic outcomes was limited. Our data revealed similar rates of glenoid radiolucencies between the 2 approaches. The clinical relevance of radiolucencies is questioned by some authors, and, indeed, Razmjou and colleagues25 found no correlation of radiolucencies with patient satisfaction. Nevertheless, early presence of radiolucencies may raise concerns about progressive loss of fixation,35,36 so this should be monitored.

Limitations of this systematic review reflect the studies analyzed. We minimized selection bias by including level I to IV evidence, but most studies were level IV, and only 1 was level I. As such, there was a relative paucity of consistent clinical and radiographic data. For instance, although many ST studies reported patient satisfaction as an outcomes measure, only 1 LTO study commented on it. Perhaps the relative novelty of the LTO approach has prompted some authors to focus more on technical details and less on reporting a variety of outcome measures. As mentioned earlier, the significance of radiolucency data is controversial, and determination of their presence or absence depends on the observer. A radiolucency found in one study may not qualify as one in a study that uses different criteria. However, lucency data were the most frequently and reliably reported radiographic parameter, so we deemed it the most appropriate method for comparing radiographic outcomes. Finally, the baseline differences in diagnosis between the ST and LTO groups complicated comparisons. We stratified the groups by component design because use of keeled or pegged implants or humeral cemented or press-fit stems was usually a uniform feature of each study—enabling removal of certain studies for data stratification. However, we were unable to stratify by original diagnosis because these groups were not stratified within the individual studies.

 

 

Conclusion

Our systematic review found similar Constant scores, pain scores, radiographic outcomes, and complication rates for the ST and LTO approaches. Compared with the LTO approach, the ST approach produced significantly more forward elevation improvement and trended toward more external rotation and abduction and fewer revisions. Although not definitive, these data suggest the ST approach may provide more stability over the long term, but additional comprehensive studies are needed to increase the sample size and the power of the trends elucidated in this review. According to the orthopedic literature, both techniques produce excellent clinical outcomes, and technique selection should be based on surgeon discretion and expertise.

Am J Orthop. 2017;46(2):E131-E138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • According to the orthopedic literature, ST and LTO for a TSA produce excellent clinical outcomes, and technique selection should be based on surgeon discretion and expertise.
  • Compared with the LTO approach, the ST approach produced significantly more forward elevation improvement and trended toward more external rotation and abduction and fewer revisions.
  • ST and LTO approaches for a TSA result in similar Constant scores, pain scores, radiographic outcomes, and complication rates.

During total shoulder arthroplasty (TSA) exposure, the subscapularis muscle must be mobilized; its repair is crucial to the stability of the arthroplasty. The subscapularis is the largest rotator cuff muscle and has a contractile force equal to that of the other 3 muscles combined.1,2 Traditionally it is mobilized with a tenotomy just medial to the tendon’s insertion onto the lesser tuberosity. Over the past 15 years, however, numerous authors have reported dysfunction after subscapularis tenotomy (ST). In 2003, Miller and colleagues3 reported that, at 2-year follow-up, almost 70% of patients had abnormal belly-press and liftoff tests, surrogate markers of subscapularis function. Other authors have found increased rates of anterior instability after subscapularis rupture.4,5

In 2005, Gerber and colleagues6 introduced a technique for circumventing surgical division of the subscapularis. They described a lesser tuberosity osteotomy (LTO), in which the subscapularis tendon is detached with a bone fragment 5 mm to 10 mm in thickness and 3 cm to 4 cm in length. This approach was based on the premise that bone-to-bone healing is more reliable than tendon-to-tendon healing. Initial studies reported successful osteotomy healing, improved clinical outcome scores, and fewer abnormalities with belly-press and liftoff tests.2,6 More recent literature, however, has questioned the necessity of LTO.2,4,7-9We performed a systematic review to evaluate the literature, describe ST and LTO, and summarize the radiographic and clinical outcomes of both techniques. We hypothesized there would be no significant clinical differences between these approaches.

Methods

Search Strategy and Study Selection

Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we systematically reviewed the literature.10 Searches were completed in September 2014 using the PubMed Medline database and the Cochrane Central Register of Clinical Trials. Two reviewers (Dr. Louie, Dr. Levy) independently performed the search and assessed eligibility of all relevant studies based on predetermined inclusion criteria. Disagreements between reviewers were resolved by discussion. Key word selection was designed to capture all English-language studies with clinical and/or radiographic outcomes and level I to IV evidence. We used an electronic search algorithm with key words and a series of NOT phrases to match certain exclusion criteria:

(((((((((((((((((((((((((((((((((((((total[Text Word]) AND shoulder[Title]) AND arthroplasty[Title] AND (English[lang]))) NOT reverse[Title/Abstract]) NOT hemiarthroplasty[Title]) NOT nonoperative[Title]) NOT nonsurgical[Title] AND (English[lang]))) NOT rheumatoid[Title/Abstract]) NOT inflammatory[Title/Abstract]) NOT elbow[Title/Abstract]) NOT wrist[Title/Abstract]) NOT hip[Title/Abstract]) NOT knee[Title/Abstract]) NOT ankle[Title/Abstract] AND (English[lang]))) NOT biomechanic[Title/Abstract]) NOT biomechanics[Title/Abstract]) NOT biomechanical [Title/Abstract]) NOT cadaveric[Title/Abstract]) NOT revision[Title]) NOT resurfacing[Title/Abstract]) NOT surface[Title/Abstract]) NOT interphalangeal[Title/Abstract] AND (English[lang]))) NOT radiostereometric[Title/Abstract] AND (English[lang]))) NOT cmc[Title/Abstract]) NOT carpometacarpal[Title/Abstract]) NOT cervical[Title/Abstract]) NOT histology[Title/Abstract]) NOT histological[Title/Abstract]) NOT collagen[Title/Abstract] AND (English[lang]))) NOT kinematic[Title/Abstract]) NOT kinematics[Title/Abstract] AND (English[lang]))) NOT vitro[Title/Abstract] AND (English[lang]))) NOT inverted[Title/Abstract]) NOT grammont[Title/Abstract]) NOT arthrodesis[Title/Abstract]) NOT fusion[Title/Abstract]) NOT reverse[Title/Abstract] AND (English[lang]))

Study exclusion criteria consisted of cadaveric, biomechanical, histologic, and kinematic results as well as analyses of nonoperative management, hemiarthroplasty, or reverse TSA. Studies were excluded if they did not report clinical and/or radiographic data. Minimum mean follow-up was 2 years. To discount the effect of other TSA technical innovations, we evaluated the same period for the 2 surgical approaches. The first study with clinical outcomes after LTO was published in early 2005,6 so all studies published before 2005 were excluded.

We reviewed all references within the studies included by the initial search algorithm: randomized control trials, retrospective and prospective cohort designs, case series, and treatment studies. Technical notes, review papers, letters to the editor, and level V evidence reviews were excluded. To avoid counting patients twice, we compared each study’s authors and data collection period with those of the other studies. If there was overlap in authorship, period, and place, only the study with the longer follow-up or more comprehensive data was included. All trials comparing ST and LTO were included. If the authors of a TSA study did not describe the approach used, that study was excluded from our review.

Data Extraction

We collected details of study design, sample size, and patient demographics (sex, age, hand dominance, primary diagnosis). We also abstracted surgical factors about the glenoid component (cemented vs uncemented; pegged vs keeled; all-polyethylene vs metal-backed) and the humeral component (cemented vs press-fit; stemmed vs stemless). Clinical outcomes included pain scores, functional scores, number of revisions, range of motion (ROM), and subscapularis-specific tests (eg, belly-press, liftoff). As pain scales varied between studies, all values were converted to a 10-point scoring scale (0 = no pain; 10 = maximum pain) for comparisons. Numerous functional outcome scores were reported, but the Constant score was the only one consistently used across studies, making it a good choice for comparisons. One study used Penn Shoulder Scores (PSSs) and directly compared ST and LTO groups, so its data were included. In addition, radiographic data were compiled: radiolucencies around the humeral stem and glenoid component, humeral head subluxation/migration, and osteotomy healing. The only consistent radiographic parameter available for comparisons between groups was the presence of radiolucencies.

 

 

The Modified Coleman Methodology Score (MCMS), described by Cowan and colleagues,11 was used to evaluate the methodologic quality of each study. The MCMS is a 15-item instrument that has been used to assess both randomized and nonrandomized trials.12,13 It has a scaled score ranging from 0 to 100 (85-100, excellent; 70-84, good; 55-69, fair; <55, poor). Study quality was not factored into the data synthesis analysis.

Statistical Analysis

Data are reported as weighted means and standard deviations. A mean was calculated for each study reporting on a respective data point and was then weighed according to the study sample size. The result was that the nonweighted means from studies with smaller samples did not carry as much weight as those from studies with larger samples. Student t tests and 2-way analysis of variance were used to compare the ST and LTO groups and assess differences over time (SPSS Version 18; IBM). An α of 0.05 was set as statistically significant.

Results

Twenty studies (1420 shoulders, 1392 patients) were included in the final dataset (Figure).2,6,8,14-30 

Figure.
Table 1 lists the demographic characteristics of included patients. Of the 20 studies, 12 reported level IV evidence, 6 reported level III, 1 reported level II, and 1 reported level I. Mean (SD) MCMS was 51.9 (11.2) for ST studies and 46.3 (8.1) for LTO studies.

The youngest patients in the ST and LTO groups were 22 years and 19 years of age, respectively.

Table 1.
The oldest patient in each group was 92 years of age. On average, the ST study populations (mean age, 66.6 years; SD, 2.0 years) were older (P = .04) than the LTO populations (mean age, 62.1 years; SD, 4.2 years). The ST group had a higher percentage of patients with osteoarthritis (P = .03) and fewer patients with posttraumatic arthritis (P = .04). There were no significant differences in sex, shoulder side, or shoulder dominance between the 2 groups.

Table 2 lists the details regarding the surgical components. For glenoid components, the ST and LTO groups’ fixation types and material used were not significantly different.
Table 2.
There was a significant (P < .01) difference in use of pegged (vs keeled) glenoid components (all LTO components were pegged). There was also a significant (P = .04) difference in use of cement for humeral components (the ST group had a larger percentage of cemented humeral components). There were no other significant differences in components between the groups. When subgroup analysis was applied to keeled glenoid components and uncemented humeral components in the ST study populations, there were no significant changes in the radiographic or clinical trends.

Table 3 lists the clinical and radiographic outcomes most consistently reported in the literature. Physical examination data were reported in 18 ST populations8,14-16,21-30 and 11 LTO populations.2,6,14-20
Table 3.
Mean (SD) forward elevation improvements were significantly (P < .01) larger for the ST group, +50.9° (17.5°), than for the LTO group, +31.3° (0.9°). There were no significant differences in preoperative/postoperative shoulder external rotation or abduction. In a common method of testing internal rotation, the patient is asked to internally rotate the surgical arm as high as possible behind the back. Internal rotation improved from L4–S1 (before surgery) to T5–T12 (after surgery) in the ST group8,16,24,26,28,29 and from S1 to T7–T12 in the LTO group.16,31 There were isolated improvements in other subscapularis-specific tests, such as belly-press resistance (lb),14 belly-press force (N),15 bear hug resistance (lb),14,23 liftoff,2,8,16 and ability to tuck in one’s shirt,2,16,23 but data were insufficient for comparisons between the 2 groups.

Constant scores were reported in 4 ST studies14,22,24,27 and 3 LTO studies14,17,18 (Table 3). There was no significant difference (P = .37) in post-TSA Constant score improvement between the 2 groups. In the one study that performed direct comparisons, PSS improved on average from 29 to 81 in the ST group and from 29 to 92 in the LTO group.15 Several ST studies reported improved scores on various indices: WOOS (Western Ontario Osteoarthritis of the Shoulder), ASES (American Shoulder and Elbow Surgeons), SST (Simple Shoulder Test), DASH (Disabilities of the Arm, Shoulder, and Hand), SF-12 (Short Form 12-Item Health Survey), MACTAR (McMaster Toronto Arthritis Patient Preference Disability Questionnaire), and Neer shoulder impingement test.8,14,15,21,23-25,27-30 However, these outcomes were not reported in LTO cohorts for comparison. Similarly, 2 LTO cohorts reported improvements in SSV (subjective shoulder value) scores, but this measure was not used in the ST cohorts.6,17 Five ST studies recorded patients’ subjective satisfaction: 58% of patients indicated an excellent outcome, 35% a satisfactory outcome, and 7% a less than satisfactory outcome.21,23,25,26,29 Only 1 LTO study reported patient satisfaction: 69% excellent, 31% satisfactory, 0% dissatisfied.17

Complications were reported in 16 ST studies8,15,21-30 and 6 LTO studies.15,17-19 There were 117 complications (17.8%) and 58 revisions (10.0%) in the ST group and 52 complications (17.2%) and 49 revisions (16.2%) in the LTO group. In the ST group, aseptic loosening (6.2%) was the most common complication, followed by subscapularis tear or attenuation (5.2%), dislocation (2.1%), and deep infection (0.5%). In the LTO group, aseptic loosening was again the most common (9.0%), followed by dislocation (4.0%), subscapularis tear or attenuation (2.2%), and deep infection (0.7%). There were no significant differences in the incidence of individual complications between groups. The difference in revision rates was not statistically significant (P = .31).

Radiolucency data were reported in 12 ST studies19,21-26,28,30 and 2 LTO studies.17,18 There were no discussions of humeral component radiolucencies in the LTO studies. At final follow-up, radiolucencies of the glenoid component were detected in 42.3% of patients in the ST group and 40.7% of patients in the LTO group (P = .76).

 

 

Discussion

Our goal in this systematic review was to analyze outcomes associated with ST and LTO in a heterogenous TSA population. We hypothesized TSA with ST or LTO would produce similar clinical and radiographic outcomes. There were no significant differences in Constant scores, pain scores, radiolucencies, or complications between the 2 groups. The ST group showed trends toward wider ROM improvements and fewer revisions, but only the change in forward elevation was significant. The components used in the 2 groups were similar with the exception of a lack of keeled glenoids and cemented humeral stems in the LTO group; data stratification controlling for these differences revealed no change in outcomes.

The optimal method of subscapularis mobilization for TSA remains a source of debate. Jackson and colleagues23 found significant improvements in Neer and DASH scores after ST. However, 7 of 15 patients ruptured the subscapularis after 6 months and had significantly lower DASH scores. In 2005, Gerber and colleagues6 first described the LTO technique as an alternative to ST. After a mean of 39 months, 89% of their patients had a negative belly-press test, and 75% had a normal liftoff test. Radiographic evaluation revealed that the osteotomized fragment had healed in an anatomical position in all shoulders. In a large case series, Small and colleagues20 used radiographs and computed tomography to further investigate LTO healing rates and found that 89% of patients had bony union by 6 months and that smoking was a significant risk factor for nonunion.

Biomechanical studies comparing ST and LTO approaches have shown mixed results. Ponce and colleagues2 found decreased cyclic displacement and increased maximum load to failure with LTO, but Giuseffi and colleagues32 showed less cyclic displacement with ST and no difference in load to failure. Others authors have found no significant differences in stiffness or maximum load to failure.33 Van den Berghe and colleagues7 reported a higher failure rate in bone-to-bone repairs compared with tendon-to-tendon constructs. Moreover, they found that suture cut-out through bone tunnels is the primary mode of LTO failure, so many LTO surgeons now pass sutures around the humeral stem instead.

Three TSA studies directly compared ST and LTO approaches. Buckley and colleagues14 analyzed 60 TSAs and found no significant differences in WOOS, DASH, or Constant scores between groups. The authors described an ST subgroup with subscapularis attenuation on ultrasound but did not report the group as having any inferior functional outcome. Scalise and colleagues15 showed improved strength and PSSs in both groups after 2 years. However, the LTO group had a lower rate of subscapularis tears and significantly higher PSSs. Finally, Jandhyala and colleagues16 reported more favorable outcomes with LTO, which trended toward wider ROM and significantly higher belly-press test grades. Lapner and colleagues34 conducted a randomized, controlled trial (often referenced) and found no significant differences between the 2 groups in terms of strength or functional outcome at 2-year follow-up. Their study, however, included hemiarthroplasties and did not substratify the TSA population, so we did not include it in our review.

Our systematic review found significantly more forward elevation improvement for the ST group than the LTO group, which may suggest improved ROM with a soft-tissue approach than a bony approach. At the same time, the ST group trended toward better passive external rotation relative to the LTO group. This trend indicates fewer constraints to external rotation in the ST group, possibly attributable to a more attenuated subscapularis after tenotomy. Subscapularis tear or attenuation was more commonly reported in the ST group than in the LTO group, though not significantly so. This may indicate that more ST studies than LTO studies specially emphasized postoperative subscapularis function, but these data also highlight some authors’ concerns regarding subscapularis dysfunction after tenotomy.6,15,16The study populations’ complication rates were similar, just over 17%. The LTO group trended toward a higher revision rate, but it was not statistically significant. The LTO group also had significantly fewer patients with osteoarthritis and more patients with posttraumatic arthritis, so this group may have had more complex patients predisposed to a higher likelihood of revision surgery. Revisions were most commonly performed for aseptic loosening; theoretically, if osteotomies heal less effectively than tenotomies, the LTO approach could produce component instability and aseptic loosening. However, no prior studies or other clinical findings from this review suggest LTO predisposes to aseptic loosening. Overall, the uneven revision rates represent a clinical concern that should be monitored as larger samples of patients undergo ST and LTO procedures.

Glenoid radiolucencies were the only radiographic parameter consistently reported in the included studies. Twelve ST studies had radiolucency data—compared with only 2 LTO studies. Thus, our ability to compare radiographic outcomes was limited. Our data revealed similar rates of glenoid radiolucencies between the 2 approaches. The clinical relevance of radiolucencies is questioned by some authors, and, indeed, Razmjou and colleagues25 found no correlation of radiolucencies with patient satisfaction. Nevertheless, early presence of radiolucencies may raise concerns about progressive loss of fixation,35,36 so this should be monitored.

Limitations of this systematic review reflect the studies analyzed. We minimized selection bias by including level I to IV evidence, but most studies were level IV, and only 1 was level I. As such, there was a relative paucity of consistent clinical and radiographic data. For instance, although many ST studies reported patient satisfaction as an outcomes measure, only 1 LTO study commented on it. Perhaps the relative novelty of the LTO approach has prompted some authors to focus more on technical details and less on reporting a variety of outcome measures. As mentioned earlier, the significance of radiolucency data is controversial, and determination of their presence or absence depends on the observer. A radiolucency found in one study may not qualify as one in a study that uses different criteria. However, lucency data were the most frequently and reliably reported radiographic parameter, so we deemed it the most appropriate method for comparing radiographic outcomes. Finally, the baseline differences in diagnosis between the ST and LTO groups complicated comparisons. We stratified the groups by component design because use of keeled or pegged implants or humeral cemented or press-fit stems was usually a uniform feature of each study—enabling removal of certain studies for data stratification. However, we were unable to stratify by original diagnosis because these groups were not stratified within the individual studies.

 

 

Conclusion

Our systematic review found similar Constant scores, pain scores, radiographic outcomes, and complication rates for the ST and LTO approaches. Compared with the LTO approach, the ST approach produced significantly more forward elevation improvement and trended toward more external rotation and abduction and fewer revisions. Although not definitive, these data suggest the ST approach may provide more stability over the long term, but additional comprehensive studies are needed to increase the sample size and the power of the trends elucidated in this review. According to the orthopedic literature, both techniques produce excellent clinical outcomes, and technique selection should be based on surgeon discretion and expertise.

Am J Orthop. 2017;46(2):E131-E138. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Keating JF, Waterworth P, Shaw-Dunn J, Crossan J. The relative strengths of the rotator cuff muscles. A cadaver study. J Bone Joint Surg Br. 1993;75(1):137-140.

2. Ponce BA, Ahluwalia RS, Mazzocca AD, Gobezie RG, Warner JJ, Millett PJ. Biomechanical and clinical evaluation of a novel lesser tuberosity repair technique in total shoulder arthroplasty. J Bone Joint Surg Am. 2005;87(suppl 2):1-8.

3. Miller SL, Hazrati Y, Klepps S, Chiang A, Flatow EL. Loss of subscapularis function after total shoulder replacement: a seldom recognized problem. J Shoulder Elbow Surg. 2003;12(1):29-34.

4. Gerber A, Ghalambor N, Warner JJ. Instability of shoulder arthroplasty: balancing mobility and stability. Orthop Clin North Am. 2001;32(4):661-670, ix.

5. Moeckel BH, Altchek DW, Warren RF, Wickiewicz TL, Dines DM. Instability of the shoulder after arthroplasty. J Bone Joint Surg Am. 1993;75(4):492-497.

6. Gerber C, Yian EH, Pfirrmann CA, Zumstein MA, Werner CM. Subscapularis muscle function and structure after total shoulder replacement with lesser tuberosity osteotomy and repair. J Bone Joint Surg Am. 2005;87(8):1739-1745.

7. Van den Berghe GR, Nguyen B, Patil S, et al. A biomechanical evaluation of three surgical techniques for subscapularis repair. J Shoulder Elbow Surg. 2008;17(1):156-161.

8. Caplan JL, Whitfield B, Neviaser RJ. Subscapularis function after primary tendon to tendon repair in patients after replacement arthroplasty of the shoulder. J Shoulder Elbow Surg. 2009;18(2):193-196.

9. Armstrong A, Lashgari C, Teefey S, Menendez J, Yamaguchi K, Galatz LM. Ultrasound evaluation and clinical correlation of subscapularis repair after total shoulder arthroplasty. J Shoulder Elbow Surg. 2006;15(5):541-548.

10. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred Reporting Items for Systematic Reviews and Meta-Analyses: the PRISMA statement. Int J Surg. 2010;8(5):336-341.

11. Cowan J, Lozano-Calderón S, Ring D. Quality of prospective controlled randomized trials. Analysis of trials of treatment for lateral epicondylitis as an example. J Bone Joint Surg Am. 2007;89(8):1693-1699.

12. Harris JD, Siston RA, Pan X, Flanigan DC. Autologous chondrocyte implantation: a systematic review. J Bone Joint Surg Am. 2010;92(12):2220-2233.

13. Harris JD, Siston RA, Brophy RH, Lattermann C, Carey JL, Flanigan DC. Failures, re-operations, and complications after autologous chondrocyte implantation—a systematic review. Osteoarthritis Cartilage. 2011;19(7):779-791.

14. Buckley T, Miller R, Nicandri G, Lewis R, Voloshin I. Analysis of subscapularis integrity and function after lesser tuberosity osteotomy versus subscapularis tenotomy in total shoulder arthroplasty using ultrasound and validated clinical outcome measures. J Shoulder Elbow Surg. 2014;23(9):1309-1317.

15. Scalise JJ, Ciccone J, Iannotti JP. Clinical, radiographic, and ultrasonographic comparison of subscapularis tenotomy and lesser tuberosity osteotomy for total shoulder arthroplasty. J Bone Joint Surg Am. 2010;92(7):1627-1634.

16. Jandhyala S, Unnithan A, Hughes S, Hong T. Subscapularis tenotomy versus lesser tuberosity osteotomy during total shoulder replacement: a comparison of patient outcomes. J Shoulder Elbow Surg. 2011;20(7):1102-1107.

17. Fucentese SF, Costouros JG, Kühnel SP, Gerber C. Total shoulder arthroplasty with an uncemented soft-metal-backed glenoid component. J Shoulder Elbow Surg. 2010;19(4):624-631.

18. Clement ND, Duckworth AD, Colling RC, Stirrat AN. An uncemented metal-backed glenoid component in total shoulder arthroplasty for osteoarthritis: factors affecting survival and outcome. J Orthop Sci. 2013;18(1):22-28.

19. Rosenberg N, Neumann L, Modi A, Mersich IJ, Wallace AW. Improvements in survival of the uncemented Nottingham Total Shoulder prosthesis: a prospective comparative study. BMC Musculoskelet Disord. 2007;8(1):76.

20. Small KM, Siegel EJ, Miller LR, Higgins LD. Imaging characteristics of lesser tuberosity osteotomy after total shoulder replacement: a study of 220 patients. J Shoulder Elbow Surg. 2014;23(9):1318-1326.

21. Mileti J, Sperling JW, Cofield RH, Harrington JR, Hoskin TL. Monoblock and modular total shoulder arthroplasty for osteoarthritis. J Bone Joint Surg Br. 2005;87(4):496-500.

22. Merolla G, Paladini P, Campi F, Porcellini G. Efficacy of anatomical prostheses in primary glenohumeral osteoarthritis. Chir Organi Mov. 2008;91(2):109-115.

23. Jackson JD, Cil A, Smith J, Steinmann SP. Integrity and function of the subscapularis after total shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(7):1085-1090.

24. Jost PW, Dines JS, Griffith MH, Angel M, Altchek DW, Dines DM. Total shoulder arthroplasty utilizing mini-stem humeral components: technique and short-term results. HSS J. 2011;7(3):213-217.

25. Razmjou H, Holtby R, Christakis M, Axelrod T, Richards R. Impact of prosthetic design on clinical and radiologic outcomes of total shoulder arthroplasty: a prospective study. J Shoulder Elbow Surg. 2013;22(2):206-214.

26. Raiss P, Schmitt M, Bruckner T, et al. Results of cemented total shoulder replacement with a minimum follow-up of ten years. J Bone Joint Surg Am. 2012;94(23):e1711-1710.

27. Litchfied RB, McKee MD, Balyk R, et al. Cemented versus uncemented fixation of humeral components in total shoulder arthroplasty for osteoarthritis of the shoulder: a prospective, randomized, double-blind clinical trial—a JOINTs Canada Project. J Shoulder Elbow Surg. 2011;20(4):529-536.

28. Martin SD, Zurakowski D, Thornhill TS. Uncemented glenoid component in total shoulder arthroplasty. Survivorship and outcomes. J Bone Joint Surg Am. 2005;87(6):1284-1292.

29. Taunton MJ, McIntosh AL, Sperling JW, Cofield RH. Total shoulder arthroplasty with a metal-backed, bone-ingrowth glenoid component. Medium to long-term results. J Bone Joint Surg Am. 2008;90(10):2180-2188.

30. Budge MD, Nolan EM, Heisey MH, Baker K, Wiater JM. Results of total shoulder arthroplasty with a monoblock porous tantalum glenoid component: a prospective minimum 2-year follow-up study. J Shoulder Elbow Surg. 2013;22(4):535-541.

31. Gerber C, Costouros JG, Sukthankar A, Fucentese SF. Static posterior humeral head subluxation and total shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(4):505-510.

32. Giuseffi SA, Wongtriratanachai P, Omae H, et al. Biomechanical comparison of lesser tuberosity osteotomy versus subscapularis tenotomy in total shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(8):1087-1095.

 

 

33. Van Thiel GS, Wang VM, Wang FC, et al. Biomechanical similarities among subscapularis repairs after shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(5):657-663.

34. Lapner PL, Sabri E, Rakhra K, Bell K, Athwal GS. Comparison of lesser tuberosity osteotomy to subscapularis peel in shoulder arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2012;94(24):2239-2246.

35. Cofield RH. Total shoulder arthroplasty with the Neer prosthesis. J Bone Joint Surg Am. 1984;66(6):899-906.

36. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.

References

1. Keating JF, Waterworth P, Shaw-Dunn J, Crossan J. The relative strengths of the rotator cuff muscles. A cadaver study. J Bone Joint Surg Br. 1993;75(1):137-140.

2. Ponce BA, Ahluwalia RS, Mazzocca AD, Gobezie RG, Warner JJ, Millett PJ. Biomechanical and clinical evaluation of a novel lesser tuberosity repair technique in total shoulder arthroplasty. J Bone Joint Surg Am. 2005;87(suppl 2):1-8.

3. Miller SL, Hazrati Y, Klepps S, Chiang A, Flatow EL. Loss of subscapularis function after total shoulder replacement: a seldom recognized problem. J Shoulder Elbow Surg. 2003;12(1):29-34.

4. Gerber A, Ghalambor N, Warner JJ. Instability of shoulder arthroplasty: balancing mobility and stability. Orthop Clin North Am. 2001;32(4):661-670, ix.

5. Moeckel BH, Altchek DW, Warren RF, Wickiewicz TL, Dines DM. Instability of the shoulder after arthroplasty. J Bone Joint Surg Am. 1993;75(4):492-497.

6. Gerber C, Yian EH, Pfirrmann CA, Zumstein MA, Werner CM. Subscapularis muscle function and structure after total shoulder replacement with lesser tuberosity osteotomy and repair. J Bone Joint Surg Am. 2005;87(8):1739-1745.

7. Van den Berghe GR, Nguyen B, Patil S, et al. A biomechanical evaluation of three surgical techniques for subscapularis repair. J Shoulder Elbow Surg. 2008;17(1):156-161.

8. Caplan JL, Whitfield B, Neviaser RJ. Subscapularis function after primary tendon to tendon repair in patients after replacement arthroplasty of the shoulder. J Shoulder Elbow Surg. 2009;18(2):193-196.

9. Armstrong A, Lashgari C, Teefey S, Menendez J, Yamaguchi K, Galatz LM. Ultrasound evaluation and clinical correlation of subscapularis repair after total shoulder arthroplasty. J Shoulder Elbow Surg. 2006;15(5):541-548.

10. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred Reporting Items for Systematic Reviews and Meta-Analyses: the PRISMA statement. Int J Surg. 2010;8(5):336-341.

11. Cowan J, Lozano-Calderón S, Ring D. Quality of prospective controlled randomized trials. Analysis of trials of treatment for lateral epicondylitis as an example. J Bone Joint Surg Am. 2007;89(8):1693-1699.

12. Harris JD, Siston RA, Pan X, Flanigan DC. Autologous chondrocyte implantation: a systematic review. J Bone Joint Surg Am. 2010;92(12):2220-2233.

13. Harris JD, Siston RA, Brophy RH, Lattermann C, Carey JL, Flanigan DC. Failures, re-operations, and complications after autologous chondrocyte implantation—a systematic review. Osteoarthritis Cartilage. 2011;19(7):779-791.

14. Buckley T, Miller R, Nicandri G, Lewis R, Voloshin I. Analysis of subscapularis integrity and function after lesser tuberosity osteotomy versus subscapularis tenotomy in total shoulder arthroplasty using ultrasound and validated clinical outcome measures. J Shoulder Elbow Surg. 2014;23(9):1309-1317.

15. Scalise JJ, Ciccone J, Iannotti JP. Clinical, radiographic, and ultrasonographic comparison of subscapularis tenotomy and lesser tuberosity osteotomy for total shoulder arthroplasty. J Bone Joint Surg Am. 2010;92(7):1627-1634.

16. Jandhyala S, Unnithan A, Hughes S, Hong T. Subscapularis tenotomy versus lesser tuberosity osteotomy during total shoulder replacement: a comparison of patient outcomes. J Shoulder Elbow Surg. 2011;20(7):1102-1107.

17. Fucentese SF, Costouros JG, Kühnel SP, Gerber C. Total shoulder arthroplasty with an uncemented soft-metal-backed glenoid component. J Shoulder Elbow Surg. 2010;19(4):624-631.

18. Clement ND, Duckworth AD, Colling RC, Stirrat AN. An uncemented metal-backed glenoid component in total shoulder arthroplasty for osteoarthritis: factors affecting survival and outcome. J Orthop Sci. 2013;18(1):22-28.

19. Rosenberg N, Neumann L, Modi A, Mersich IJ, Wallace AW. Improvements in survival of the uncemented Nottingham Total Shoulder prosthesis: a prospective comparative study. BMC Musculoskelet Disord. 2007;8(1):76.

20. Small KM, Siegel EJ, Miller LR, Higgins LD. Imaging characteristics of lesser tuberosity osteotomy after total shoulder replacement: a study of 220 patients. J Shoulder Elbow Surg. 2014;23(9):1318-1326.

21. Mileti J, Sperling JW, Cofield RH, Harrington JR, Hoskin TL. Monoblock and modular total shoulder arthroplasty for osteoarthritis. J Bone Joint Surg Br. 2005;87(4):496-500.

22. Merolla G, Paladini P, Campi F, Porcellini G. Efficacy of anatomical prostheses in primary glenohumeral osteoarthritis. Chir Organi Mov. 2008;91(2):109-115.

23. Jackson JD, Cil A, Smith J, Steinmann SP. Integrity and function of the subscapularis after total shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(7):1085-1090.

24. Jost PW, Dines JS, Griffith MH, Angel M, Altchek DW, Dines DM. Total shoulder arthroplasty utilizing mini-stem humeral components: technique and short-term results. HSS J. 2011;7(3):213-217.

25. Razmjou H, Holtby R, Christakis M, Axelrod T, Richards R. Impact of prosthetic design on clinical and radiologic outcomes of total shoulder arthroplasty: a prospective study. J Shoulder Elbow Surg. 2013;22(2):206-214.

26. Raiss P, Schmitt M, Bruckner T, et al. Results of cemented total shoulder replacement with a minimum follow-up of ten years. J Bone Joint Surg Am. 2012;94(23):e1711-1710.

27. Litchfied RB, McKee MD, Balyk R, et al. Cemented versus uncemented fixation of humeral components in total shoulder arthroplasty for osteoarthritis of the shoulder: a prospective, randomized, double-blind clinical trial—a JOINTs Canada Project. J Shoulder Elbow Surg. 2011;20(4):529-536.

28. Martin SD, Zurakowski D, Thornhill TS. Uncemented glenoid component in total shoulder arthroplasty. Survivorship and outcomes. J Bone Joint Surg Am. 2005;87(6):1284-1292.

29. Taunton MJ, McIntosh AL, Sperling JW, Cofield RH. Total shoulder arthroplasty with a metal-backed, bone-ingrowth glenoid component. Medium to long-term results. J Bone Joint Surg Am. 2008;90(10):2180-2188.

30. Budge MD, Nolan EM, Heisey MH, Baker K, Wiater JM. Results of total shoulder arthroplasty with a monoblock porous tantalum glenoid component: a prospective minimum 2-year follow-up study. J Shoulder Elbow Surg. 2013;22(4):535-541.

31. Gerber C, Costouros JG, Sukthankar A, Fucentese SF. Static posterior humeral head subluxation and total shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(4):505-510.

32. Giuseffi SA, Wongtriratanachai P, Omae H, et al. Biomechanical comparison of lesser tuberosity osteotomy versus subscapularis tenotomy in total shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(8):1087-1095.

 

 

33. Van Thiel GS, Wang VM, Wang FC, et al. Biomechanical similarities among subscapularis repairs after shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(5):657-663.

34. Lapner PL, Sabri E, Rakhra K, Bell K, Athwal GS. Comparison of lesser tuberosity osteotomy to subscapularis peel in shoulder arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2012;94(24):2239-2246.

35. Cofield RH. Total shoulder arthroplasty with the Neer prosthesis. J Bone Joint Surg Am. 1984;66(6):899-906.

36. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.

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Subscapularis Tenotomy Versus Lesser Tuberosity Osteotomy for Total Shoulder Arthroplasty: A Systematic Review
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Pronator Teres Myotendinous Tear

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Pronator Teres Myotendinous Tear

Take-Home Points

  • Pronator teres muscle injuries are rare.
  • Injury can be mistaken for MUCL injury in athletes.
  • Tenderness and weak/painful forearm pronation are common findings.
  • MRI confirms the diagnosis and helps grade the muscle strain injury.
  • Conservative treatment is recommended and prognosis is excellent even for high-grade strains.

Pronator teres muscle strain is a rare sporting injury reported only in cricket players, and now in a golfer whose forearm experienced an eccentric force during resisted elbow flexion and pronation.1,2 The injury occurs when the sporting club or racket strikes the ground during a swing, impeding forward progress and subjecting the pronator teres muscle to eccentric forces in excess of what it can withstand. The pronator teres, one of several muscles that comprise the flexor wad of the forearm, consists of 2 heads, originating proximally from the medical epicondyle and attaching distally to the shaft of the radius on its lateral surface and just distal to the supinator. The oblique orientation of the muscle belly allows it to serve in its primary rotatory role as the main pronator of the forearm. Injuries to the soft tissue of the medial forearm are common in both elite and recreational athletes, especially in racket and club sports.3 Often, these injuries are related to overuse and chronic fatigue of the surrounding soft tissue—caused by repetitive flexing, gripping, or swinging. Even when identified early, these injuries can result in a significant loss of training time.4 In this article, we report a case of pronator teres muscle tear at the myotendinous junction. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A right-hand–dominant 36-year-old man presented to the clinic with pain on the medial side of his right elbow after sustaining an injury to the elbow while playing golf several days earlier. The patient, an advertising executive, was playing recreational golf several times a month and had no significant medical history or previous symptoms related to the elbow. Initial pain symptoms began during a second round of play, immediately after the patient miss-hit an iron shot, making contact mostly with the ground and causing the club to forcefully stop. The pain was on the medial side of the elbow and forearm. The patient noted progressive swelling and bruising at the pain site and development of forearm weakness. Physical examination during the clinic presentation revealed ecchymosis on the anterior medial forearm, medial elbow, and medial triceps (Figure 1).

Figure 1.
Mild tenderness to palpation was elicited over the medial elbow, specifically over the course of the flexor pronator mass. When the elbow was assessed for tender areas, the medial epicondyle was not tender. Range of motion (ROM) testing revealed 120° of flexion and 10° short of full extension, attributed to swelling from acute injury. The patient had full supination and pronation, but the pain was reproduced with either movement. The pain produced weakness with flexion and pronation. Valgus stress test results were normal; there was no re-creation of symptoms. The median nerve was negative for the Tinel sign, and the rest of the neurovascular examination was unremarkable. The ipsilateral shoulder was normal on examination.

Noncontrast magnetic resonance imaging (MRI) showed a high-grade partial tear of the pronator teres myotendinous junction (Figures 2A-2C).

Figure 2.
In the surrounding tissue there was an associated increased signal representing edema. Also found was a small intramuscular hematoma. The median nerve, medial collateral ligament, distal biceps, and triceps were uninjured.

The patient was instructed to rest the elbow from strenuous activity, golf in particular, for 4 weeks. Physical therapy for ROM and forearm strengthening of the surrounding flexor wad was initiated at 2 weeks and continued for 4 weeks. The patient was advised to take over-the-counter nonsteroidal anti-inflammatory drugs as needed for comfort. On repeat examination at 4 weeks, with tenderness or weakness with pronation absent and full ROM regained, the patient was released back to full activity. He was able to return to golf and reported being symptom-free and having no sense of weakness or loss of control.

Discussion

A tear of the pronator teres is an exceedingly rare injury. Our results with conservative treatment and a full return to previous activity level are consistent with the only other case reported in the literature.5 In contrast to our patient, the previous patient sustained a tear of the pronator teres after a prolonged period of batting during a recreational cricket match.

 

 

Our patient’s pronator teres injury occurred at the myotendinous junction, a muscle-tendon transition zone often susceptible to injury. What is unusual for this athletic medial elbow injury is that the patient reported no previous symptoms, and it appears that, though the surrounding muscle may have been fatigued by overuse from the round of golf earlier that day, the pathology was caused by an acute eccentric force. During a golf swing, tremendous forces are put on the entire body, from the lower extremities to the forearm and the fingers. Successful completion of the transfer of energy from the golf club to the ball requires both proper technique and proper functioning of key muscles. Specifically, parameters such as ball positioning, club angle, and wrist control play a major role.6 Altered forearm positioning or swing arc can significantly affect club head velocity and energy transfer without putting more stress on the golfer.7 Therefore, it is easy to understand how prolonged or extended play may fatigue the surrounding elbow muscles, leading to altered technique and increased susceptibility to acute injury. Biomechanical analysis of shoulder motion can provide a helpful baseline for assessing injury-related changes in golf swing and developing specific exercise and rehabilitation programs.8,9Although injury to the pronator teres is rare, sport physicians should be aware that, after a valgus stress or force, bruising and swelling along the medial elbow do not always indicate a medial ulnar collateral ligament (MUCL) tear or medial epicondylitis. The key examination findings that differentiate this injury from a MUCL injury are the exact location of pain, the milking maneuver for MUCL incompetence, and the extensive bruising over the muscle course of the pronator teres. MRI plays a pivotal role in proper diagnosis.4 In addition, MRI allows for evaluation of any concomitant injuries that may be obscuring the clinical presentation.

Successful treatment of such injuries is important for both elite and recreational athletes. With rest and physical therapy, our patient recovered from this rare isolated injury to the pronator teres with complete resolution of symptoms and full ROM. In the literature, we found no other reports of isolated full-thickness myotendinous rupture of the pronator teres or avulsion from the medial epicondyle. Therefore, it is unclear whether the same outcome can be expected with conservative therapy. However, because of the good outcomes for partial-thickness injuries treated conservatively and the lack of robust tendinous tissue to repair at the myotendinous junction, we recommend an initial course of conservative treatment. Sports physicians should be aware of this exceedingly rare injury to the elbow and understand the large forces experienced by the soft tissues of the forearm during the golf swing.9,10

Conclusion

Pronator teres muscle strain is a rare sporting injury reported in cricket and golf players. The elbow experiences a large eccentric force during resisted elbow flexion and pronation. The injury appears to occur when the sporting club or racket strikes the ground during a forceful swing impeding forward progress of the arm. The injury can be confused with a MUCL injury, or exacerbation of medial epicondylitis. Physical examination reveals bruising and tenderness over the course of the pronator teres, often distal to the elbow. Advanced imaging confirms the diagnosis and helps grade the severity of muscle strain. Treatment is often conservative, with return to function and sport after 4 to 6 weeks of rest and restricted activities. The patient in this case report had complete return to sporting function, with no residual weakness or pain.

Am J Orthop. 2017;46(2):E105-E107. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Field LD, Savoie FH. Common elbow injuries in sport. Sports Med. 1998;26(3):193-205.

2. Loomer RL. Elbow injuries in athletes. Can J Appl Sport Sci. 1982;7(3):164-166.

3. Dines JS, Bedi A, Williams PN, et al. Tennis injuries: epidemiology, pathophysiology, and treatment. J Am Acad Orthop Surg. 2015;23(3):181-189.

4. Banks KPLy JQBeall DPGrayson DEBancroft LWTall MA. Overuse injuries of the upper extremity in the competitive athlete: magnetic resonance imaging findings associated with repetitive trauma. Curr Probl Diagn Radiol2005;34(4):127-142.

5. Niebulski HZ, Richardson ML. High-grade pronator teres tear in a cricket batsman. Radiol Case Rep. 2015;6(3):540.

6. Zhang X, Shan G. Where do golf drive swings go wrong? Factors influencing driver swing consistency.
Scand J Med Sci Sports. 2014;24(5):749-757.

7. Nesbit SM, McGinnis RS. Kinetic constrained optimization of the golf swing hub path. J Sports Sci Med. 2014;13(4):859-873.

8. Helton MS. Conservative treatment of a proximal full-thickness biceps brachii muscle tear in a special operations soldier.
Phys Ther. 2014;94(4):571-577.

9. Mitchell K, Banks S, Morgan D, Sugaya H. Shoulder motions during the golf swing in male amateur golfers.
J Orthop Sports Phys Ther. 2003;33(4):196-203.

10. Grimshaw P, Giles A, Tong R, Grimmer K. Lower back and elbow injuries in golf. Sports Med. 2002;32(10):655-666.

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Take-Home Points

  • Pronator teres muscle injuries are rare.
  • Injury can be mistaken for MUCL injury in athletes.
  • Tenderness and weak/painful forearm pronation are common findings.
  • MRI confirms the diagnosis and helps grade the muscle strain injury.
  • Conservative treatment is recommended and prognosis is excellent even for high-grade strains.

Pronator teres muscle strain is a rare sporting injury reported only in cricket players, and now in a golfer whose forearm experienced an eccentric force during resisted elbow flexion and pronation.1,2 The injury occurs when the sporting club or racket strikes the ground during a swing, impeding forward progress and subjecting the pronator teres muscle to eccentric forces in excess of what it can withstand. The pronator teres, one of several muscles that comprise the flexor wad of the forearm, consists of 2 heads, originating proximally from the medical epicondyle and attaching distally to the shaft of the radius on its lateral surface and just distal to the supinator. The oblique orientation of the muscle belly allows it to serve in its primary rotatory role as the main pronator of the forearm. Injuries to the soft tissue of the medial forearm are common in both elite and recreational athletes, especially in racket and club sports.3 Often, these injuries are related to overuse and chronic fatigue of the surrounding soft tissue—caused by repetitive flexing, gripping, or swinging. Even when identified early, these injuries can result in a significant loss of training time.4 In this article, we report a case of pronator teres muscle tear at the myotendinous junction. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A right-hand–dominant 36-year-old man presented to the clinic with pain on the medial side of his right elbow after sustaining an injury to the elbow while playing golf several days earlier. The patient, an advertising executive, was playing recreational golf several times a month and had no significant medical history or previous symptoms related to the elbow. Initial pain symptoms began during a second round of play, immediately after the patient miss-hit an iron shot, making contact mostly with the ground and causing the club to forcefully stop. The pain was on the medial side of the elbow and forearm. The patient noted progressive swelling and bruising at the pain site and development of forearm weakness. Physical examination during the clinic presentation revealed ecchymosis on the anterior medial forearm, medial elbow, and medial triceps (Figure 1).

Figure 1.
Mild tenderness to palpation was elicited over the medial elbow, specifically over the course of the flexor pronator mass. When the elbow was assessed for tender areas, the medial epicondyle was not tender. Range of motion (ROM) testing revealed 120° of flexion and 10° short of full extension, attributed to swelling from acute injury. The patient had full supination and pronation, but the pain was reproduced with either movement. The pain produced weakness with flexion and pronation. Valgus stress test results were normal; there was no re-creation of symptoms. The median nerve was negative for the Tinel sign, and the rest of the neurovascular examination was unremarkable. The ipsilateral shoulder was normal on examination.

Noncontrast magnetic resonance imaging (MRI) showed a high-grade partial tear of the pronator teres myotendinous junction (Figures 2A-2C).

Figure 2.
In the surrounding tissue there was an associated increased signal representing edema. Also found was a small intramuscular hematoma. The median nerve, medial collateral ligament, distal biceps, and triceps were uninjured.

The patient was instructed to rest the elbow from strenuous activity, golf in particular, for 4 weeks. Physical therapy for ROM and forearm strengthening of the surrounding flexor wad was initiated at 2 weeks and continued for 4 weeks. The patient was advised to take over-the-counter nonsteroidal anti-inflammatory drugs as needed for comfort. On repeat examination at 4 weeks, with tenderness or weakness with pronation absent and full ROM regained, the patient was released back to full activity. He was able to return to golf and reported being symptom-free and having no sense of weakness or loss of control.

Discussion

A tear of the pronator teres is an exceedingly rare injury. Our results with conservative treatment and a full return to previous activity level are consistent with the only other case reported in the literature.5 In contrast to our patient, the previous patient sustained a tear of the pronator teres after a prolonged period of batting during a recreational cricket match.

 

 

Our patient’s pronator teres injury occurred at the myotendinous junction, a muscle-tendon transition zone often susceptible to injury. What is unusual for this athletic medial elbow injury is that the patient reported no previous symptoms, and it appears that, though the surrounding muscle may have been fatigued by overuse from the round of golf earlier that day, the pathology was caused by an acute eccentric force. During a golf swing, tremendous forces are put on the entire body, from the lower extremities to the forearm and the fingers. Successful completion of the transfer of energy from the golf club to the ball requires both proper technique and proper functioning of key muscles. Specifically, parameters such as ball positioning, club angle, and wrist control play a major role.6 Altered forearm positioning or swing arc can significantly affect club head velocity and energy transfer without putting more stress on the golfer.7 Therefore, it is easy to understand how prolonged or extended play may fatigue the surrounding elbow muscles, leading to altered technique and increased susceptibility to acute injury. Biomechanical analysis of shoulder motion can provide a helpful baseline for assessing injury-related changes in golf swing and developing specific exercise and rehabilitation programs.8,9Although injury to the pronator teres is rare, sport physicians should be aware that, after a valgus stress or force, bruising and swelling along the medial elbow do not always indicate a medial ulnar collateral ligament (MUCL) tear or medial epicondylitis. The key examination findings that differentiate this injury from a MUCL injury are the exact location of pain, the milking maneuver for MUCL incompetence, and the extensive bruising over the muscle course of the pronator teres. MRI plays a pivotal role in proper diagnosis.4 In addition, MRI allows for evaluation of any concomitant injuries that may be obscuring the clinical presentation.

Successful treatment of such injuries is important for both elite and recreational athletes. With rest and physical therapy, our patient recovered from this rare isolated injury to the pronator teres with complete resolution of symptoms and full ROM. In the literature, we found no other reports of isolated full-thickness myotendinous rupture of the pronator teres or avulsion from the medial epicondyle. Therefore, it is unclear whether the same outcome can be expected with conservative therapy. However, because of the good outcomes for partial-thickness injuries treated conservatively and the lack of robust tendinous tissue to repair at the myotendinous junction, we recommend an initial course of conservative treatment. Sports physicians should be aware of this exceedingly rare injury to the elbow and understand the large forces experienced by the soft tissues of the forearm during the golf swing.9,10

Conclusion

Pronator teres muscle strain is a rare sporting injury reported in cricket and golf players. The elbow experiences a large eccentric force during resisted elbow flexion and pronation. The injury appears to occur when the sporting club or racket strikes the ground during a forceful swing impeding forward progress of the arm. The injury can be confused with a MUCL injury, or exacerbation of medial epicondylitis. Physical examination reveals bruising and tenderness over the course of the pronator teres, often distal to the elbow. Advanced imaging confirms the diagnosis and helps grade the severity of muscle strain. Treatment is often conservative, with return to function and sport after 4 to 6 weeks of rest and restricted activities. The patient in this case report had complete return to sporting function, with no residual weakness or pain.

Am J Orthop. 2017;46(2):E105-E107. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Pronator teres muscle injuries are rare.
  • Injury can be mistaken for MUCL injury in athletes.
  • Tenderness and weak/painful forearm pronation are common findings.
  • MRI confirms the diagnosis and helps grade the muscle strain injury.
  • Conservative treatment is recommended and prognosis is excellent even for high-grade strains.

Pronator teres muscle strain is a rare sporting injury reported only in cricket players, and now in a golfer whose forearm experienced an eccentric force during resisted elbow flexion and pronation.1,2 The injury occurs when the sporting club or racket strikes the ground during a swing, impeding forward progress and subjecting the pronator teres muscle to eccentric forces in excess of what it can withstand. The pronator teres, one of several muscles that comprise the flexor wad of the forearm, consists of 2 heads, originating proximally from the medical epicondyle and attaching distally to the shaft of the radius on its lateral surface and just distal to the supinator. The oblique orientation of the muscle belly allows it to serve in its primary rotatory role as the main pronator of the forearm. Injuries to the soft tissue of the medial forearm are common in both elite and recreational athletes, especially in racket and club sports.3 Often, these injuries are related to overuse and chronic fatigue of the surrounding soft tissue—caused by repetitive flexing, gripping, or swinging. Even when identified early, these injuries can result in a significant loss of training time.4 In this article, we report a case of pronator teres muscle tear at the myotendinous junction. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A right-hand–dominant 36-year-old man presented to the clinic with pain on the medial side of his right elbow after sustaining an injury to the elbow while playing golf several days earlier. The patient, an advertising executive, was playing recreational golf several times a month and had no significant medical history or previous symptoms related to the elbow. Initial pain symptoms began during a second round of play, immediately after the patient miss-hit an iron shot, making contact mostly with the ground and causing the club to forcefully stop. The pain was on the medial side of the elbow and forearm. The patient noted progressive swelling and bruising at the pain site and development of forearm weakness. Physical examination during the clinic presentation revealed ecchymosis on the anterior medial forearm, medial elbow, and medial triceps (Figure 1).

Figure 1.
Mild tenderness to palpation was elicited over the medial elbow, specifically over the course of the flexor pronator mass. When the elbow was assessed for tender areas, the medial epicondyle was not tender. Range of motion (ROM) testing revealed 120° of flexion and 10° short of full extension, attributed to swelling from acute injury. The patient had full supination and pronation, but the pain was reproduced with either movement. The pain produced weakness with flexion and pronation. Valgus stress test results were normal; there was no re-creation of symptoms. The median nerve was negative for the Tinel sign, and the rest of the neurovascular examination was unremarkable. The ipsilateral shoulder was normal on examination.

Noncontrast magnetic resonance imaging (MRI) showed a high-grade partial tear of the pronator teres myotendinous junction (Figures 2A-2C).

Figure 2.
In the surrounding tissue there was an associated increased signal representing edema. Also found was a small intramuscular hematoma. The median nerve, medial collateral ligament, distal biceps, and triceps were uninjured.

The patient was instructed to rest the elbow from strenuous activity, golf in particular, for 4 weeks. Physical therapy for ROM and forearm strengthening of the surrounding flexor wad was initiated at 2 weeks and continued for 4 weeks. The patient was advised to take over-the-counter nonsteroidal anti-inflammatory drugs as needed for comfort. On repeat examination at 4 weeks, with tenderness or weakness with pronation absent and full ROM regained, the patient was released back to full activity. He was able to return to golf and reported being symptom-free and having no sense of weakness or loss of control.

Discussion

A tear of the pronator teres is an exceedingly rare injury. Our results with conservative treatment and a full return to previous activity level are consistent with the only other case reported in the literature.5 In contrast to our patient, the previous patient sustained a tear of the pronator teres after a prolonged period of batting during a recreational cricket match.

 

 

Our patient’s pronator teres injury occurred at the myotendinous junction, a muscle-tendon transition zone often susceptible to injury. What is unusual for this athletic medial elbow injury is that the patient reported no previous symptoms, and it appears that, though the surrounding muscle may have been fatigued by overuse from the round of golf earlier that day, the pathology was caused by an acute eccentric force. During a golf swing, tremendous forces are put on the entire body, from the lower extremities to the forearm and the fingers. Successful completion of the transfer of energy from the golf club to the ball requires both proper technique and proper functioning of key muscles. Specifically, parameters such as ball positioning, club angle, and wrist control play a major role.6 Altered forearm positioning or swing arc can significantly affect club head velocity and energy transfer without putting more stress on the golfer.7 Therefore, it is easy to understand how prolonged or extended play may fatigue the surrounding elbow muscles, leading to altered technique and increased susceptibility to acute injury. Biomechanical analysis of shoulder motion can provide a helpful baseline for assessing injury-related changes in golf swing and developing specific exercise and rehabilitation programs.8,9Although injury to the pronator teres is rare, sport physicians should be aware that, after a valgus stress or force, bruising and swelling along the medial elbow do not always indicate a medial ulnar collateral ligament (MUCL) tear or medial epicondylitis. The key examination findings that differentiate this injury from a MUCL injury are the exact location of pain, the milking maneuver for MUCL incompetence, and the extensive bruising over the muscle course of the pronator teres. MRI plays a pivotal role in proper diagnosis.4 In addition, MRI allows for evaluation of any concomitant injuries that may be obscuring the clinical presentation.

Successful treatment of such injuries is important for both elite and recreational athletes. With rest and physical therapy, our patient recovered from this rare isolated injury to the pronator teres with complete resolution of symptoms and full ROM. In the literature, we found no other reports of isolated full-thickness myotendinous rupture of the pronator teres or avulsion from the medial epicondyle. Therefore, it is unclear whether the same outcome can be expected with conservative therapy. However, because of the good outcomes for partial-thickness injuries treated conservatively and the lack of robust tendinous tissue to repair at the myotendinous junction, we recommend an initial course of conservative treatment. Sports physicians should be aware of this exceedingly rare injury to the elbow and understand the large forces experienced by the soft tissues of the forearm during the golf swing.9,10

Conclusion

Pronator teres muscle strain is a rare sporting injury reported in cricket and golf players. The elbow experiences a large eccentric force during resisted elbow flexion and pronation. The injury appears to occur when the sporting club or racket strikes the ground during a forceful swing impeding forward progress of the arm. The injury can be confused with a MUCL injury, or exacerbation of medial epicondylitis. Physical examination reveals bruising and tenderness over the course of the pronator teres, often distal to the elbow. Advanced imaging confirms the diagnosis and helps grade the severity of muscle strain. Treatment is often conservative, with return to function and sport after 4 to 6 weeks of rest and restricted activities. The patient in this case report had complete return to sporting function, with no residual weakness or pain.

Am J Orthop. 2017;46(2):E105-E107. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Field LD, Savoie FH. Common elbow injuries in sport. Sports Med. 1998;26(3):193-205.

2. Loomer RL. Elbow injuries in athletes. Can J Appl Sport Sci. 1982;7(3):164-166.

3. Dines JS, Bedi A, Williams PN, et al. Tennis injuries: epidemiology, pathophysiology, and treatment. J Am Acad Orthop Surg. 2015;23(3):181-189.

4. Banks KPLy JQBeall DPGrayson DEBancroft LWTall MA. Overuse injuries of the upper extremity in the competitive athlete: magnetic resonance imaging findings associated with repetitive trauma. Curr Probl Diagn Radiol2005;34(4):127-142.

5. Niebulski HZ, Richardson ML. High-grade pronator teres tear in a cricket batsman. Radiol Case Rep. 2015;6(3):540.

6. Zhang X, Shan G. Where do golf drive swings go wrong? Factors influencing driver swing consistency.
Scand J Med Sci Sports. 2014;24(5):749-757.

7. Nesbit SM, McGinnis RS. Kinetic constrained optimization of the golf swing hub path. J Sports Sci Med. 2014;13(4):859-873.

8. Helton MS. Conservative treatment of a proximal full-thickness biceps brachii muscle tear in a special operations soldier.
Phys Ther. 2014;94(4):571-577.

9. Mitchell K, Banks S, Morgan D, Sugaya H. Shoulder motions during the golf swing in male amateur golfers.
J Orthop Sports Phys Ther. 2003;33(4):196-203.

10. Grimshaw P, Giles A, Tong R, Grimmer K. Lower back and elbow injuries in golf. Sports Med. 2002;32(10):655-666.

References

1. Field LD, Savoie FH. Common elbow injuries in sport. Sports Med. 1998;26(3):193-205.

2. Loomer RL. Elbow injuries in athletes. Can J Appl Sport Sci. 1982;7(3):164-166.

3. Dines JS, Bedi A, Williams PN, et al. Tennis injuries: epidemiology, pathophysiology, and treatment. J Am Acad Orthop Surg. 2015;23(3):181-189.

4. Banks KPLy JQBeall DPGrayson DEBancroft LWTall MA. Overuse injuries of the upper extremity in the competitive athlete: magnetic resonance imaging findings associated with repetitive trauma. Curr Probl Diagn Radiol2005;34(4):127-142.

5. Niebulski HZ, Richardson ML. High-grade pronator teres tear in a cricket batsman. Radiol Case Rep. 2015;6(3):540.

6. Zhang X, Shan G. Where do golf drive swings go wrong? Factors influencing driver swing consistency.
Scand J Med Sci Sports. 2014;24(5):749-757.

7. Nesbit SM, McGinnis RS. Kinetic constrained optimization of the golf swing hub path. J Sports Sci Med. 2014;13(4):859-873.

8. Helton MS. Conservative treatment of a proximal full-thickness biceps brachii muscle tear in a special operations soldier.
Phys Ther. 2014;94(4):571-577.

9. Mitchell K, Banks S, Morgan D, Sugaya H. Shoulder motions during the golf swing in male amateur golfers.
J Orthop Sports Phys Ther. 2003;33(4):196-203.

10. Grimshaw P, Giles A, Tong R, Grimmer K. Lower back and elbow injuries in golf. Sports Med. 2002;32(10):655-666.

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Novel Solution for Massive Glenoid Defects in Shoulder Arthroplasty: A Patient-Specific Glenoid Vault Reconstruction System

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Novel Solution for Massive Glenoid Defects in Shoulder Arthroplasty: A Patient-Specific Glenoid Vault Reconstruction System

Take-Home Points

  • With more shoulder arthroplasties being performed on younger patients, we can expect more revisions in the future.
  • Many of these revision cases will have profound glenoid bone loss.
  • Bone grafting the glenoid defects in shoulder arthroplasty has been less successful especially with significant vault defects.
  • Based on the CAD-CAM success in total hip and knee replacement surgery, a patient-specific glenoid vault reconstruction system has been developed by Zimmer Biomet to deal with profound glenoid bone loss and cuff insufficiency.
  • Early results of this vault reconstruction system have been promising in these most difficult clinical situations.

Early results of this vault reconstruction system have been promising in these most difficult clinical situations. Complex glenoid deformities present the most difficult challenges in shoulder arthroplasty (SA). These deformities may be caused by severe degenerative or congenital deformity, posttraumatic anatomy, tumor, or, in most cases, bone loss after glenoid failure in anatomical total SA.

Walch and colleagues1 described the pathologic glenoid lesions seen in progressive degenerative arthritis and some congenital defects. The most severe were initially characterized as Walch B2 and Walch C deformities. These lesions have been further classified to include Walch B3 posteroinferior glenoid deformities.2,3 Each of these deformities can result in severe glenoid vault deficiency.

In some revision cases and in severe rheumatoid cases, these deformities can present as cavitary lesions with or without failure of the glenoid rim or wall resulting in significant compromise of glenoid vault lesions.4,5 In these cases, the degree of “medialization” of the native glenohumeral joint line and the amount of peripheral bone loss can have profound effects on the amount of bone available for fixation and on the ability to allow component positioning for best surgical and biomechanical outcomes.

Other bone loss deformities, which have been described by Antuna and colleagues6 and Seebauer and colleagues,7 often accompany disease processes with severe cuff deficiency. These deformities historically have been treated with intercalary-type bone grafts in 1- or 2-stage revision of reverse SA or in salvage to hemiarthroplasty. Treatment of these pathologies with the technique described produced only fair results in short-term to midterm follow-up. The most commonly reported complications have been component loosening, bone graft failure, infection, and instability.8-11Borrowing from hip and knee arthroplasty surgeons’ experience in using CAD/CAM (computer-aided design/computer-aided manufacturing) patient-specific implants to fill significant bony defects, Dr. D. M. Dines and Dr. Craig developed a patient-specific glenoid vault reconstruction system (VRS) in conjunction with the Comprehensive Shoulder Arthroplasty System (Zimmer Biomet). For a number of years, the Food and Drug Administration allowed this patient-specific glenoid VRS component to be made available only as a custom implant. Recently, however, full 510K clearance was granted to use the VRS in reverse SA patients with severe soft-tissue deficiency and significant glenoid bone loss.

In this article, we describe the implant and its indications, technical aspects of production, and surgical technique.

Vault Reconstruction System

Severe glenoid bone loss often requires an implant that specifically matches the patient’s anatomy. The patient-specific glenoid VRS (Figure 1) is made from a 3-dimensional reconstruction of a 2-dimensional computed tomography image.

Figure 1.
CAD/CAM reconstruction allows for preoperative planning, visualization, and development of patient-specific implants. The patient-specific images used for the glenoid VRS detail implant position, orientation, and size to create a more normal gleno­humeral center of rotation. The model allows for the planning, placement, size, and trajectory of the central and peripheral screws, ensuring the best possible fixation (Figures 2A, 2B).
Figure 2.
Most important, the model is used to create patient-matched implants that fill bone voids with porous plasma spray–coated titanium, which provides high strength and flexibility and allows for biological fixation. This system can accommodate a bone loss envelope of about 50 mm × 50 mm × 35 mm based on evaluation of all implants created in the custom scenario.

In some cases in which the bone is sufficient to enhance fixation in the deficient glenoid vault, a custom boss may be added to the implant, as well as a custom guide matching the implant.

Figure 3.
The implant model, the bone model, and the custom boss reaming guide are all constructed from a sterilizable material and are intended to be single-use disposable instruments as well as tools for the initial plan review (Figures 3A, 3B).

Glenoid Exposure

In most cases of severe glenoid bone loss, the associated soft-tissue deficiency allows for easier glenoid exposure. In this implant system, however, maximal peripheral en face exposure of the glenoid is required. In addition, it is mandatory to avoid disturbing the remaining glenoid bone surfaces, which often are thin or fragile, because the patient-specific implant is referenced to this anatomy. Bone that is not maintained changes the orientation of the patient-specific guide and ultimately the fixation of the component. Using the correct retractors and meticulously excising soft-tissue scar tissue are crucial for success.

 

 

Implant Positioning

With the glenoid surface properly exposed, the removable inserter handle and the built-in lip on the implant are used to position the patient-specific guide. Next, a central guide pin is placed through the inserter for temporary fixation and further instrumentation. If enough bone is present, a boss reamer can be used over the guide pin to prepare and increase the fixation surface.

Figure 4.
Next, the real implant is placed in the ideal position as defined in the preoperative plan. The implant is fixed provisionally through special guides in the peripheral screw holes (Figures 4A, 4B).

The central 6.5-mm nonlocking compression screw is placed to provide strong initial compressive fixation in best bone.

Figure 5.
Then, in sequence, the temporary fixation pins are removed and are replaced with the 4.75-mm locking or nonlocking screws in the real implant to secure the implant in the planned anatomical position (Figure 5).

With the patient-specific glenoid VRS implant now rigidly fixed in the glenoid, the sized and offset glenosphere is properly positioned, and the reverse SA is completed in routine fashion.

Case Examples

A 49-year-old man underwent hemiarthroplasty for osteoarthritis. The procedure failed and, 3 years later, was revised to conventional total SA. Unfortunately, the cemented all-polyethylene glenoid loosened secondary to active Propionibacterium acnes infection, which required excisional arthroplasty with antibiotic spacer. Significant cavitary bone loss was found with anterior glenoid wall bone loss compromising the glenoid vault. Given the history of bone loss and infection, patient-specific glenoid vault reconstruction was performed after infection eradication. Within 4 years after this surgery, the patient had resumed all activities. At age 57 years, he had restricted active forward elevation and abduction to 120° but was satisfied with the outcome.

Figure 6.
There was no evidence of infection or component loosening, but close monitoring was continued (Figures 6A-6D).

A 71-year-old man underwent reverse SA for rotator cuff-deficient osteoarthritis. After implant excision and spacer placement, he was left with severe soft-tissue deficiency and glenoid bone loss, which caused substantial disability. After treatment for infection, a work-up was performed for glenoid bone deficiency and insertion of a patient-specific glenoid VRS implant.

Figure 7.
Eighteen months after surgery, active range of motion was 130° forward elevation and limited (20°) external rotation (Figures 7A-7D).

Discussion

Glenoid bone deformity and deficiency are among the most difficult challenges in SA—a particularly compelling fact given the increasing number of SAs being performed in younger, more active patients. SA surgeons can now expect to be performing even more revisions with concomitant bone defects, which may be severe in some cases.

In addition to these causes of extreme bone loss, recent awareness of the importance of recognizing and treating bone deficits in osteoarthritis, rheumatoid arthritis, trauma, and instability has led to the development of patient-specific guides, instrumentation, and implants. Concepts from the use of CAD/CAM acetabular implants in total hip arthroplasty for severe acetabular bony defects were applied to the use of patient-specific glenoid reconstruction implants without bone graft augmentation.12 In different form, this idea was reported by Chammaa and colleagues13 in 30 cases, and clinical and durable results were very promising.

We have described use of this technique in 2 extreme cases of glenoid vault deficiency. In each case, short-term results were quite satisfactory. However, both patients were relatively young, and long-term clinical and radiographic follow-up is needed.

Many of the severe cases of glenoid bone loss require an implant that specifically matches the patient’s anatomy. The glenoid VRS implant described here may be of great benefit in these difficult reconstructions and is a valuable addition to the armamentarium of treatments for distorted glenoid anatomy. Eventually, the idea may become useful in treating other, less significant defects by re-creating more-normal biomechanics in SA without bone graft.


Am J Orthop. 2017;46(2):104-108. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.

2. Chan K, Knowles NK, Chaoui J, et al. Characterization of the Walch B3 glenoid in primary osteoarthritis [published online January 11, 2017]. J Shoulder Elbow Surg. doi:10.1016/j.jse.2016.10.003.

3. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.

4. Sears BW, Johnston PS, Ramsay ML, Williams GR. Glenoid bone loss in primary total shoulder arthroplasty: evaluation and management. J Am Acad Orthop Surg. 2012;20(9):604-613.

5. Kocsis G, Thyagarajan DS, Fairbairn KJ, Wallace WA. A new classification of glenoid bone loss to help plan the implantation of a glenoid component before revision arthroplasty of the shoulder. Bone Joint J. 2016;98(3):374-380.

6. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.

7. Seebauer L, Walter W, Keyl W. Reverse total shoulder arthroplasty for the treatment of defect arthropathy [in English, German]. Oper Orthop Traumatol. 2005;17(1):1-24.

8. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012:21(6):765-771.

9. Hill JM, Norris TR. Long-term results of total shoulder arthroplasty following bone-grafting of the glenoid. J Bone Joint Surg Am. 2001;83(6):877-883.

10. Steinmann SP, Cofield RH. Bone grafting for glenoid deficiency in total shoulder replacement. J Shoulder Elbow Surg. 2000;9(5):361-367.

11. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymptomatic posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308.

12. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684.

13. Chammaa R, Uri O, Lambert S. Primary shoulder arthroplasty using a custom-made hip-inspired implant for the treatment of advanced glenohumeral arthritis in the presence of severe glenoid bone loss. J Shoulder Elbow Surg. 2017;26(1):101-107.

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Authors’ Disclosure Statement: Dr. D. M. Dines reports that he is a paid consultant to and receives royalties and advisory board compensation from Zimmer Biomet for his development of its Comprehensive Shoulder Arthroplasty System, which relates directly to this article. He also receives royalties on textbooks published by Thieme and is a shareholder in VuMedi. Dr. Gulotta reports that he is a consultant to Zimmer Biomet. Dr. Craig reports that he receives royalties from Zimmer Biomet. Dr. J. S. Dines reports that he is a consultant to Arthrex.

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Authors’ Disclosure Statement: Dr. D. M. Dines reports that he is a paid consultant to and receives royalties and advisory board compensation from Zimmer Biomet for his development of its Comprehensive Shoulder Arthroplasty System, which relates directly to this article. He also receives royalties on textbooks published by Thieme and is a shareholder in VuMedi. Dr. Gulotta reports that he is a consultant to Zimmer Biomet. Dr. Craig reports that he receives royalties from Zimmer Biomet. Dr. J. S. Dines reports that he is a consultant to Arthrex.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. D. M. Dines reports that he is a paid consultant to and receives royalties and advisory board compensation from Zimmer Biomet for his development of its Comprehensive Shoulder Arthroplasty System, which relates directly to this article. He also receives royalties on textbooks published by Thieme and is a shareholder in VuMedi. Dr. Gulotta reports that he is a consultant to Zimmer Biomet. Dr. Craig reports that he receives royalties from Zimmer Biomet. Dr. J. S. Dines reports that he is a consultant to Arthrex.

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Take-Home Points

  • With more shoulder arthroplasties being performed on younger patients, we can expect more revisions in the future.
  • Many of these revision cases will have profound glenoid bone loss.
  • Bone grafting the glenoid defects in shoulder arthroplasty has been less successful especially with significant vault defects.
  • Based on the CAD-CAM success in total hip and knee replacement surgery, a patient-specific glenoid vault reconstruction system has been developed by Zimmer Biomet to deal with profound glenoid bone loss and cuff insufficiency.
  • Early results of this vault reconstruction system have been promising in these most difficult clinical situations.

Early results of this vault reconstruction system have been promising in these most difficult clinical situations. Complex glenoid deformities present the most difficult challenges in shoulder arthroplasty (SA). These deformities may be caused by severe degenerative or congenital deformity, posttraumatic anatomy, tumor, or, in most cases, bone loss after glenoid failure in anatomical total SA.

Walch and colleagues1 described the pathologic glenoid lesions seen in progressive degenerative arthritis and some congenital defects. The most severe were initially characterized as Walch B2 and Walch C deformities. These lesions have been further classified to include Walch B3 posteroinferior glenoid deformities.2,3 Each of these deformities can result in severe glenoid vault deficiency.

In some revision cases and in severe rheumatoid cases, these deformities can present as cavitary lesions with or without failure of the glenoid rim or wall resulting in significant compromise of glenoid vault lesions.4,5 In these cases, the degree of “medialization” of the native glenohumeral joint line and the amount of peripheral bone loss can have profound effects on the amount of bone available for fixation and on the ability to allow component positioning for best surgical and biomechanical outcomes.

Other bone loss deformities, which have been described by Antuna and colleagues6 and Seebauer and colleagues,7 often accompany disease processes with severe cuff deficiency. These deformities historically have been treated with intercalary-type bone grafts in 1- or 2-stage revision of reverse SA or in salvage to hemiarthroplasty. Treatment of these pathologies with the technique described produced only fair results in short-term to midterm follow-up. The most commonly reported complications have been component loosening, bone graft failure, infection, and instability.8-11Borrowing from hip and knee arthroplasty surgeons’ experience in using CAD/CAM (computer-aided design/computer-aided manufacturing) patient-specific implants to fill significant bony defects, Dr. D. M. Dines and Dr. Craig developed a patient-specific glenoid vault reconstruction system (VRS) in conjunction with the Comprehensive Shoulder Arthroplasty System (Zimmer Biomet). For a number of years, the Food and Drug Administration allowed this patient-specific glenoid VRS component to be made available only as a custom implant. Recently, however, full 510K clearance was granted to use the VRS in reverse SA patients with severe soft-tissue deficiency and significant glenoid bone loss.

In this article, we describe the implant and its indications, technical aspects of production, and surgical technique.

Vault Reconstruction System

Severe glenoid bone loss often requires an implant that specifically matches the patient’s anatomy. The patient-specific glenoid VRS (Figure 1) is made from a 3-dimensional reconstruction of a 2-dimensional computed tomography image.

Figure 1.
CAD/CAM reconstruction allows for preoperative planning, visualization, and development of patient-specific implants. The patient-specific images used for the glenoid VRS detail implant position, orientation, and size to create a more normal gleno­humeral center of rotation. The model allows for the planning, placement, size, and trajectory of the central and peripheral screws, ensuring the best possible fixation (Figures 2A, 2B).
Figure 2.
Most important, the model is used to create patient-matched implants that fill bone voids with porous plasma spray–coated titanium, which provides high strength and flexibility and allows for biological fixation. This system can accommodate a bone loss envelope of about 50 mm × 50 mm × 35 mm based on evaluation of all implants created in the custom scenario.

In some cases in which the bone is sufficient to enhance fixation in the deficient glenoid vault, a custom boss may be added to the implant, as well as a custom guide matching the implant.

Figure 3.
The implant model, the bone model, and the custom boss reaming guide are all constructed from a sterilizable material and are intended to be single-use disposable instruments as well as tools for the initial plan review (Figures 3A, 3B).

Glenoid Exposure

In most cases of severe glenoid bone loss, the associated soft-tissue deficiency allows for easier glenoid exposure. In this implant system, however, maximal peripheral en face exposure of the glenoid is required. In addition, it is mandatory to avoid disturbing the remaining glenoid bone surfaces, which often are thin or fragile, because the patient-specific implant is referenced to this anatomy. Bone that is not maintained changes the orientation of the patient-specific guide and ultimately the fixation of the component. Using the correct retractors and meticulously excising soft-tissue scar tissue are crucial for success.

 

 

Implant Positioning

With the glenoid surface properly exposed, the removable inserter handle and the built-in lip on the implant are used to position the patient-specific guide. Next, a central guide pin is placed through the inserter for temporary fixation and further instrumentation. If enough bone is present, a boss reamer can be used over the guide pin to prepare and increase the fixation surface.

Figure 4.
Next, the real implant is placed in the ideal position as defined in the preoperative plan. The implant is fixed provisionally through special guides in the peripheral screw holes (Figures 4A, 4B).

The central 6.5-mm nonlocking compression screw is placed to provide strong initial compressive fixation in best bone.

Figure 5.
Then, in sequence, the temporary fixation pins are removed and are replaced with the 4.75-mm locking or nonlocking screws in the real implant to secure the implant in the planned anatomical position (Figure 5).

With the patient-specific glenoid VRS implant now rigidly fixed in the glenoid, the sized and offset glenosphere is properly positioned, and the reverse SA is completed in routine fashion.

Case Examples

A 49-year-old man underwent hemiarthroplasty for osteoarthritis. The procedure failed and, 3 years later, was revised to conventional total SA. Unfortunately, the cemented all-polyethylene glenoid loosened secondary to active Propionibacterium acnes infection, which required excisional arthroplasty with antibiotic spacer. Significant cavitary bone loss was found with anterior glenoid wall bone loss compromising the glenoid vault. Given the history of bone loss and infection, patient-specific glenoid vault reconstruction was performed after infection eradication. Within 4 years after this surgery, the patient had resumed all activities. At age 57 years, he had restricted active forward elevation and abduction to 120° but was satisfied with the outcome.

Figure 6.
There was no evidence of infection or component loosening, but close monitoring was continued (Figures 6A-6D).

A 71-year-old man underwent reverse SA for rotator cuff-deficient osteoarthritis. After implant excision and spacer placement, he was left with severe soft-tissue deficiency and glenoid bone loss, which caused substantial disability. After treatment for infection, a work-up was performed for glenoid bone deficiency and insertion of a patient-specific glenoid VRS implant.

Figure 7.
Eighteen months after surgery, active range of motion was 130° forward elevation and limited (20°) external rotation (Figures 7A-7D).

Discussion

Glenoid bone deformity and deficiency are among the most difficult challenges in SA—a particularly compelling fact given the increasing number of SAs being performed in younger, more active patients. SA surgeons can now expect to be performing even more revisions with concomitant bone defects, which may be severe in some cases.

In addition to these causes of extreme bone loss, recent awareness of the importance of recognizing and treating bone deficits in osteoarthritis, rheumatoid arthritis, trauma, and instability has led to the development of patient-specific guides, instrumentation, and implants. Concepts from the use of CAD/CAM acetabular implants in total hip arthroplasty for severe acetabular bony defects were applied to the use of patient-specific glenoid reconstruction implants without bone graft augmentation.12 In different form, this idea was reported by Chammaa and colleagues13 in 30 cases, and clinical and durable results were very promising.

We have described use of this technique in 2 extreme cases of glenoid vault deficiency. In each case, short-term results were quite satisfactory. However, both patients were relatively young, and long-term clinical and radiographic follow-up is needed.

Many of the severe cases of glenoid bone loss require an implant that specifically matches the patient’s anatomy. The glenoid VRS implant described here may be of great benefit in these difficult reconstructions and is a valuable addition to the armamentarium of treatments for distorted glenoid anatomy. Eventually, the idea may become useful in treating other, less significant defects by re-creating more-normal biomechanics in SA without bone graft.


Am J Orthop. 2017;46(2):104-108. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • With more shoulder arthroplasties being performed on younger patients, we can expect more revisions in the future.
  • Many of these revision cases will have profound glenoid bone loss.
  • Bone grafting the glenoid defects in shoulder arthroplasty has been less successful especially with significant vault defects.
  • Based on the CAD-CAM success in total hip and knee replacement surgery, a patient-specific glenoid vault reconstruction system has been developed by Zimmer Biomet to deal with profound glenoid bone loss and cuff insufficiency.
  • Early results of this vault reconstruction system have been promising in these most difficult clinical situations.

Early results of this vault reconstruction system have been promising in these most difficult clinical situations. Complex glenoid deformities present the most difficult challenges in shoulder arthroplasty (SA). These deformities may be caused by severe degenerative or congenital deformity, posttraumatic anatomy, tumor, or, in most cases, bone loss after glenoid failure in anatomical total SA.

Walch and colleagues1 described the pathologic glenoid lesions seen in progressive degenerative arthritis and some congenital defects. The most severe were initially characterized as Walch B2 and Walch C deformities. These lesions have been further classified to include Walch B3 posteroinferior glenoid deformities.2,3 Each of these deformities can result in severe glenoid vault deficiency.

In some revision cases and in severe rheumatoid cases, these deformities can present as cavitary lesions with or without failure of the glenoid rim or wall resulting in significant compromise of glenoid vault lesions.4,5 In these cases, the degree of “medialization” of the native glenohumeral joint line and the amount of peripheral bone loss can have profound effects on the amount of bone available for fixation and on the ability to allow component positioning for best surgical and biomechanical outcomes.

Other bone loss deformities, which have been described by Antuna and colleagues6 and Seebauer and colleagues,7 often accompany disease processes with severe cuff deficiency. These deformities historically have been treated with intercalary-type bone grafts in 1- or 2-stage revision of reverse SA or in salvage to hemiarthroplasty. Treatment of these pathologies with the technique described produced only fair results in short-term to midterm follow-up. The most commonly reported complications have been component loosening, bone graft failure, infection, and instability.8-11Borrowing from hip and knee arthroplasty surgeons’ experience in using CAD/CAM (computer-aided design/computer-aided manufacturing) patient-specific implants to fill significant bony defects, Dr. D. M. Dines and Dr. Craig developed a patient-specific glenoid vault reconstruction system (VRS) in conjunction with the Comprehensive Shoulder Arthroplasty System (Zimmer Biomet). For a number of years, the Food and Drug Administration allowed this patient-specific glenoid VRS component to be made available only as a custom implant. Recently, however, full 510K clearance was granted to use the VRS in reverse SA patients with severe soft-tissue deficiency and significant glenoid bone loss.

In this article, we describe the implant and its indications, technical aspects of production, and surgical technique.

Vault Reconstruction System

Severe glenoid bone loss often requires an implant that specifically matches the patient’s anatomy. The patient-specific glenoid VRS (Figure 1) is made from a 3-dimensional reconstruction of a 2-dimensional computed tomography image.

Figure 1.
CAD/CAM reconstruction allows for preoperative planning, visualization, and development of patient-specific implants. The patient-specific images used for the glenoid VRS detail implant position, orientation, and size to create a more normal gleno­humeral center of rotation. The model allows for the planning, placement, size, and trajectory of the central and peripheral screws, ensuring the best possible fixation (Figures 2A, 2B).
Figure 2.
Most important, the model is used to create patient-matched implants that fill bone voids with porous plasma spray–coated titanium, which provides high strength and flexibility and allows for biological fixation. This system can accommodate a bone loss envelope of about 50 mm × 50 mm × 35 mm based on evaluation of all implants created in the custom scenario.

In some cases in which the bone is sufficient to enhance fixation in the deficient glenoid vault, a custom boss may be added to the implant, as well as a custom guide matching the implant.

Figure 3.
The implant model, the bone model, and the custom boss reaming guide are all constructed from a sterilizable material and are intended to be single-use disposable instruments as well as tools for the initial plan review (Figures 3A, 3B).

Glenoid Exposure

In most cases of severe glenoid bone loss, the associated soft-tissue deficiency allows for easier glenoid exposure. In this implant system, however, maximal peripheral en face exposure of the glenoid is required. In addition, it is mandatory to avoid disturbing the remaining glenoid bone surfaces, which often are thin or fragile, because the patient-specific implant is referenced to this anatomy. Bone that is not maintained changes the orientation of the patient-specific guide and ultimately the fixation of the component. Using the correct retractors and meticulously excising soft-tissue scar tissue are crucial for success.

 

 

Implant Positioning

With the glenoid surface properly exposed, the removable inserter handle and the built-in lip on the implant are used to position the patient-specific guide. Next, a central guide pin is placed through the inserter for temporary fixation and further instrumentation. If enough bone is present, a boss reamer can be used over the guide pin to prepare and increase the fixation surface.

Figure 4.
Next, the real implant is placed in the ideal position as defined in the preoperative plan. The implant is fixed provisionally through special guides in the peripheral screw holes (Figures 4A, 4B).

The central 6.5-mm nonlocking compression screw is placed to provide strong initial compressive fixation in best bone.

Figure 5.
Then, in sequence, the temporary fixation pins are removed and are replaced with the 4.75-mm locking or nonlocking screws in the real implant to secure the implant in the planned anatomical position (Figure 5).

With the patient-specific glenoid VRS implant now rigidly fixed in the glenoid, the sized and offset glenosphere is properly positioned, and the reverse SA is completed in routine fashion.

Case Examples

A 49-year-old man underwent hemiarthroplasty for osteoarthritis. The procedure failed and, 3 years later, was revised to conventional total SA. Unfortunately, the cemented all-polyethylene glenoid loosened secondary to active Propionibacterium acnes infection, which required excisional arthroplasty with antibiotic spacer. Significant cavitary bone loss was found with anterior glenoid wall bone loss compromising the glenoid vault. Given the history of bone loss and infection, patient-specific glenoid vault reconstruction was performed after infection eradication. Within 4 years after this surgery, the patient had resumed all activities. At age 57 years, he had restricted active forward elevation and abduction to 120° but was satisfied with the outcome.

Figure 6.
There was no evidence of infection or component loosening, but close monitoring was continued (Figures 6A-6D).

A 71-year-old man underwent reverse SA for rotator cuff-deficient osteoarthritis. After implant excision and spacer placement, he was left with severe soft-tissue deficiency and glenoid bone loss, which caused substantial disability. After treatment for infection, a work-up was performed for glenoid bone deficiency and insertion of a patient-specific glenoid VRS implant.

Figure 7.
Eighteen months after surgery, active range of motion was 130° forward elevation and limited (20°) external rotation (Figures 7A-7D).

Discussion

Glenoid bone deformity and deficiency are among the most difficult challenges in SA—a particularly compelling fact given the increasing number of SAs being performed in younger, more active patients. SA surgeons can now expect to be performing even more revisions with concomitant bone defects, which may be severe in some cases.

In addition to these causes of extreme bone loss, recent awareness of the importance of recognizing and treating bone deficits in osteoarthritis, rheumatoid arthritis, trauma, and instability has led to the development of patient-specific guides, instrumentation, and implants. Concepts from the use of CAD/CAM acetabular implants in total hip arthroplasty for severe acetabular bony defects were applied to the use of patient-specific glenoid reconstruction implants without bone graft augmentation.12 In different form, this idea was reported by Chammaa and colleagues13 in 30 cases, and clinical and durable results were very promising.

We have described use of this technique in 2 extreme cases of glenoid vault deficiency. In each case, short-term results were quite satisfactory. However, both patients were relatively young, and long-term clinical and radiographic follow-up is needed.

Many of the severe cases of glenoid bone loss require an implant that specifically matches the patient’s anatomy. The glenoid VRS implant described here may be of great benefit in these difficult reconstructions and is a valuable addition to the armamentarium of treatments for distorted glenoid anatomy. Eventually, the idea may become useful in treating other, less significant defects by re-creating more-normal biomechanics in SA without bone graft.


Am J Orthop. 2017;46(2):104-108. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.

2. Chan K, Knowles NK, Chaoui J, et al. Characterization of the Walch B3 glenoid in primary osteoarthritis [published online January 11, 2017]. J Shoulder Elbow Surg. doi:10.1016/j.jse.2016.10.003.

3. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.

4. Sears BW, Johnston PS, Ramsay ML, Williams GR. Glenoid bone loss in primary total shoulder arthroplasty: evaluation and management. J Am Acad Orthop Surg. 2012;20(9):604-613.

5. Kocsis G, Thyagarajan DS, Fairbairn KJ, Wallace WA. A new classification of glenoid bone loss to help plan the implantation of a glenoid component before revision arthroplasty of the shoulder. Bone Joint J. 2016;98(3):374-380.

6. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.

7. Seebauer L, Walter W, Keyl W. Reverse total shoulder arthroplasty for the treatment of defect arthropathy [in English, German]. Oper Orthop Traumatol. 2005;17(1):1-24.

8. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012:21(6):765-771.

9. Hill JM, Norris TR. Long-term results of total shoulder arthroplasty following bone-grafting of the glenoid. J Bone Joint Surg Am. 2001;83(6):877-883.

10. Steinmann SP, Cofield RH. Bone grafting for glenoid deficiency in total shoulder replacement. J Shoulder Elbow Surg. 2000;9(5):361-367.

11. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymptomatic posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308.

12. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684.

13. Chammaa R, Uri O, Lambert S. Primary shoulder arthroplasty using a custom-made hip-inspired implant for the treatment of advanced glenohumeral arthritis in the presence of severe glenoid bone loss. J Shoulder Elbow Surg. 2017;26(1):101-107.

References

1. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.

2. Chan K, Knowles NK, Chaoui J, et al. Characterization of the Walch B3 glenoid in primary osteoarthritis [published online January 11, 2017]. J Shoulder Elbow Surg. doi:10.1016/j.jse.2016.10.003.

3. Bercik MJ, Kruse K 2nd, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606.

4. Sears BW, Johnston PS, Ramsay ML, Williams GR. Glenoid bone loss in primary total shoulder arthroplasty: evaluation and management. J Am Acad Orthop Surg. 2012;20(9):604-613.

5. Kocsis G, Thyagarajan DS, Fairbairn KJ, Wallace WA. A new classification of glenoid bone loss to help plan the implantation of a glenoid component before revision arthroplasty of the shoulder. Bone Joint J. 2016;98(3):374-380.

6. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.

7. Seebauer L, Walter W, Keyl W. Reverse total shoulder arthroplasty for the treatment of defect arthropathy [in English, German]. Oper Orthop Traumatol. 2005;17(1):1-24.

8. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012:21(6):765-771.

9. Hill JM, Norris TR. Long-term results of total shoulder arthroplasty following bone-grafting of the glenoid. J Bone Joint Surg Am. 2001;83(6):877-883.

10. Steinmann SP, Cofield RH. Bone grafting for glenoid deficiency in total shoulder replacement. J Shoulder Elbow Surg. 2000;9(5):361-367.

11. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymptomatic posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308.

12. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684.

13. Chammaa R, Uri O, Lambert S. Primary shoulder arthroplasty using a custom-made hip-inspired implant for the treatment of advanced glenohumeral arthritis in the presence of severe glenoid bone loss. J Shoulder Elbow Surg. 2017;26(1):101-107.

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Novel Solution for Massive Glenoid Defects in Shoulder Arthroplasty: A Patient-Specific Glenoid Vault Reconstruction System
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Management of Proximal Biceps Pathology in Overhead Athletes: What Is the Role of Biceps Tenodesis?

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Management of Proximal Biceps Pathology in Overhead Athletes: What Is the Role of Biceps Tenodesis?

Take Home Points

  • Outcomes after SLAP repair remain guarded.
  • Physical examination is key in determining proper management of biceps pathology.
  • When performing SLAP repair, knotless technology may prevent future cartilage or rotator cuff injury.
  • Revision of SLAP repair is best handled with biceps tenodesis.
  • Subpectoral biceps tenodesis avoids residual groove pain.

In recent decades, the long head of the biceps (LHB) tendon has been recognized as a pain generator in the shoulder of throwing athletes. The LHB muscle and its role in glenohumeral kinematics remains largely in question. The LHB tendon varies in size but most commonly is 5 mm to 6mm in diameter and about 9 cm in length, inserting on the superior labrum and supraglenoid tubercle after traveling through the bicipital groove.1 The many conditions that can develop along the course of the biceps tendon include overall biceps tendonitis, biceps tendon subluxation or instability, and injuries to the superior anterior to posterior area of the labrum.

These injuries can occur in young overhead athletes as well as manual laborers and older overhead recreational athletes. Pitching is the most common activity that leads to proximal biceps tendon disorders. The 6 phases of the pitch are linked in a kinetic chain that generates energy that is then translated to high velocity. The amount of force that is exerted on the shoulder during pitching and especially after ball release is impressive, and the athlete’s shoulder changes in many ways as it adapts to the motion.2-5 The late-cocking and deceleration phases are most commonly associated with proximal biceps pathology and the “peel-back” phenomenon. Other common activities that lead to biceps tendon issues in a young population are volleyball, baseball, tennis, softball, swimming, and cricket. Shoulder arthroscopies performed in older patients show degenerative biceps and labrum tears, which should be treated appropriately but perhaps different from how they are treated in overhead athletes.6-8 Further, many professional athletes have asymptomatic superior labrum anterior-posterior (SLAP) tears.9

Mechanism of Injury

Overhead throwing is commonly thought to be the mechanism by which lesions are created in the biceps–labrum complex (BLC). Pitching in particular generates incredible force and torque within the shoulder. In professional pitchers, the resulting throwing speed creates forces regularly in excess of 1000 N.3 These forces effect internal compensatory changes and internal derangement of the BLC. These changes often involve internal rotation deficits and alterations in the rotator cuff, which may contribute to glenohumeral instability and altered joint kinematics.10

Repetitive overhead activity is largely considered the mechanism of injury in this population, though more specific mechanisms have been described, including the peel-back mechanism11 and the posterior superior glenoid impingement. There is little evidence that preventive programs have any effect on decreasing the incidence of SLAP tears in overhead athletes.

Preoperative Evaluation

Preoperative evaluation is arguably the most important step in treating a patient with persistent or recurrent symptoms consistent with a SLAP tear. Evaluation includes thorough history, physical examination, and review of any prior injuries or surgical procedures. The physical examination should focus on maneuvers that define where the problem is occurring. Although SLAP tears are most common in this population, disorders of the biceps tendon within the groove, including inflammation and instability, should be ruled out with physical examination and advanced imaging. Palpation for groove tenderness, impingement-type complaints, internal rotation loss, and SLAP provocative testing are crucial in the diagnosis.12,13 The cause of symptoms may be multifactorial and include the often encountered concomitant pathology of rotator cuff tears, internal impingement, and instability.

Standard radiographs (Grashey anteroposterior, scapular/lateral, axillary lateral) and magnetic resonance imaging (MRI) with or without arthrography can be helpful in identifying and characterizing most SLAP tears as well as failed SLAP tear repairs. However, MRI is often positive for SLAP tears in asymptomatic patients, and diagnosing SLAP tears with MRI is often a challenge.14 MRI can help in determining concomitant pathology, including rotator cuff injury and cysts causing nerve compression. Correlation with clinical examination and patient history is most crucial. Conservative treatment (rest, activity modification, use of oral anti-inflammatory medications) typically is attempted and coordinated with respect to the athlete’s season of play.15,16

Classification

In overhead throwing athletes, SLAP tears typically are associated with anterior shoulder pain. Associated shoulder instability and significant glenohumeral dysfunction are not uncommon in athletes with lesions of the BLC. In 1985, Andrews and colleagues17 were the first to describe SLAP tears in overhead athletes (73 patients). Later, Snyder and colleagues18,19 further classified these lesions into 4 types based on tear stability and location, and they coined the acronym SLAP (Figure 1).

Figure 1.
Morgan and colleagues20 subclassified type II lesions into 3 groups based on location (anterior SLAP, posterior SLAP, and combined SLAP tear).

 

 

Type I lesions typically are described as fraying at the inner margin of the labrum and are common in throwers, even asymptomatic throwers. Type II lesions, separations of the biceps and labrum from the superior glenoid (≥5 mm of excursion), are the most commonly occurring and treated variant in throwing athletes.20-22 Intraoperative evaluation for a peel-back lesion (placing the arm in abduction with external rotation), rather than for a sulcus of 1 mm to 2 mm, may confirm a type II SLAP tear.20,23,24 It is often important to consider the direction of tear propagation as well. Type III lesions include those with an intact BLC (but with a bucket-handle tear of the superior labral complex and an intact biceps tendon), whereas type IV lesions involve additional extension of the tear into the biceps tendon.18,19The classification systems are well defined. Nevertheless, management of SLAP lesions remains controversial.

Options for Surgical Treatment

SLAP Tear Repair—Outcomes

The incidence of SLAP tear repairs has increased dramatically in recent years.6,25 There are various SLAP tear repair methods, but the most common consists of repairing the labrum and biceps anchor. Management of type II SLAP lesions remains controversial. Several prospective studies have found overall improvement after SLAP tear repair.26-31 Other series have reported less encouraging outcomes, including dissatisfaction with persistent pain and inability to return to throwing.28,32 A 2010 systematic review found that the percentage of patients who returned to their preinjury level of play was only 64%, and outcomes for overhead throwing athletes were even worse—only 22% to 60% of these patients returned to their previous level.33 The right surgery for SLAP tears in this population continues to be an area of uncertainty for many surgeons.

Failed SLAP tear repairs (poor outcomes) have become common in overhead throwing athletes. The reasons for these failed repairs are unclear, but several possible explanations have been offered. One is that labral repair may result in permanent alterations in pitching biomechanics, which may lead to an inability to regain velocity and command.3 Another is that the athlete’s shoulder may remain unstable even after repair.10Hardware complications are a significant concern in this high-level population. Suture anchor pullout or iatrogenic cartilage damage may occur during instrumentation or as a result of suture anchor reactive changes. In addition, there are several reports of glenoid osteochondrolysis (Figure 2) caused by prominent hardware or prominent knots.34-39

Figure 2.
Intra-articular hardware concerns aside, lack of healing is another reason for failed SLAP tear repairs, as the vascular supply to the superior labrum is scarce near the biceps attachment, where shear forces are high.38,40,41 The intra-articular portion of the biceps tendon, as well as the portion within the bicipital groove, contains sensory fibers, which may become the source of persistent pain and inflammation after SLAP tear repair.24,42,43
Figure 3.
Several studies have reported this phenomenon (Figure 3), leading some authors to perform primary biceps tenodesis in an attempt to avoid revision surgery.42,44-47

Stiffness after SLAP tear repair is a significant problem, with most patients taking up to 6 months to regain full motion.26,48 Overtensioning of the labrum and the glenohumeral ligaments may be the cause, and the solution may be to place anchors posterior (vs anterior) to the biceps insertion. In a large prospective military study, mean forward flexion and external rotation were reduced at final follow-up.31 These outcomes are less acceptable to overhead throwing athletes, who rely on motion for high-end throwing activities.

Primary Biceps Tenodesis—Outcomes

A 2015 database study found a 1.7-fold increase in biceps tenodesis over the preceding 5 years.49 However, relatively few procedures included in the study were performed in patients age younger than 30 years. For many older non-overhead throwers with type II tears, SLAP tear repair has become less popular as a treatment option.32 There is a dearth of knowledge about the outcomes of subpectoral biceps tenodesis as a primary treatment for biceps tendonitis and an associated SLAP tear. Although type I tears historically have been treated with débridement, débridement is seldom used for concomitant biceps tendonitis. It should be coupled with careful clinical examination.

In recent years, biceps tenodesis has been proposed as an alternative to repair for SLAP tears, particularly in older patients.24,44 For obvious reasons, however, there has been some trepidation about performing biceps tenodesis in throwing athletes. Some authors have proposed biceps tenodesis as primary treatment for isolated SLAP tears. Boileau and colleagues44 compared the outcomes of treatment of isolated type II SLAP lesions in 25 consecutive patients. For 10 patients, repair involved suture anchors; for the other 15, arthroscopic biceps tenodesis was performed with an absorbable interference screw. Six of the 10 suture anchor patients were disappointed with their outcome (persistent pain or inability to return to sport), whereas 14 of the 15 biceps tenodesis patients were satisfied. The authors concluded that arthroscopic biceps tenodesis is an effective alternative to repair for type II SLAP lesions, though their study was not isolated to overhead athletes (tenodesis group mean age, 52 years).

In a 2014 series of cases, Ek and colleagues50 reported good outcomes of SLAP tear repair and biceps tenodesis. Again, though, tenodesis was used in older patients, and repair in younger, more active patients, with no high-level athletes in either group. There was no difference in return to sport between groups. In a study of patients who underwent primary biceps tenodesis, Gupta and colleagues51 found 80% excellent outcomes (improved shoulder outcome scores) in select SLAP tear patients, including 8 athletes, 88% of whom were overhead athletes. Gottschalk and colleagues52 reported on differences in prospectively collected outcome data (age, sex, SLAP lesion type II or IV) for primary biceps tenodesis in a series of 33 patients. Twenty-six of the 29 patients who completed follow-up returned to their previous level of activity. These studies suggest that primary biceps tenodesis may be an alternative with lower failure rates in the treatment of SLAP tears in middle-aged patients, and in overhead athletes, though additional specific studies are needed to focus on overhead athletes on a larger scale.

 

 

Revision SLAP Tear Repair Versus Biceps Tenodesis

Failed arthroscopic SLAP tear repairs, which are increasingly common, present a unique treatment challenge. In a 2013 prospective cohort series, Gupta and colleagues46 found excellent clinical outcomes of subpectoral biceps tenodesis for failed type II SLAP tears. The authors reported a postoperative SANE (Single Assessment Numeric Evaluation) score of 70.4%, an SST (Simple Shoulder Test) score of 9.33, and an ASES (American Shoulder and Elbow Surgeons) score of 77.96, along with reasonable health-related quality-of-life scores. Werner and colleagues53 evaluated 2-year outcomes of biceps tenodesis performed after SLAP tear repair in 24 patients and found a return to almost normal range of motion as well as good clinical outcome scores. Significantly worse outcomes were found for patients with open worker’s compensation claims.

McCormick and colleagues26 prospectively evaluated the efficacy of biceps tenodesis for failed type II SLAP tear repair in 46 patients. Improvement was noted across all outcome assessments during follow-up (mean, 3.6 years). From these findings, we might conclude that biceps tenodesis is a more predictable option for failed SLAP tear repair, and that it has a relatively low complication rate. However, most investigators have used a heterogeneous patient population, as opposed to overhead athletes specifically. To our knowledge, no one has evaluated the specific population of overhead throwers with failed SLAP tear repairs. In addition, no one has conducted randomized controlled trials comparing débridement, biceps tenodesis, and repair for failed SLAP tear repairs.

Postoperative Considerations

When overhead athletes and their surgeons are considering surgical options, they must take rehabilitation and return to play into account. Many surgeons think the possible marginal clinical benefit of SLAP tear repair may not be worth the protracted rehabilitation. In most practices, rehabilitation after biceps tenodesis is less involved. Discussing the advantages and disadvantages of these 2 procedures can be helpful in decision making.

Dein and colleagues54 reported the case of a middle-aged pitcher who sustained a fracture after biceps tenodesis with an interference screw. Cases like this are concerning. Surgeons should consider altering the rehabilitation regimen when planning postoperative care in cases of biceps tenodesis in throwers. Other reported complications of open tenodesis are deep infection, thrombosis, postoperative stiffness, and nerve injury.55-58

Consequences for Overhead Throwers

The unknown role of the BLC leaves surgeons wary when considering biceps tenodesis for elite athletes. Some have postulated that removing the intra-articular portion of the LHB may cause microinstability and alter joint kinematics.10,59-61 Others have suggested the biceps is desynchronized from the other musculature and is not functionally important.62 Disruption of one portion of the superior labrum may result in instability on the opposite side of the glenoid.10,61 Biomechanical studies, both cadaveric and in vivo, have tried to create proper loads to the LHB and evaluate the kinematics of the shoulder before and after biceps tenodesis and SLAP tear repair.59,60 Using a cadaveric model, Strauss and colleagues63 found that type II SLAP lesions resulted in increased glenohumeral translation compared with baseline. Biceps tenodesis did not restore normal translation, but this did not negatively affect stability in the presence of a SLAP lesion. The consensus is that the role of the biceps is controversial at best.

Several studies have used electromyography (EMG) to evaluate LHB functioning. In 2014, Chalmers and colleagues59 used surface EMG and motion analysis to evaluate 18 pitchers: 6 underwent SLAP tear repair, 5 underwent biceps tenodesis, and 7 were uninjured controls. There were no significant differences in the activity of the LHB muscle, the short head of the biceps muscle, the deltoid, the infraspinatus, or the latissimus among the 3 groups. Motion analysis showed that the normal pattern of muscular activation within the LHB muscle was more closely restored by biceps tenodesis than by SLAP tear repair. In addition, thoracic rotation patterns were significantly more altered in the SLAP tear repair patients than in the uninjured controls. As the authors noted, given the low frequency with which biceps tenodesis is performed in overhead athletes, it is unlikely that larger scale studies will be conducted without a multicenter effort.

Recommendations and Our Preferred Technique

Which surgical option is best for treating symptomatic SLAP lesions in overhead athletes remains unclear. Many athletes struggle to return to high-level play after SLAP tear repair. Whether the same is true after biceps tenodesis is yet to be determined because of the low frequency with which biceps tenodesis is performed in high-level overhead athletes. The options for fixation, technique, and fixation location are equally broad. In this section, we outline our general line of thinking for cases of proximal biceps pathology.

 

 

In each case, we perform glenohumeral arthroscopy to evaluate the BLC and identify any other pathology. For overhead athletes who are younger than 30 years and lack bicipital groove pain or signs of gross tendinopathy, we favor arthroscopic SLAP tear repair. Repair is usually performed through an anterior working portal for suture passage and a Wilmington portal for anchor placement. We use knotless technology to achieve stable fixation and stay posterior to the biceps anchor insertion.

For the prevention of any potential pain from the bicipital groove in carefully selected patients—recreational overhead athletes and patients who want a less involved surgical recovery—we favor open subpectoral biceps tenodesis rather than arthroscopic tenodesis. The outcomes of biceps tenodesis are consistent, according to the literature.47,57,64 Moreover, the open approach is favored for the incidence of postoperative stiffness in the arthroscopic population.65 Tendons can be fixed with multiple procedures, including soft-tissue tenodesis, interference screw fixation, and surface anchors. We favor using a tenodesis screw in the subpectoral location, as outlined by Mazzocca and colleagues.64Our algorithm for SLAP lesions is evolving with our understanding of this complex disease process. For young overhead throwers with type II SLAP lesions, we favor arthroscopic SLAP tear repair with knotless technology. For older recreational overhead athletes, we favor biceps tenodesis in the subpectoral region after diagnostic arthroscopy plus biceps tenotomy with or without additional SLAP tear fixation, depending on the stability of the biceps anchor (Figures 4A, 4B).

Figure 4.
In this procedure, a unicortical hole is drilled in the center of the bicipital groove, with careful attention given to restoring the anatomical length–tension relationship.66 For revision of SLAP tear repair, we recommend revision to a biceps tenodesis using our published technique.57,67 Postoperative rehabilitation is crucial, as failure to return to play may stem from poor throwing mechanics rather than from the surgical fixation technique used.

Conclusion

Overhead athletes who present with symptomatic SLAP lesions often provide a treatment dilemma. Although SLAP tear repair historically has been standard treatment, biceps tenodesis represents a consistent surgical option with low complication rates and low revision rates. It is likely that, as additional data on glenohumeral kinematics and outcomes in young athletes become available, improved decision-making algorithms will follow.

Am J Orthop. 2017;46(1):E71-E78. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

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Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Romeo reports that he receives royalties from Arthrex and Elsevier; is a consultant for Arthrex; receives research support from Arthrex, Smith & Nephew, Össur, MioMed Orthopaedics, DJO Global, ConMed Linvatec, and Athletico; is on the editorial board of Orthopedics Today, Journal of Shoulder and Elbow Surgery, Techniques in Shoulder and Elbow Surgery, Operative Techniques in Sports Medicine, Sports Health, and Orthopedics; and receives publisher support from Elsevier and Orthopedics Today. The other authors report no actual or potential conflict of interest in relation to this article.

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The American Journal of Orthopedics - 46(1)
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Authors’ Disclosure Statement: Dr. Romeo reports that he receives royalties from Arthrex and Elsevier; is a consultant for Arthrex; receives research support from Arthrex, Smith & Nephew, Össur, MioMed Orthopaedics, DJO Global, ConMed Linvatec, and Athletico; is on the editorial board of Orthopedics Today, Journal of Shoulder and Elbow Surgery, Techniques in Shoulder and Elbow Surgery, Operative Techniques in Sports Medicine, Sports Health, and Orthopedics; and receives publisher support from Elsevier and Orthopedics Today. The other authors report no actual or potential conflict of interest in relation to this article.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr. Romeo reports that he receives royalties from Arthrex and Elsevier; is a consultant for Arthrex; receives research support from Arthrex, Smith & Nephew, Össur, MioMed Orthopaedics, DJO Global, ConMed Linvatec, and Athletico; is on the editorial board of Orthopedics Today, Journal of Shoulder and Elbow Surgery, Techniques in Shoulder and Elbow Surgery, Operative Techniques in Sports Medicine, Sports Health, and Orthopedics; and receives publisher support from Elsevier and Orthopedics Today. The other authors report no actual or potential conflict of interest in relation to this article.

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Take Home Points

  • Outcomes after SLAP repair remain guarded.
  • Physical examination is key in determining proper management of biceps pathology.
  • When performing SLAP repair, knotless technology may prevent future cartilage or rotator cuff injury.
  • Revision of SLAP repair is best handled with biceps tenodesis.
  • Subpectoral biceps tenodesis avoids residual groove pain.

In recent decades, the long head of the biceps (LHB) tendon has been recognized as a pain generator in the shoulder of throwing athletes. The LHB muscle and its role in glenohumeral kinematics remains largely in question. The LHB tendon varies in size but most commonly is 5 mm to 6mm in diameter and about 9 cm in length, inserting on the superior labrum and supraglenoid tubercle after traveling through the bicipital groove.1 The many conditions that can develop along the course of the biceps tendon include overall biceps tendonitis, biceps tendon subluxation or instability, and injuries to the superior anterior to posterior area of the labrum.

These injuries can occur in young overhead athletes as well as manual laborers and older overhead recreational athletes. Pitching is the most common activity that leads to proximal biceps tendon disorders. The 6 phases of the pitch are linked in a kinetic chain that generates energy that is then translated to high velocity. The amount of force that is exerted on the shoulder during pitching and especially after ball release is impressive, and the athlete’s shoulder changes in many ways as it adapts to the motion.2-5 The late-cocking and deceleration phases are most commonly associated with proximal biceps pathology and the “peel-back” phenomenon. Other common activities that lead to biceps tendon issues in a young population are volleyball, baseball, tennis, softball, swimming, and cricket. Shoulder arthroscopies performed in older patients show degenerative biceps and labrum tears, which should be treated appropriately but perhaps different from how they are treated in overhead athletes.6-8 Further, many professional athletes have asymptomatic superior labrum anterior-posterior (SLAP) tears.9

Mechanism of Injury

Overhead throwing is commonly thought to be the mechanism by which lesions are created in the biceps–labrum complex (BLC). Pitching in particular generates incredible force and torque within the shoulder. In professional pitchers, the resulting throwing speed creates forces regularly in excess of 1000 N.3 These forces effect internal compensatory changes and internal derangement of the BLC. These changes often involve internal rotation deficits and alterations in the rotator cuff, which may contribute to glenohumeral instability and altered joint kinematics.10

Repetitive overhead activity is largely considered the mechanism of injury in this population, though more specific mechanisms have been described, including the peel-back mechanism11 and the posterior superior glenoid impingement. There is little evidence that preventive programs have any effect on decreasing the incidence of SLAP tears in overhead athletes.

Preoperative Evaluation

Preoperative evaluation is arguably the most important step in treating a patient with persistent or recurrent symptoms consistent with a SLAP tear. Evaluation includes thorough history, physical examination, and review of any prior injuries or surgical procedures. The physical examination should focus on maneuvers that define where the problem is occurring. Although SLAP tears are most common in this population, disorders of the biceps tendon within the groove, including inflammation and instability, should be ruled out with physical examination and advanced imaging. Palpation for groove tenderness, impingement-type complaints, internal rotation loss, and SLAP provocative testing are crucial in the diagnosis.12,13 The cause of symptoms may be multifactorial and include the often encountered concomitant pathology of rotator cuff tears, internal impingement, and instability.

Standard radiographs (Grashey anteroposterior, scapular/lateral, axillary lateral) and magnetic resonance imaging (MRI) with or without arthrography can be helpful in identifying and characterizing most SLAP tears as well as failed SLAP tear repairs. However, MRI is often positive for SLAP tears in asymptomatic patients, and diagnosing SLAP tears with MRI is often a challenge.14 MRI can help in determining concomitant pathology, including rotator cuff injury and cysts causing nerve compression. Correlation with clinical examination and patient history is most crucial. Conservative treatment (rest, activity modification, use of oral anti-inflammatory medications) typically is attempted and coordinated with respect to the athlete’s season of play.15,16

Classification

In overhead throwing athletes, SLAP tears typically are associated with anterior shoulder pain. Associated shoulder instability and significant glenohumeral dysfunction are not uncommon in athletes with lesions of the BLC. In 1985, Andrews and colleagues17 were the first to describe SLAP tears in overhead athletes (73 patients). Later, Snyder and colleagues18,19 further classified these lesions into 4 types based on tear stability and location, and they coined the acronym SLAP (Figure 1).

Figure 1.
Morgan and colleagues20 subclassified type II lesions into 3 groups based on location (anterior SLAP, posterior SLAP, and combined SLAP tear).

 

 

Type I lesions typically are described as fraying at the inner margin of the labrum and are common in throwers, even asymptomatic throwers. Type II lesions, separations of the biceps and labrum from the superior glenoid (≥5 mm of excursion), are the most commonly occurring and treated variant in throwing athletes.20-22 Intraoperative evaluation for a peel-back lesion (placing the arm in abduction with external rotation), rather than for a sulcus of 1 mm to 2 mm, may confirm a type II SLAP tear.20,23,24 It is often important to consider the direction of tear propagation as well. Type III lesions include those with an intact BLC (but with a bucket-handle tear of the superior labral complex and an intact biceps tendon), whereas type IV lesions involve additional extension of the tear into the biceps tendon.18,19The classification systems are well defined. Nevertheless, management of SLAP lesions remains controversial.

Options for Surgical Treatment

SLAP Tear Repair—Outcomes

The incidence of SLAP tear repairs has increased dramatically in recent years.6,25 There are various SLAP tear repair methods, but the most common consists of repairing the labrum and biceps anchor. Management of type II SLAP lesions remains controversial. Several prospective studies have found overall improvement after SLAP tear repair.26-31 Other series have reported less encouraging outcomes, including dissatisfaction with persistent pain and inability to return to throwing.28,32 A 2010 systematic review found that the percentage of patients who returned to their preinjury level of play was only 64%, and outcomes for overhead throwing athletes were even worse—only 22% to 60% of these patients returned to their previous level.33 The right surgery for SLAP tears in this population continues to be an area of uncertainty for many surgeons.

Failed SLAP tear repairs (poor outcomes) have become common in overhead throwing athletes. The reasons for these failed repairs are unclear, but several possible explanations have been offered. One is that labral repair may result in permanent alterations in pitching biomechanics, which may lead to an inability to regain velocity and command.3 Another is that the athlete’s shoulder may remain unstable even after repair.10Hardware complications are a significant concern in this high-level population. Suture anchor pullout or iatrogenic cartilage damage may occur during instrumentation or as a result of suture anchor reactive changes. In addition, there are several reports of glenoid osteochondrolysis (Figure 2) caused by prominent hardware or prominent knots.34-39

Figure 2.
Intra-articular hardware concerns aside, lack of healing is another reason for failed SLAP tear repairs, as the vascular supply to the superior labrum is scarce near the biceps attachment, where shear forces are high.38,40,41 The intra-articular portion of the biceps tendon, as well as the portion within the bicipital groove, contains sensory fibers, which may become the source of persistent pain and inflammation after SLAP tear repair.24,42,43
Figure 3.
Several studies have reported this phenomenon (Figure 3), leading some authors to perform primary biceps tenodesis in an attempt to avoid revision surgery.42,44-47

Stiffness after SLAP tear repair is a significant problem, with most patients taking up to 6 months to regain full motion.26,48 Overtensioning of the labrum and the glenohumeral ligaments may be the cause, and the solution may be to place anchors posterior (vs anterior) to the biceps insertion. In a large prospective military study, mean forward flexion and external rotation were reduced at final follow-up.31 These outcomes are less acceptable to overhead throwing athletes, who rely on motion for high-end throwing activities.

Primary Biceps Tenodesis—Outcomes

A 2015 database study found a 1.7-fold increase in biceps tenodesis over the preceding 5 years.49 However, relatively few procedures included in the study were performed in patients age younger than 30 years. For many older non-overhead throwers with type II tears, SLAP tear repair has become less popular as a treatment option.32 There is a dearth of knowledge about the outcomes of subpectoral biceps tenodesis as a primary treatment for biceps tendonitis and an associated SLAP tear. Although type I tears historically have been treated with débridement, débridement is seldom used for concomitant biceps tendonitis. It should be coupled with careful clinical examination.

In recent years, biceps tenodesis has been proposed as an alternative to repair for SLAP tears, particularly in older patients.24,44 For obvious reasons, however, there has been some trepidation about performing biceps tenodesis in throwing athletes. Some authors have proposed biceps tenodesis as primary treatment for isolated SLAP tears. Boileau and colleagues44 compared the outcomes of treatment of isolated type II SLAP lesions in 25 consecutive patients. For 10 patients, repair involved suture anchors; for the other 15, arthroscopic biceps tenodesis was performed with an absorbable interference screw. Six of the 10 suture anchor patients were disappointed with their outcome (persistent pain or inability to return to sport), whereas 14 of the 15 biceps tenodesis patients were satisfied. The authors concluded that arthroscopic biceps tenodesis is an effective alternative to repair for type II SLAP lesions, though their study was not isolated to overhead athletes (tenodesis group mean age, 52 years).

In a 2014 series of cases, Ek and colleagues50 reported good outcomes of SLAP tear repair and biceps tenodesis. Again, though, tenodesis was used in older patients, and repair in younger, more active patients, with no high-level athletes in either group. There was no difference in return to sport between groups. In a study of patients who underwent primary biceps tenodesis, Gupta and colleagues51 found 80% excellent outcomes (improved shoulder outcome scores) in select SLAP tear patients, including 8 athletes, 88% of whom were overhead athletes. Gottschalk and colleagues52 reported on differences in prospectively collected outcome data (age, sex, SLAP lesion type II or IV) for primary biceps tenodesis in a series of 33 patients. Twenty-six of the 29 patients who completed follow-up returned to their previous level of activity. These studies suggest that primary biceps tenodesis may be an alternative with lower failure rates in the treatment of SLAP tears in middle-aged patients, and in overhead athletes, though additional specific studies are needed to focus on overhead athletes on a larger scale.

 

 

Revision SLAP Tear Repair Versus Biceps Tenodesis

Failed arthroscopic SLAP tear repairs, which are increasingly common, present a unique treatment challenge. In a 2013 prospective cohort series, Gupta and colleagues46 found excellent clinical outcomes of subpectoral biceps tenodesis for failed type II SLAP tears. The authors reported a postoperative SANE (Single Assessment Numeric Evaluation) score of 70.4%, an SST (Simple Shoulder Test) score of 9.33, and an ASES (American Shoulder and Elbow Surgeons) score of 77.96, along with reasonable health-related quality-of-life scores. Werner and colleagues53 evaluated 2-year outcomes of biceps tenodesis performed after SLAP tear repair in 24 patients and found a return to almost normal range of motion as well as good clinical outcome scores. Significantly worse outcomes were found for patients with open worker’s compensation claims.

McCormick and colleagues26 prospectively evaluated the efficacy of biceps tenodesis for failed type II SLAP tear repair in 46 patients. Improvement was noted across all outcome assessments during follow-up (mean, 3.6 years). From these findings, we might conclude that biceps tenodesis is a more predictable option for failed SLAP tear repair, and that it has a relatively low complication rate. However, most investigators have used a heterogeneous patient population, as opposed to overhead athletes specifically. To our knowledge, no one has evaluated the specific population of overhead throwers with failed SLAP tear repairs. In addition, no one has conducted randomized controlled trials comparing débridement, biceps tenodesis, and repair for failed SLAP tear repairs.

Postoperative Considerations

When overhead athletes and their surgeons are considering surgical options, they must take rehabilitation and return to play into account. Many surgeons think the possible marginal clinical benefit of SLAP tear repair may not be worth the protracted rehabilitation. In most practices, rehabilitation after biceps tenodesis is less involved. Discussing the advantages and disadvantages of these 2 procedures can be helpful in decision making.

Dein and colleagues54 reported the case of a middle-aged pitcher who sustained a fracture after biceps tenodesis with an interference screw. Cases like this are concerning. Surgeons should consider altering the rehabilitation regimen when planning postoperative care in cases of biceps tenodesis in throwers. Other reported complications of open tenodesis are deep infection, thrombosis, postoperative stiffness, and nerve injury.55-58

Consequences for Overhead Throwers

The unknown role of the BLC leaves surgeons wary when considering biceps tenodesis for elite athletes. Some have postulated that removing the intra-articular portion of the LHB may cause microinstability and alter joint kinematics.10,59-61 Others have suggested the biceps is desynchronized from the other musculature and is not functionally important.62 Disruption of one portion of the superior labrum may result in instability on the opposite side of the glenoid.10,61 Biomechanical studies, both cadaveric and in vivo, have tried to create proper loads to the LHB and evaluate the kinematics of the shoulder before and after biceps tenodesis and SLAP tear repair.59,60 Using a cadaveric model, Strauss and colleagues63 found that type II SLAP lesions resulted in increased glenohumeral translation compared with baseline. Biceps tenodesis did not restore normal translation, but this did not negatively affect stability in the presence of a SLAP lesion. The consensus is that the role of the biceps is controversial at best.

Several studies have used electromyography (EMG) to evaluate LHB functioning. In 2014, Chalmers and colleagues59 used surface EMG and motion analysis to evaluate 18 pitchers: 6 underwent SLAP tear repair, 5 underwent biceps tenodesis, and 7 were uninjured controls. There were no significant differences in the activity of the LHB muscle, the short head of the biceps muscle, the deltoid, the infraspinatus, or the latissimus among the 3 groups. Motion analysis showed that the normal pattern of muscular activation within the LHB muscle was more closely restored by biceps tenodesis than by SLAP tear repair. In addition, thoracic rotation patterns were significantly more altered in the SLAP tear repair patients than in the uninjured controls. As the authors noted, given the low frequency with which biceps tenodesis is performed in overhead athletes, it is unlikely that larger scale studies will be conducted without a multicenter effort.

Recommendations and Our Preferred Technique

Which surgical option is best for treating symptomatic SLAP lesions in overhead athletes remains unclear. Many athletes struggle to return to high-level play after SLAP tear repair. Whether the same is true after biceps tenodesis is yet to be determined because of the low frequency with which biceps tenodesis is performed in high-level overhead athletes. The options for fixation, technique, and fixation location are equally broad. In this section, we outline our general line of thinking for cases of proximal biceps pathology.

 

 

In each case, we perform glenohumeral arthroscopy to evaluate the BLC and identify any other pathology. For overhead athletes who are younger than 30 years and lack bicipital groove pain or signs of gross tendinopathy, we favor arthroscopic SLAP tear repair. Repair is usually performed through an anterior working portal for suture passage and a Wilmington portal for anchor placement. We use knotless technology to achieve stable fixation and stay posterior to the biceps anchor insertion.

For the prevention of any potential pain from the bicipital groove in carefully selected patients—recreational overhead athletes and patients who want a less involved surgical recovery—we favor open subpectoral biceps tenodesis rather than arthroscopic tenodesis. The outcomes of biceps tenodesis are consistent, according to the literature.47,57,64 Moreover, the open approach is favored for the incidence of postoperative stiffness in the arthroscopic population.65 Tendons can be fixed with multiple procedures, including soft-tissue tenodesis, interference screw fixation, and surface anchors. We favor using a tenodesis screw in the subpectoral location, as outlined by Mazzocca and colleagues.64Our algorithm for SLAP lesions is evolving with our understanding of this complex disease process. For young overhead throwers with type II SLAP lesions, we favor arthroscopic SLAP tear repair with knotless technology. For older recreational overhead athletes, we favor biceps tenodesis in the subpectoral region after diagnostic arthroscopy plus biceps tenotomy with or without additional SLAP tear fixation, depending on the stability of the biceps anchor (Figures 4A, 4B).

Figure 4.
In this procedure, a unicortical hole is drilled in the center of the bicipital groove, with careful attention given to restoring the anatomical length–tension relationship.66 For revision of SLAP tear repair, we recommend revision to a biceps tenodesis using our published technique.57,67 Postoperative rehabilitation is crucial, as failure to return to play may stem from poor throwing mechanics rather than from the surgical fixation technique used.

Conclusion

Overhead athletes who present with symptomatic SLAP lesions often provide a treatment dilemma. Although SLAP tear repair historically has been standard treatment, biceps tenodesis represents a consistent surgical option with low complication rates and low revision rates. It is likely that, as additional data on glenohumeral kinematics and outcomes in young athletes become available, improved decision-making algorithms will follow.

Am J Orthop. 2017;46(1):E71-E78. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

Take Home Points

  • Outcomes after SLAP repair remain guarded.
  • Physical examination is key in determining proper management of biceps pathology.
  • When performing SLAP repair, knotless technology may prevent future cartilage or rotator cuff injury.
  • Revision of SLAP repair is best handled with biceps tenodesis.
  • Subpectoral biceps tenodesis avoids residual groove pain.

In recent decades, the long head of the biceps (LHB) tendon has been recognized as a pain generator in the shoulder of throwing athletes. The LHB muscle and its role in glenohumeral kinematics remains largely in question. The LHB tendon varies in size but most commonly is 5 mm to 6mm in diameter and about 9 cm in length, inserting on the superior labrum and supraglenoid tubercle after traveling through the bicipital groove.1 The many conditions that can develop along the course of the biceps tendon include overall biceps tendonitis, biceps tendon subluxation or instability, and injuries to the superior anterior to posterior area of the labrum.

These injuries can occur in young overhead athletes as well as manual laborers and older overhead recreational athletes. Pitching is the most common activity that leads to proximal biceps tendon disorders. The 6 phases of the pitch are linked in a kinetic chain that generates energy that is then translated to high velocity. The amount of force that is exerted on the shoulder during pitching and especially after ball release is impressive, and the athlete’s shoulder changes in many ways as it adapts to the motion.2-5 The late-cocking and deceleration phases are most commonly associated with proximal biceps pathology and the “peel-back” phenomenon. Other common activities that lead to biceps tendon issues in a young population are volleyball, baseball, tennis, softball, swimming, and cricket. Shoulder arthroscopies performed in older patients show degenerative biceps and labrum tears, which should be treated appropriately but perhaps different from how they are treated in overhead athletes.6-8 Further, many professional athletes have asymptomatic superior labrum anterior-posterior (SLAP) tears.9

Mechanism of Injury

Overhead throwing is commonly thought to be the mechanism by which lesions are created in the biceps–labrum complex (BLC). Pitching in particular generates incredible force and torque within the shoulder. In professional pitchers, the resulting throwing speed creates forces regularly in excess of 1000 N.3 These forces effect internal compensatory changes and internal derangement of the BLC. These changes often involve internal rotation deficits and alterations in the rotator cuff, which may contribute to glenohumeral instability and altered joint kinematics.10

Repetitive overhead activity is largely considered the mechanism of injury in this population, though more specific mechanisms have been described, including the peel-back mechanism11 and the posterior superior glenoid impingement. There is little evidence that preventive programs have any effect on decreasing the incidence of SLAP tears in overhead athletes.

Preoperative Evaluation

Preoperative evaluation is arguably the most important step in treating a patient with persistent or recurrent symptoms consistent with a SLAP tear. Evaluation includes thorough history, physical examination, and review of any prior injuries or surgical procedures. The physical examination should focus on maneuvers that define where the problem is occurring. Although SLAP tears are most common in this population, disorders of the biceps tendon within the groove, including inflammation and instability, should be ruled out with physical examination and advanced imaging. Palpation for groove tenderness, impingement-type complaints, internal rotation loss, and SLAP provocative testing are crucial in the diagnosis.12,13 The cause of symptoms may be multifactorial and include the often encountered concomitant pathology of rotator cuff tears, internal impingement, and instability.

Standard radiographs (Grashey anteroposterior, scapular/lateral, axillary lateral) and magnetic resonance imaging (MRI) with or without arthrography can be helpful in identifying and characterizing most SLAP tears as well as failed SLAP tear repairs. However, MRI is often positive for SLAP tears in asymptomatic patients, and diagnosing SLAP tears with MRI is often a challenge.14 MRI can help in determining concomitant pathology, including rotator cuff injury and cysts causing nerve compression. Correlation with clinical examination and patient history is most crucial. Conservative treatment (rest, activity modification, use of oral anti-inflammatory medications) typically is attempted and coordinated with respect to the athlete’s season of play.15,16

Classification

In overhead throwing athletes, SLAP tears typically are associated with anterior shoulder pain. Associated shoulder instability and significant glenohumeral dysfunction are not uncommon in athletes with lesions of the BLC. In 1985, Andrews and colleagues17 were the first to describe SLAP tears in overhead athletes (73 patients). Later, Snyder and colleagues18,19 further classified these lesions into 4 types based on tear stability and location, and they coined the acronym SLAP (Figure 1).

Figure 1.
Morgan and colleagues20 subclassified type II lesions into 3 groups based on location (anterior SLAP, posterior SLAP, and combined SLAP tear).

 

 

Type I lesions typically are described as fraying at the inner margin of the labrum and are common in throwers, even asymptomatic throwers. Type II lesions, separations of the biceps and labrum from the superior glenoid (≥5 mm of excursion), are the most commonly occurring and treated variant in throwing athletes.20-22 Intraoperative evaluation for a peel-back lesion (placing the arm in abduction with external rotation), rather than for a sulcus of 1 mm to 2 mm, may confirm a type II SLAP tear.20,23,24 It is often important to consider the direction of tear propagation as well. Type III lesions include those with an intact BLC (but with a bucket-handle tear of the superior labral complex and an intact biceps tendon), whereas type IV lesions involve additional extension of the tear into the biceps tendon.18,19The classification systems are well defined. Nevertheless, management of SLAP lesions remains controversial.

Options for Surgical Treatment

SLAP Tear Repair—Outcomes

The incidence of SLAP tear repairs has increased dramatically in recent years.6,25 There are various SLAP tear repair methods, but the most common consists of repairing the labrum and biceps anchor. Management of type II SLAP lesions remains controversial. Several prospective studies have found overall improvement after SLAP tear repair.26-31 Other series have reported less encouraging outcomes, including dissatisfaction with persistent pain and inability to return to throwing.28,32 A 2010 systematic review found that the percentage of patients who returned to their preinjury level of play was only 64%, and outcomes for overhead throwing athletes were even worse—only 22% to 60% of these patients returned to their previous level.33 The right surgery for SLAP tears in this population continues to be an area of uncertainty for many surgeons.

Failed SLAP tear repairs (poor outcomes) have become common in overhead throwing athletes. The reasons for these failed repairs are unclear, but several possible explanations have been offered. One is that labral repair may result in permanent alterations in pitching biomechanics, which may lead to an inability to regain velocity and command.3 Another is that the athlete’s shoulder may remain unstable even after repair.10Hardware complications are a significant concern in this high-level population. Suture anchor pullout or iatrogenic cartilage damage may occur during instrumentation or as a result of suture anchor reactive changes. In addition, there are several reports of glenoid osteochondrolysis (Figure 2) caused by prominent hardware or prominent knots.34-39

Figure 2.
Intra-articular hardware concerns aside, lack of healing is another reason for failed SLAP tear repairs, as the vascular supply to the superior labrum is scarce near the biceps attachment, where shear forces are high.38,40,41 The intra-articular portion of the biceps tendon, as well as the portion within the bicipital groove, contains sensory fibers, which may become the source of persistent pain and inflammation after SLAP tear repair.24,42,43
Figure 3.
Several studies have reported this phenomenon (Figure 3), leading some authors to perform primary biceps tenodesis in an attempt to avoid revision surgery.42,44-47

Stiffness after SLAP tear repair is a significant problem, with most patients taking up to 6 months to regain full motion.26,48 Overtensioning of the labrum and the glenohumeral ligaments may be the cause, and the solution may be to place anchors posterior (vs anterior) to the biceps insertion. In a large prospective military study, mean forward flexion and external rotation were reduced at final follow-up.31 These outcomes are less acceptable to overhead throwing athletes, who rely on motion for high-end throwing activities.

Primary Biceps Tenodesis—Outcomes

A 2015 database study found a 1.7-fold increase in biceps tenodesis over the preceding 5 years.49 However, relatively few procedures included in the study were performed in patients age younger than 30 years. For many older non-overhead throwers with type II tears, SLAP tear repair has become less popular as a treatment option.32 There is a dearth of knowledge about the outcomes of subpectoral biceps tenodesis as a primary treatment for biceps tendonitis and an associated SLAP tear. Although type I tears historically have been treated with débridement, débridement is seldom used for concomitant biceps tendonitis. It should be coupled with careful clinical examination.

In recent years, biceps tenodesis has been proposed as an alternative to repair for SLAP tears, particularly in older patients.24,44 For obvious reasons, however, there has been some trepidation about performing biceps tenodesis in throwing athletes. Some authors have proposed biceps tenodesis as primary treatment for isolated SLAP tears. Boileau and colleagues44 compared the outcomes of treatment of isolated type II SLAP lesions in 25 consecutive patients. For 10 patients, repair involved suture anchors; for the other 15, arthroscopic biceps tenodesis was performed with an absorbable interference screw. Six of the 10 suture anchor patients were disappointed with their outcome (persistent pain or inability to return to sport), whereas 14 of the 15 biceps tenodesis patients were satisfied. The authors concluded that arthroscopic biceps tenodesis is an effective alternative to repair for type II SLAP lesions, though their study was not isolated to overhead athletes (tenodesis group mean age, 52 years).

In a 2014 series of cases, Ek and colleagues50 reported good outcomes of SLAP tear repair and biceps tenodesis. Again, though, tenodesis was used in older patients, and repair in younger, more active patients, with no high-level athletes in either group. There was no difference in return to sport between groups. In a study of patients who underwent primary biceps tenodesis, Gupta and colleagues51 found 80% excellent outcomes (improved shoulder outcome scores) in select SLAP tear patients, including 8 athletes, 88% of whom were overhead athletes. Gottschalk and colleagues52 reported on differences in prospectively collected outcome data (age, sex, SLAP lesion type II or IV) for primary biceps tenodesis in a series of 33 patients. Twenty-six of the 29 patients who completed follow-up returned to their previous level of activity. These studies suggest that primary biceps tenodesis may be an alternative with lower failure rates in the treatment of SLAP tears in middle-aged patients, and in overhead athletes, though additional specific studies are needed to focus on overhead athletes on a larger scale.

 

 

Revision SLAP Tear Repair Versus Biceps Tenodesis

Failed arthroscopic SLAP tear repairs, which are increasingly common, present a unique treatment challenge. In a 2013 prospective cohort series, Gupta and colleagues46 found excellent clinical outcomes of subpectoral biceps tenodesis for failed type II SLAP tears. The authors reported a postoperative SANE (Single Assessment Numeric Evaluation) score of 70.4%, an SST (Simple Shoulder Test) score of 9.33, and an ASES (American Shoulder and Elbow Surgeons) score of 77.96, along with reasonable health-related quality-of-life scores. Werner and colleagues53 evaluated 2-year outcomes of biceps tenodesis performed after SLAP tear repair in 24 patients and found a return to almost normal range of motion as well as good clinical outcome scores. Significantly worse outcomes were found for patients with open worker’s compensation claims.

McCormick and colleagues26 prospectively evaluated the efficacy of biceps tenodesis for failed type II SLAP tear repair in 46 patients. Improvement was noted across all outcome assessments during follow-up (mean, 3.6 years). From these findings, we might conclude that biceps tenodesis is a more predictable option for failed SLAP tear repair, and that it has a relatively low complication rate. However, most investigators have used a heterogeneous patient population, as opposed to overhead athletes specifically. To our knowledge, no one has evaluated the specific population of overhead throwers with failed SLAP tear repairs. In addition, no one has conducted randomized controlled trials comparing débridement, biceps tenodesis, and repair for failed SLAP tear repairs.

Postoperative Considerations

When overhead athletes and their surgeons are considering surgical options, they must take rehabilitation and return to play into account. Many surgeons think the possible marginal clinical benefit of SLAP tear repair may not be worth the protracted rehabilitation. In most practices, rehabilitation after biceps tenodesis is less involved. Discussing the advantages and disadvantages of these 2 procedures can be helpful in decision making.

Dein and colleagues54 reported the case of a middle-aged pitcher who sustained a fracture after biceps tenodesis with an interference screw. Cases like this are concerning. Surgeons should consider altering the rehabilitation regimen when planning postoperative care in cases of biceps tenodesis in throwers. Other reported complications of open tenodesis are deep infection, thrombosis, postoperative stiffness, and nerve injury.55-58

Consequences for Overhead Throwers

The unknown role of the BLC leaves surgeons wary when considering biceps tenodesis for elite athletes. Some have postulated that removing the intra-articular portion of the LHB may cause microinstability and alter joint kinematics.10,59-61 Others have suggested the biceps is desynchronized from the other musculature and is not functionally important.62 Disruption of one portion of the superior labrum may result in instability on the opposite side of the glenoid.10,61 Biomechanical studies, both cadaveric and in vivo, have tried to create proper loads to the LHB and evaluate the kinematics of the shoulder before and after biceps tenodesis and SLAP tear repair.59,60 Using a cadaveric model, Strauss and colleagues63 found that type II SLAP lesions resulted in increased glenohumeral translation compared with baseline. Biceps tenodesis did not restore normal translation, but this did not negatively affect stability in the presence of a SLAP lesion. The consensus is that the role of the biceps is controversial at best.

Several studies have used electromyography (EMG) to evaluate LHB functioning. In 2014, Chalmers and colleagues59 used surface EMG and motion analysis to evaluate 18 pitchers: 6 underwent SLAP tear repair, 5 underwent biceps tenodesis, and 7 were uninjured controls. There were no significant differences in the activity of the LHB muscle, the short head of the biceps muscle, the deltoid, the infraspinatus, or the latissimus among the 3 groups. Motion analysis showed that the normal pattern of muscular activation within the LHB muscle was more closely restored by biceps tenodesis than by SLAP tear repair. In addition, thoracic rotation patterns were significantly more altered in the SLAP tear repair patients than in the uninjured controls. As the authors noted, given the low frequency with which biceps tenodesis is performed in overhead athletes, it is unlikely that larger scale studies will be conducted without a multicenter effort.

Recommendations and Our Preferred Technique

Which surgical option is best for treating symptomatic SLAP lesions in overhead athletes remains unclear. Many athletes struggle to return to high-level play after SLAP tear repair. Whether the same is true after biceps tenodesis is yet to be determined because of the low frequency with which biceps tenodesis is performed in high-level overhead athletes. The options for fixation, technique, and fixation location are equally broad. In this section, we outline our general line of thinking for cases of proximal biceps pathology.

 

 

In each case, we perform glenohumeral arthroscopy to evaluate the BLC and identify any other pathology. For overhead athletes who are younger than 30 years and lack bicipital groove pain or signs of gross tendinopathy, we favor arthroscopic SLAP tear repair. Repair is usually performed through an anterior working portal for suture passage and a Wilmington portal for anchor placement. We use knotless technology to achieve stable fixation and stay posterior to the biceps anchor insertion.

For the prevention of any potential pain from the bicipital groove in carefully selected patients—recreational overhead athletes and patients who want a less involved surgical recovery—we favor open subpectoral biceps tenodesis rather than arthroscopic tenodesis. The outcomes of biceps tenodesis are consistent, according to the literature.47,57,64 Moreover, the open approach is favored for the incidence of postoperative stiffness in the arthroscopic population.65 Tendons can be fixed with multiple procedures, including soft-tissue tenodesis, interference screw fixation, and surface anchors. We favor using a tenodesis screw in the subpectoral location, as outlined by Mazzocca and colleagues.64Our algorithm for SLAP lesions is evolving with our understanding of this complex disease process. For young overhead throwers with type II SLAP lesions, we favor arthroscopic SLAP tear repair with knotless technology. For older recreational overhead athletes, we favor biceps tenodesis in the subpectoral region after diagnostic arthroscopy plus biceps tenotomy with or without additional SLAP tear fixation, depending on the stability of the biceps anchor (Figures 4A, 4B).

Figure 4.
In this procedure, a unicortical hole is drilled in the center of the bicipital groove, with careful attention given to restoring the anatomical length–tension relationship.66 For revision of SLAP tear repair, we recommend revision to a biceps tenodesis using our published technique.57,67 Postoperative rehabilitation is crucial, as failure to return to play may stem from poor throwing mechanics rather than from the surgical fixation technique used.

Conclusion

Overhead athletes who present with symptomatic SLAP lesions often provide a treatment dilemma. Although SLAP tear repair historically has been standard treatment, biceps tenodesis represents a consistent surgical option with low complication rates and low revision rates. It is likely that, as additional data on glenohumeral kinematics and outcomes in young athletes become available, improved decision-making algorithms will follow.

Am J Orthop. 2017;46(1):E71-E78. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.

References

1. 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.

2. Fedoriw WW, Ramkumar P, McCulloch PC, Lintner DM. Return to play after treatment of superior labral tears in professional baseball players. Am J Sports Med. 2014;42(5):1155-1160.

3. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF. Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med. 1995;23(2):233-239.

4. Aydin N, Sirin E, Arya A. Superior labrum anterior to posterior lesions of the shoulder: diagnosis and arthroscopic management. World J Orthop. 2014;5(3):344-350.

5. Barber A, Field LD, Ryu R. Biceps tendon and superior labrum injuries: decision-marking. J Bone Joint Surg Am. 2007;89(8):1844-1855.

6. Onyekwelu I, Khatib O, Zuckerman JD, Rokito AS, Kwon YW. The rising incidence of arthroscopic superior labrum anterior and posterior (SLAP) repairs. J Shoulder Elbow Surg. 2012;21(6):728-731.

7. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery Certification Examination Database. Am J Sports Med. 2014;42(8):1904-1910.

8. Walton DM, Sadi J. Identifying SLAP lesions: a meta-analysis of clinical tests and exercise in clinical reasoning. Phys Ther Sport. 2008;9(4):167-176.

9. Lesniak BP, Baraga MG, Jose J, Smith MK, Cunningham S, Kaplan LD. Glenohumeral findings on magnetic resonance imaging correlate with innings pitched in asymptomatic pitchers. Am J Sports Med. 2013;41(9):2022-2027.

10. Mihata T, McGarry MH, Tibone JE, Fitzpatrick MJ, Kinoshita M, Lee TQ. Biomechanical assessment of type II superior labral anterior-posterior (SLAP) lesions associated with anterior shoulder capsular laxity as seen in throwers: a cadaveric study. Am J Sports Med. 2008;36(8):1604-1610.

11. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part II: evaluation and treatment of SLAP lesions in throwers. Arthroscopy. 2003;19(5):531-539.

12. Meserve BB, Cleland JA, Boucher TR. A meta-analysis examining clinical test utility for assessing superior labral anterior posterior lesions. Am J Sports Med. 2009;37(11):2252-2258.

13. Pandya NK, Colton A, Webner D, Sennett B, Huffman GR. Physical examination and magnetic resonance imaging in the diagnosis of superior labrum anterior-posterior lesions of the shoulder: a sensitivity analysis. Arthroscopy. 2008;24(3):311-317.

14. Amin MF, Youssef AO. The diagnostic value of magnetic resonance arthrography of the shoulder in detection and grading of SLAP lesions: comparison with arthroscopic findings. Eur J Radiol. 2012;81(9):2343-2347.

15. Cook C, Beaty S, Kissenberth MJ, Siffri P, Pill SG, Hawkins RJ. Diagnostic accuracy of five orthopedic clinical tests for diagnosis of superior labrum anterior posterior (SLAP) lesions. J Shoulder Elbow Surg. 2012;21(1):13-22.

16. Edwards SL, Lee JA, Bell JE, et al. Nonoperative treatment of superior labrum anterior posterior tears: improvements in pain, function, and quality of life. Am J Sports Med. 2010;38(7):1456-1461.

17. Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.

18. Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274-279.

19. Snyder SJ, Banas MP, Karzel RP. An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg. 1995;4(4):243-248.

20. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.

21. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

22. Keener JD, Brophy RH. Superior labral tears of the shoulder: pathogenesis, evaluation, and treatment. J Am Acad Orthop Surg. 2009;17(10):627-637.

23. Chen CH, Hsu KY, Chen WJ, Shih CH. Incidence and severity of biceps long head tendon lesion in patients with complete rotator cuff tears. J Trauma. 2005;58(6):1189-1193.

24. Nho SJ, Strauss EJ, Lenart BA, et al. Long head of the biceps tendinopathy: diagnosis and management. J Am Acad Orthop Surg. 2010;18(11):645-656.

25. Zhang AL, Kreulen C, Ngo SS, Hame SL, Wang JC, Gamradt SC. Demographic trends in arthroscopic SLAP repair in the United States. Am J Sports Med. 2012;40(5):1144-1147.

26. McCormick F, Bhatia S, Chalmers P, Gupta A, Verma N, Romeo AA. The management of type II superior labral anterior to posterior injuries. Orthop Clin North Am. 2014;45(1):121-128.

27. Brockmeier SF, Voos JE, Williams RJ 3rd, Altchek DW, Cordasco FA, Allen AA; Hospital for Special Surgery Sports Medicine and Shoulder Service. Outcomes after arthroscopic repair of type-II SLAP lesions. J Bone Joint Surg Am. 2009;91(7):1595-1603.

28. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37(5):929-936.

29. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.

30. Friel NA, Karas V, Slabaugh MA, Cole BJ. Outcomes of type II superior labrum, anterior to posterior (SLAP) repair: prospective evaluation at a minimum two-year follow-up. J Shoulder Elbow Surg. 2010;19(6):859-867.

31. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

32. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

 

 

33. Gorantla K, Gill C, Wright RW. The outcome of type II SLAP repair: a systematic review. Arthroscopy. 2010;26(4):537-545.

34. Katz LM, Hsu S, Miller SL, et al. Poor outcomes after SLAP repair: descriptive analysis and prognosis. Arthroscopy. 2009;25(8):849-855.

35. Park MJ, Hsu JE, Harper C, Sennett BJ, Huffman GR. Poly-L/D-lactic acid anchors are associated with reoperation and failure of SLAP repairs. Arthroscopy. 2011;27(10):1335-1340.

36. Sassmannshausen G, Sukay M, Mair SD. Broken or dislodged poly-L-lactic acid bioabsorbable tacks in patients after SLAP lesion surgery. Arthroscopy. 2006;22(6):615-619.

37. Uggen C, Wei A, Glousman RE, et al. Biomechanical comparison of knotless anchor repair versus simple suture repair for type II SLAP lesions. Arthroscopy. 2009;25(10):1085-1092.

38. Weber SC. Surgical management of the failed SLAP repair. Sports Med Arthrosc. 2010;18(3):162-166.

39. Wilkerson JP, Zvijac JE, Uribe JW, Schürhoff MR, Green JB. Failure of polymerized lactic acid tacks in shoulder surgery. J Shoulder Elbow Surg. 2003;12(2):117-121.

40. Weber S. Surgical management of the failed SLAP lesion. Arthroscopy. 2008;24(suppl):e8-e9.

41. Schrøder CP, Skare O, Gjengedal E, Uppheim G, Reikerås O, Brox JI. Long-term results after SLAP repair: a 5-year follow-up study of 107 patients with comparison of patients aged over and under 40 years. Arthroscopy. 2012;28(11):1601-1607.

42. 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.

43. Mazzocca AD, McCarthy MB, Ledgard FA, et al. Histomorphologic changes of the long head of the biceps tendon in common shoulder pathologies. Arthroscopy. 2013;29(6):972-981.

44. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37(5):929-936.

45. Boileau P, Krishnan SG, Coste JS, Walch G. Arthroscopic biceps tenodesis: a new technique using bioabsorbable interference screw fixation. Arthroscopy. 2002;18(9):1002-1012.

46. Gupta AK, Bruce B, Klosterman EL, McCormick F, Harris J, Romeo AA. Subpectoral biceps tenodesis for failed type II SLAP repair. Orthopedics. 2013;36(6):e723-e728.

47. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc. 2008;16(3):170-176.

48. McCarty LP 3rd, Buss DD, Datta MW, Freehill MQ, Giveans MR. Complications observed following labral or rotator cuff repair with use of poly-L-lactic acid implants. J Bone Joint Surg Am. 2013;95(6):507-511.

49. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

50. Ek ET, Shi LL, Tompson JD, Freehill MT, Warner JJ. Surgical treatment of isolated type II superior labrum anterior-posterior (SLAP) lesions: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2014;23(7):1059-1065.

51. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

52. Gottschalk MB, Karas SG, Ghattas TN, Burdette R. Subpectoral biceps tenodesis for the treatment of type II and IV superior labral anterior and posterior lesions. Am J Sports Med. 2014;42(9):2128-2135.

53. Werner BC, Pehlivan HC, Hart JM, et al. Biceps tenodesis is a viable option for salvage of failed SLAP repair. J Shoulder Elbow Surg. 2014;23(8):e179-e184.

54. Dein EJ, Huri G, Gordon JC, McFarland EG. A humerus fracture in a baseball pitcher after biceps tenodesis [published correction appears in Am J Sports Med. 2014;42(6):NP39]. Am J Sports Med. 2014;42(4):877-879.

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. Osbahr DC, Diamond AB, Speer KP. The cosmetic appearance of the biceps muscle after long-head tenotomy versus tenodesis. Arthroscopy. 2002;18(5):483-487.

57. Romeo AA, Mazzocca AD, Tauro JC. Arthroscopic biceps tenodesis. Arthroscopy. 2004;20(2):206-213.

58. 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.

59. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

60. Giphart JE, Elser F, Dewing CB, Torry MR, Millett PJ. The long head of the biceps tendon has minimal effect on in vivo glenohumeral kinematics: a biplane fluoroscopy study. Am J Sports Med. 2012;40(1):202-212.

61. Grossman MG, Tibone JE, McGarry MH, Schneider DJ, Veneziani S, Lee TQ. A cadaveric model of the throwing shoulder: a possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am. 2005;87(4):824-831.

62. Hawkes DH, Alizadehkhaiyat O, Fisher AC, Kemp GJ, Roebuck MM, Frostick SP. Normal shoulder muscular activation and co-ordination during a shoulder elevation task based on activities of daily living: an electromyographic study. J Orthop Res. 2012;30(1):53-60.

63. Strauss EJ, Salata MJ, Sershon RA, et al. Role of the superior labrum after biceps tenodesis in glenohumeral stability. J Shoulder Elbow Surg. 2014;23(4):485-491.

64. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.

 

 

65. 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.

66. 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.

67. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.

References

1. 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.

2. Fedoriw WW, Ramkumar P, McCulloch PC, Lintner DM. Return to play after treatment of superior labral tears in professional baseball players. Am J Sports Med. 2014;42(5):1155-1160.

3. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF. Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med. 1995;23(2):233-239.

4. Aydin N, Sirin E, Arya A. Superior labrum anterior to posterior lesions of the shoulder: diagnosis and arthroscopic management. World J Orthop. 2014;5(3):344-350.

5. Barber A, Field LD, Ryu R. Biceps tendon and superior labrum injuries: decision-marking. J Bone Joint Surg Am. 2007;89(8):1844-1855.

6. Onyekwelu I, Khatib O, Zuckerman JD, Rokito AS, Kwon YW. The rising incidence of arthroscopic superior labrum anterior and posterior (SLAP) repairs. J Shoulder Elbow Surg. 2012;21(6):728-731.

7. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery Certification Examination Database. Am J Sports Med. 2014;42(8):1904-1910.

8. Walton DM, Sadi J. Identifying SLAP lesions: a meta-analysis of clinical tests and exercise in clinical reasoning. Phys Ther Sport. 2008;9(4):167-176.

9. Lesniak BP, Baraga MG, Jose J, Smith MK, Cunningham S, Kaplan LD. Glenohumeral findings on magnetic resonance imaging correlate with innings pitched in asymptomatic pitchers. Am J Sports Med. 2013;41(9):2022-2027.

10. Mihata T, McGarry MH, Tibone JE, Fitzpatrick MJ, Kinoshita M, Lee TQ. Biomechanical assessment of type II superior labral anterior-posterior (SLAP) lesions associated with anterior shoulder capsular laxity as seen in throwers: a cadaveric study. Am J Sports Med. 2008;36(8):1604-1610.

11. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part II: evaluation and treatment of SLAP lesions in throwers. Arthroscopy. 2003;19(5):531-539.

12. Meserve BB, Cleland JA, Boucher TR. A meta-analysis examining clinical test utility for assessing superior labral anterior posterior lesions. Am J Sports Med. 2009;37(11):2252-2258.

13. Pandya NK, Colton A, Webner D, Sennett B, Huffman GR. Physical examination and magnetic resonance imaging in the diagnosis of superior labrum anterior-posterior lesions of the shoulder: a sensitivity analysis. Arthroscopy. 2008;24(3):311-317.

14. Amin MF, Youssef AO. The diagnostic value of magnetic resonance arthrography of the shoulder in detection and grading of SLAP lesions: comparison with arthroscopic findings. Eur J Radiol. 2012;81(9):2343-2347.

15. Cook C, Beaty S, Kissenberth MJ, Siffri P, Pill SG, Hawkins RJ. Diagnostic accuracy of five orthopedic clinical tests for diagnosis of superior labrum anterior posterior (SLAP) lesions. J Shoulder Elbow Surg. 2012;21(1):13-22.

16. Edwards SL, Lee JA, Bell JE, et al. Nonoperative treatment of superior labrum anterior posterior tears: improvements in pain, function, and quality of life. Am J Sports Med. 2010;38(7):1456-1461.

17. Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.

18. Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274-279.

19. Snyder SJ, Banas MP, Karzel RP. An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg. 1995;4(4):243-248.

20. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.

21. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

22. Keener JD, Brophy RH. Superior labral tears of the shoulder: pathogenesis, evaluation, and treatment. J Am Acad Orthop Surg. 2009;17(10):627-637.

23. Chen CH, Hsu KY, Chen WJ, Shih CH. Incidence and severity of biceps long head tendon lesion in patients with complete rotator cuff tears. J Trauma. 2005;58(6):1189-1193.

24. Nho SJ, Strauss EJ, Lenart BA, et al. Long head of the biceps tendinopathy: diagnosis and management. J Am Acad Orthop Surg. 2010;18(11):645-656.

25. Zhang AL, Kreulen C, Ngo SS, Hame SL, Wang JC, Gamradt SC. Demographic trends in arthroscopic SLAP repair in the United States. Am J Sports Med. 2012;40(5):1144-1147.

26. McCormick F, Bhatia S, Chalmers P, Gupta A, Verma N, Romeo AA. The management of type II superior labral anterior to posterior injuries. Orthop Clin North Am. 2014;45(1):121-128.

27. Brockmeier SF, Voos JE, Williams RJ 3rd, Altchek DW, Cordasco FA, Allen AA; Hospital for Special Surgery Sports Medicine and Shoulder Service. Outcomes after arthroscopic repair of type-II SLAP lesions. J Bone Joint Surg Am. 2009;91(7):1595-1603.

28. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37(5):929-936.

29. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.

30. Friel NA, Karas V, Slabaugh MA, Cole BJ. Outcomes of type II superior labrum, anterior to posterior (SLAP) repair: prospective evaluation at a minimum two-year follow-up. J Shoulder Elbow Surg. 2010;19(6):859-867.

31. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.

32. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

 

 

33. Gorantla K, Gill C, Wright RW. The outcome of type II SLAP repair: a systematic review. Arthroscopy. 2010;26(4):537-545.

34. Katz LM, Hsu S, Miller SL, et al. Poor outcomes after SLAP repair: descriptive analysis and prognosis. Arthroscopy. 2009;25(8):849-855.

35. Park MJ, Hsu JE, Harper C, Sennett BJ, Huffman GR. Poly-L/D-lactic acid anchors are associated with reoperation and failure of SLAP repairs. Arthroscopy. 2011;27(10):1335-1340.

36. Sassmannshausen G, Sukay M, Mair SD. Broken or dislodged poly-L-lactic acid bioabsorbable tacks in patients after SLAP lesion surgery. Arthroscopy. 2006;22(6):615-619.

37. Uggen C, Wei A, Glousman RE, et al. Biomechanical comparison of knotless anchor repair versus simple suture repair for type II SLAP lesions. Arthroscopy. 2009;25(10):1085-1092.

38. Weber SC. Surgical management of the failed SLAP repair. Sports Med Arthrosc. 2010;18(3):162-166.

39. Wilkerson JP, Zvijac JE, Uribe JW, Schürhoff MR, Green JB. Failure of polymerized lactic acid tacks in shoulder surgery. J Shoulder Elbow Surg. 2003;12(2):117-121.

40. Weber S. Surgical management of the failed SLAP lesion. Arthroscopy. 2008;24(suppl):e8-e9.

41. Schrøder CP, Skare O, Gjengedal E, Uppheim G, Reikerås O, Brox JI. Long-term results after SLAP repair: a 5-year follow-up study of 107 patients with comparison of patients aged over and under 40 years. Arthroscopy. 2012;28(11):1601-1607.

42. 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.

43. Mazzocca AD, McCarthy MB, Ledgard FA, et al. Histomorphologic changes of the long head of the biceps tendon in common shoulder pathologies. Arthroscopy. 2013;29(6):972-981.

44. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37(5):929-936.

45. Boileau P, Krishnan SG, Coste JS, Walch G. Arthroscopic biceps tenodesis: a new technique using bioabsorbable interference screw fixation. Arthroscopy. 2002;18(9):1002-1012.

46. Gupta AK, Bruce B, Klosterman EL, McCormick F, Harris J, Romeo AA. Subpectoral biceps tenodesis for failed type II SLAP repair. Orthopedics. 2013;36(6):e723-e728.

47. Provencher MT, LeClere LE, Romeo AA. Subpectoral biceps tenodesis. Sports Med Arthrosc. 2008;16(3):170-176.

48. McCarty LP 3rd, Buss DD, Datta MW, Freehill MQ, Giveans MR. Complications observed following labral or rotator cuff repair with use of poly-L-lactic acid implants. J Bone Joint Surg Am. 2013;95(6):507-511.

49. Werner BC, Brockmeier SF, Gwathmey FW. Trends in long head biceps tenodesis. Am J Sports Med. 2015;43(3):570-578.

50. Ek ET, Shi LL, Tompson JD, Freehill MT, Warner JJ. Surgical treatment of isolated type II superior labrum anterior-posterior (SLAP) lesions: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2014;23(7):1059-1065.

51. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.

52. Gottschalk MB, Karas SG, Ghattas TN, Burdette R. Subpectoral biceps tenodesis for the treatment of type II and IV superior labral anterior and posterior lesions. Am J Sports Med. 2014;42(9):2128-2135.

53. Werner BC, Pehlivan HC, Hart JM, et al. Biceps tenodesis is a viable option for salvage of failed SLAP repair. J Shoulder Elbow Surg. 2014;23(8):e179-e184.

54. Dein EJ, Huri G, Gordon JC, McFarland EG. A humerus fracture in a baseball pitcher after biceps tenodesis [published correction appears in Am J Sports Med. 2014;42(6):NP39]. Am J Sports Med. 2014;42(4):877-879.

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. Osbahr DC, Diamond AB, Speer KP. The cosmetic appearance of the biceps muscle after long-head tenotomy versus tenodesis. Arthroscopy. 2002;18(5):483-487.

57. Romeo AA, Mazzocca AD, Tauro JC. Arthroscopic biceps tenodesis. Arthroscopy. 2004;20(2):206-213.

58. 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.

59. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.

60. Giphart JE, Elser F, Dewing CB, Torry MR, Millett PJ. The long head of the biceps tendon has minimal effect on in vivo glenohumeral kinematics: a biplane fluoroscopy study. Am J Sports Med. 2012;40(1):202-212.

61. Grossman MG, Tibone JE, McGarry MH, Schneider DJ, Veneziani S, Lee TQ. A cadaveric model of the throwing shoulder: a possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am. 2005;87(4):824-831.

62. Hawkes DH, Alizadehkhaiyat O, Fisher AC, Kemp GJ, Roebuck MM, Frostick SP. Normal shoulder muscular activation and co-ordination during a shoulder elevation task based on activities of daily living: an electromyographic study. J Orthop Res. 2012;30(1):53-60.

63. Strauss EJ, Salata MJ, Sershon RA, et al. Role of the superior labrum after biceps tenodesis in glenohumeral stability. J Shoulder Elbow Surg. 2014;23(4):485-491.

64. Mazzocca AD, Bicos J, Santangelo S, Romeo AA, Arciero RA. The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis. Arthroscopy. 2005;21(11):1296-1306.

 

 

65. 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.

66. 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.

67. Mazzocca AD, Rios CG, Romeo AA, Arciero RA. Subpectoral biceps tenodesis with interference screw fixation. Arthroscopy. 2005;21(7):896.

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Safety of Superior Labrum Anterior and Posterior (SLAP) Repair Posterior to Biceps Tendon Is Improved With a Percutaneous Approach

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Safety of Superior Labrum Anterior and Posterior (SLAP) Repair Posterior to Biceps Tendon Is Improved With a Percutaneous Approach

Take-Home Points

  • Anchors placed posterior to the biceps during SLAP repair are at risk for glenoid vault penetration and/or suprascapular nerve (SSN) injury.
  • Vault penetration and SSN injury are avoided by using a Port of Wilmington (PW) portal instead of an anterior portal.
  • A percutaneous PW portal is safe and passes through the rotator cuff muscle only.

Since being classified by Snyder and colleagues,1 various arthroscopic techniques have been used to repair superior labrum anterior and posterior (SLAP) tears, particularly type II tears. Despite being commonly performed, repairs of SLAP lesions remain challenging. There is high variability in the rate of good/excellent functional outcomes and athletes’ return to previous level of play after SLAP repairs.2,3 Furthermore, the rate of complications after SLAP repair is as high as 5%.4

One of the most common complications of repair of a type II SLAP tear is nerve injury.4 In particular, suprascapular nerve (SSN) injury has occurred after arthroscopic repair of SLAP tears.5,6 Three cadaveric studies have demonstrated that glenoid vault penetration is common during placement of knotted anchors for SLAP repair and that the SSN is at risk during placement of these anchors.7-9 However, 2 of the 3 studies used only an anterior portal in their evaluation of anchor placement. Safety of anchor placement posterior to the biceps tendon may be improved with a percutaneous approach using a Port of Wilmington (PW) portal.10,11 No studies have evaluated the risk of glenoid vault penetration and SSN injury with shorter knotless anchors.

We conducted a study to compare a standard anterosuperolateral (ASL) portal with a percutaneous PW portal for knotless anchors placed posterior to the biceps tendon during repair of SLAP tears. We hypothesized that anchors placed through the PW portal would be less likely to penetrate the glenoid vault and would be farther from the SSN in the event of bone penetration.

Materials and Methods

Six matched pairs of fresh human cadaveric shoulders were used in this study. Each specimen included the scapula, the clavicle, and the humerus. All 6 specimens were male, and their mean age was 41.2 years (range, 23-59 years). Shoulder arthroscopy was performed for placement of SLAP anchors, and open dissection followed.

Anchor Placement

The scapula was clamped and the shoulder placed in the lateral decubitus position with 30° of abduction, 20° of forward flexion, and neutral rotation.10 A standard posterior glenohumeral viewing portal was established and a 30° arthroscope inserted. Both shoulders of each matched pair were randomly assigned to anchor placement through either an ASL portal or a PW portal. Two anchors were placed in the superior glenoid to simulate repair of a posterior SLAP tear.11 Each was a 2.9-mm short (12.5-mm) knotless anchor (BioComposite PushLock; Arthrex) that included a polyetheretherketone (PEEK) eyelet for threading sutures before anchor placement. A drill guide was inserted according to manufacturer guidelines, and a 2.9-mm drill was used to make a bone socket 18 mm deep. The anchor eyelet was loaded with suture tape (Labral Tape; Arthrex), and the anchor and suture were inserted into the socket. The sutures were left uncut to aid in anchor visualization during open dissection. On a right shoulder, the first anchor was placed just posterior to the biceps tendon, at 11 o’clock, and the second anchor about 1 cm posterior to the first, at 10 o’clock. All anchors were placed by an arthroscopy fellowship–trained shoulder surgeon. Before placement, anchor location was confirmed by another arthroscopy fellowship–trained shoulder surgeon.

The ASL portal was created, with an 18-gauge spinal needle and an outside-in technique, about 1 cm lateral to the anterolateral corner of the acromion.

Figure 1.
The portal was established through the rotator interval just anterior to the leading edge of the supraspinatus tendon and posterior to the long head of the biceps tendon. In this portal, an 8.25-mm threaded cannula was inserted for anchor placement (Figure 1).

In the opposite shoulder, the PW portal was created, with a percutaneous technique, about 1 cm anterior and 1 cm lateral to the posterolateral corner of the acromion. An 18-gauge spinal needle was inserted to allow a 45° angle of approach to the posterosuperior glenoid.11
Figure 2.
A guide wire was threaded through the needle, and the needle was removed. Then the portal was dilated, and a 4.5-mm metal cannula was inserted for anchor placement (Figure 2).

Cadaveric Dissection

After anchor placement, another shoulder surgeon performed the dissection. Skin, subcutaneous tissue, deltoid, and clavicle were removed. In the percutaneous specimens, PW portal location relative to rotator cuff was recorded before cuff removal. After overlying soft tissues were removed from a specimen, the anchors were examined for glenoid vault penetration. In the setting of vault penetration, digital calipers were used to measure the shortest distance from anchor to SSN.

 

 

Results

In the ASL portal group, 8 (66.7%) of 12 anchors (4/6 at 11 o’clock, 4/6 at 10 o’clock) penetrated the medial glenoid vault.

Table.
In the 8 penetration cases, mean distance to SSN was 6.8 mm (range, 0-14 mm) for 11 o’clock anchors and 4.8 mm (range, 0-14 mm) for 10 o’clock anchors (Table).

In the PW portal group, 2 (16.7%) of 12 anchors (1/6 at 11 o’clock, 1/6 at 10 o’clock, both from a single specimen) penetrated the medial glenoid vault. Actually, in each case the eyelet and not the anchor penetrated the vault. In the penetration cases, distance to SSN was 20 mm for the 11 o’clock anchor and 8 mm for the 10 o’clock anchor (Table). Of the 6 portals, 3 passed through the supraspinatus muscle, 2 through the infraspinatus musculotendinous junction, and 1 through the infraspinatus muscle.

Discussion

Our study findings support the hypothesis that SLAP repair anchors placed posterior to the biceps tendon are more likely to remain in bone with use of a percutaneous approach relative to an ASL approach. Our findings also support the growing body of evidence that such anchors placed with an anterior approach increase the risk for SSN injury.

Three other cadaveric studies have evaluated anchor placement for SLAP repair. Chan and colleagues7 evaluated drill penetration during bone socket preparation for SLAP repair in 21 matched pairs of formalin-embalmed cadavers. A 20-mm drill was used for correspondence to a 14.5-mm anchor, though no anchors were inserted, and sockets were created in an open manner. Through a mimicked ASL portal, 1 socket was made anterior to the biceps tendon, at 1 o’clock; then, through a mimicked PW portal, 2 sockets were made posterior to the tendon, at 11 o’clock and 9 to 10 o’clock. Glenoid vault penetration occurred in 29% of the 42 anterior sockets, but only 1 anchor (2.4%) touched the SSN. Penetration did not occur with the 11 o’clock anchors. The 9 to 10 o’clock anchor was at highest risk for SSN injury (9.5%, 4 cases). The study was limited by lack of anchor placement and open creation of bone sockets in embalmed cadavers.

Koh and colleagues8 evaluated arthroscopic placement of anterior SLAP anchors in 6 matched pairs of fresh-frozen cadavers. Through an ASL portal, each 14.5-mm knotted anchor was placed anterior to the biceps tendon, at 1 o’clock. As in the study by Chan and colleagues,7 drill depth was 20 mm. Notably, anchors were seated 2 mm beyond manufacturer recommendations, and the cadavers were of Asian origin, likely indicating smaller glenoids compared to specimens from North America or Europe. All 12 anchors penetrated the glenoid vault; mean distance to SSN was 3.1 mm.

Morgan and colleagues9 compared anterior and ASL portals created for SLAP repairs in 10 matched-pair cadavers. Anchors were placed at 1 o’clock, 11 o’clock, and 10 o’clock. As in the studies by Chan and colleagues7 and Koh and colleagues,8 14.5-mm knotted anchors were used. One anterior anchor (10%) placed through an ASL portal penetrated the cortex by 1 mm, and 2 anterior anchors (20%) placed through anterior portals penetrated the cortex (1 was completely out of the bone). Overall, 65% of 11 o’clock anchors and 100% of 10 o’clock anchors violated the glenoid vault. With the 11 o’clock anchors, mean distance to SSN was 6 mm for ASL portals and 4.2 mm for anterior portals; with the 10 o’clock anchors, mean distance to SSN was 8 mm for ASL portals and 2.1 mm for anterior portals.

Overall, the results of these 3 studies suggest that, with use of ASL portals, placement of SLAP anchors anterior to the biceps tendon is safe. Using the same portals, however, anchors placed posterior to the tendon are at higher risk for glenoid vault penetration. Supporting these findings are our study’s penetration rates: 66.7% for anchors placed through ASL portals and 16.7% for anchors placed through percutaneous PW portals. The different rates are not surprising given that the coracoid process projects anterior to the glenoid and provides additional bone stock for placement of anchors anteriorly vs posteriorly. Therefore, with percutaneous PW portals, the approach angle directs the anchor toward the bone of the coracoid base. Furthermore, the SSN passes nearest the posterior aspect of the glenoid. In a study by Shishido and Kikuchi,12 the distance from the posterior rim of the glenoid to the SSN was 18 mm, and from the superior rim was 29 mm. Therefore, anchors placed with an anterior approach naturally are directed toward the SSN.

Figure 3.
Given these findings, we think surgeons who repair posterior SLAP tears should place anchors through percutaneous PW portals, not ASL portals, in order to minimize the risks for glenoid vault penetration and SSN injury (Figures 3, 4A-4B).

In addition to portal placement and approach angle, anchor length likely affects the risks for glenoid vault penetration and SSN injury.
Figure 4.
Koh and colleagues8 found a mean distance of 14.2 mm from the glenoid rim to the medial cortex for anchors placed anterior to the biceps tendon and a mean distance of 20.7 mm from the glenoid rim to the SSN. Morgan and colleagues9 also evaluated the shortest distance from the glenoid rim to the SSN. Mean distance was 17.9 mm for 10 o’clock anchors and 20.9 mm for 11 o’clock anchors. Whereas the 3 cadaveric studies discussed earlier7-9 examined 14.5-mm knotted anchors with drill depths of 20 mm, we examined 12.5-mm knotless anchors with drill depths of 18 mm. Even with the 1 anchor penetration that occurred with a percutaneous portal in our study, the SSN was 20 mm from the 11 o’clock portal and 8 mm from the 10 o’clock portal. It is important to note that, for SLAP repair, the biomechanical characteristics of knotless anchors are equivalent to those of knotted anchors.13 In addition, knotless anchors offer the advantage of avoiding knot impingement and migration.14 On that basis, and given the anatomy mentioned, we primarily use short knotless anchors for SLAP repair and think that, as long as biomechanically supported, the trend should be to use shorter anchors for SLAP repair in order to minimize the risks for glenoid vault penetration and SSN injury.

One limitation of this study was the small number of cadavers, all of which were male. Female cadavers and cadavers of other ethnic origins likely have smaller glenoid vaults, and thus their inclusion would have altered our results. This issue was well described in studies mentioned in this article, and our goal was simply to compare ASL portals with percutaneous PW portals, so we think it does not change the fact that the risks for glenoid vault penetration and SSN injury are reduced with use of PW portals for anchors placed posterior to the biceps tendon.

 

 

Conclusion

This study was the first to examine glenoid vault penetration and SSN proximity with short anchors for SLAP repair. The risk for glenoid vault penetration during repair of SLAP tears posterior to the biceps tendon was reduced by anchor placement with a percutaneous posterior approach. The percutaneous posterior approach also directs the anchor away from the SSN.

Am J Orthop. 2017;46(1):E60-E64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Snyder SJ, Banas MP, Karzel RP. An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg. 1995;4(4):243-248.

2. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.

3. Gorantla K, Gill C, Wright RW. The outcome of type II SLAP repair: a systematic review. Arthroscopy. 2010;26(4):537-545.

4. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

5. Kim SH, Koh YG, Sung CH, Moon HK, Park YS. Iatrogenic suprascapular nerve injury after repair of type II SLAP lesion. Arthroscopy. 2010;26(7):1005-1008.

6. Yoo JC, Lee YS, Ahn JH, Park JH, Kang HJ, Koh KH. Isolated suprascapular nerve injury below the spinoglenoid notch after SLAP repair. J Shoulder Elbow Surg. 2009;18(4):e27-e29.

7. Chan H, Beaupre LA, Bouliane MJ. Injury of the suprascapular nerve during arthroscopic repair of superior labral tears: an anatomic study. J Shoulder Elbow Surg. 2010;19(5):709-715.

8. Koh KH, Park WH, Lim TK, Yoo JC. Medial perforation of the glenoid neck following SLAP repair places the suprascapular nerve at risk: a cadaveric study. J Shoulder Elbow Surg. 2011;20(2):245-250.

9. Morgan RT, Henn RF 3rd, Paryavi E, Dreese J. Injury to the suprascapular nerve during superior labrum anterior and posterior repair: is a rotator interval portal safer than an anterosuperior portal? Arthroscopy. 2014;30(11):1418-1423.

10. Lo IK, Lind CC, Burkhart SS. Glenohumeral arthroscopy portals established using an outside-in technique: neurovascular anatomy at risk. Arthroscopy. 2004;20(6):596-602.

11. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.

12. Shishido H, Kikuchi S. Injury of the suprascapular nerve in shoulder surgery: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):372-376.

13. Uggen C, Wei A, Glousman RE, et al. Biomechanical comparison of knotless anchor repair versus simple suture repair for type II SLAP lesions. Arthroscopy. 2009;25(10):1085-1092.

14. Kim SH, Crater RB, Hargens AR. Movement-induced knot migration after anterior stabilization in the shoulder. Arthroscopy. 2013;29(3):485-490.

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Authors’ Disclosure Statement: This study was funded by a research grant from Arthrex. Dr. Adams reports that he is Vice President of Global Medical Education at Arthrex. Dr. Denard reports that he is a consultant for Arthrex.

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Authors’ Disclosure Statement: This study was funded by a research grant from Arthrex. Dr. Adams reports that he is Vice President of Global Medical Education at Arthrex. Dr. Denard reports that he is a consultant for Arthrex.

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Authors’ Disclosure Statement: This study was funded by a research grant from Arthrex. Dr. Adams reports that he is Vice President of Global Medical Education at Arthrex. Dr. Denard reports that he is a consultant for Arthrex.

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Take-Home Points

  • Anchors placed posterior to the biceps during SLAP repair are at risk for glenoid vault penetration and/or suprascapular nerve (SSN) injury.
  • Vault penetration and SSN injury are avoided by using a Port of Wilmington (PW) portal instead of an anterior portal.
  • A percutaneous PW portal is safe and passes through the rotator cuff muscle only.

Since being classified by Snyder and colleagues,1 various arthroscopic techniques have been used to repair superior labrum anterior and posterior (SLAP) tears, particularly type II tears. Despite being commonly performed, repairs of SLAP lesions remain challenging. There is high variability in the rate of good/excellent functional outcomes and athletes’ return to previous level of play after SLAP repairs.2,3 Furthermore, the rate of complications after SLAP repair is as high as 5%.4

One of the most common complications of repair of a type II SLAP tear is nerve injury.4 In particular, suprascapular nerve (SSN) injury has occurred after arthroscopic repair of SLAP tears.5,6 Three cadaveric studies have demonstrated that glenoid vault penetration is common during placement of knotted anchors for SLAP repair and that the SSN is at risk during placement of these anchors.7-9 However, 2 of the 3 studies used only an anterior portal in their evaluation of anchor placement. Safety of anchor placement posterior to the biceps tendon may be improved with a percutaneous approach using a Port of Wilmington (PW) portal.10,11 No studies have evaluated the risk of glenoid vault penetration and SSN injury with shorter knotless anchors.

We conducted a study to compare a standard anterosuperolateral (ASL) portal with a percutaneous PW portal for knotless anchors placed posterior to the biceps tendon during repair of SLAP tears. We hypothesized that anchors placed through the PW portal would be less likely to penetrate the glenoid vault and would be farther from the SSN in the event of bone penetration.

Materials and Methods

Six matched pairs of fresh human cadaveric shoulders were used in this study. Each specimen included the scapula, the clavicle, and the humerus. All 6 specimens were male, and their mean age was 41.2 years (range, 23-59 years). Shoulder arthroscopy was performed for placement of SLAP anchors, and open dissection followed.

Anchor Placement

The scapula was clamped and the shoulder placed in the lateral decubitus position with 30° of abduction, 20° of forward flexion, and neutral rotation.10 A standard posterior glenohumeral viewing portal was established and a 30° arthroscope inserted. Both shoulders of each matched pair were randomly assigned to anchor placement through either an ASL portal or a PW portal. Two anchors were placed in the superior glenoid to simulate repair of a posterior SLAP tear.11 Each was a 2.9-mm short (12.5-mm) knotless anchor (BioComposite PushLock; Arthrex) that included a polyetheretherketone (PEEK) eyelet for threading sutures before anchor placement. A drill guide was inserted according to manufacturer guidelines, and a 2.9-mm drill was used to make a bone socket 18 mm deep. The anchor eyelet was loaded with suture tape (Labral Tape; Arthrex), and the anchor and suture were inserted into the socket. The sutures were left uncut to aid in anchor visualization during open dissection. On a right shoulder, the first anchor was placed just posterior to the biceps tendon, at 11 o’clock, and the second anchor about 1 cm posterior to the first, at 10 o’clock. All anchors were placed by an arthroscopy fellowship–trained shoulder surgeon. Before placement, anchor location was confirmed by another arthroscopy fellowship–trained shoulder surgeon.

The ASL portal was created, with an 18-gauge spinal needle and an outside-in technique, about 1 cm lateral to the anterolateral corner of the acromion.

Figure 1.
The portal was established through the rotator interval just anterior to the leading edge of the supraspinatus tendon and posterior to the long head of the biceps tendon. In this portal, an 8.25-mm threaded cannula was inserted for anchor placement (Figure 1).

In the opposite shoulder, the PW portal was created, with a percutaneous technique, about 1 cm anterior and 1 cm lateral to the posterolateral corner of the acromion. An 18-gauge spinal needle was inserted to allow a 45° angle of approach to the posterosuperior glenoid.11
Figure 2.
A guide wire was threaded through the needle, and the needle was removed. Then the portal was dilated, and a 4.5-mm metal cannula was inserted for anchor placement (Figure 2).

Cadaveric Dissection

After anchor placement, another shoulder surgeon performed the dissection. Skin, subcutaneous tissue, deltoid, and clavicle were removed. In the percutaneous specimens, PW portal location relative to rotator cuff was recorded before cuff removal. After overlying soft tissues were removed from a specimen, the anchors were examined for glenoid vault penetration. In the setting of vault penetration, digital calipers were used to measure the shortest distance from anchor to SSN.

 

 

Results

In the ASL portal group, 8 (66.7%) of 12 anchors (4/6 at 11 o’clock, 4/6 at 10 o’clock) penetrated the medial glenoid vault.

Table.
In the 8 penetration cases, mean distance to SSN was 6.8 mm (range, 0-14 mm) for 11 o’clock anchors and 4.8 mm (range, 0-14 mm) for 10 o’clock anchors (Table).

In the PW portal group, 2 (16.7%) of 12 anchors (1/6 at 11 o’clock, 1/6 at 10 o’clock, both from a single specimen) penetrated the medial glenoid vault. Actually, in each case the eyelet and not the anchor penetrated the vault. In the penetration cases, distance to SSN was 20 mm for the 11 o’clock anchor and 8 mm for the 10 o’clock anchor (Table). Of the 6 portals, 3 passed through the supraspinatus muscle, 2 through the infraspinatus musculotendinous junction, and 1 through the infraspinatus muscle.

Discussion

Our study findings support the hypothesis that SLAP repair anchors placed posterior to the biceps tendon are more likely to remain in bone with use of a percutaneous approach relative to an ASL approach. Our findings also support the growing body of evidence that such anchors placed with an anterior approach increase the risk for SSN injury.

Three other cadaveric studies have evaluated anchor placement for SLAP repair. Chan and colleagues7 evaluated drill penetration during bone socket preparation for SLAP repair in 21 matched pairs of formalin-embalmed cadavers. A 20-mm drill was used for correspondence to a 14.5-mm anchor, though no anchors were inserted, and sockets were created in an open manner. Through a mimicked ASL portal, 1 socket was made anterior to the biceps tendon, at 1 o’clock; then, through a mimicked PW portal, 2 sockets were made posterior to the tendon, at 11 o’clock and 9 to 10 o’clock. Glenoid vault penetration occurred in 29% of the 42 anterior sockets, but only 1 anchor (2.4%) touched the SSN. Penetration did not occur with the 11 o’clock anchors. The 9 to 10 o’clock anchor was at highest risk for SSN injury (9.5%, 4 cases). The study was limited by lack of anchor placement and open creation of bone sockets in embalmed cadavers.

Koh and colleagues8 evaluated arthroscopic placement of anterior SLAP anchors in 6 matched pairs of fresh-frozen cadavers. Through an ASL portal, each 14.5-mm knotted anchor was placed anterior to the biceps tendon, at 1 o’clock. As in the study by Chan and colleagues,7 drill depth was 20 mm. Notably, anchors were seated 2 mm beyond manufacturer recommendations, and the cadavers were of Asian origin, likely indicating smaller glenoids compared to specimens from North America or Europe. All 12 anchors penetrated the glenoid vault; mean distance to SSN was 3.1 mm.

Morgan and colleagues9 compared anterior and ASL portals created for SLAP repairs in 10 matched-pair cadavers. Anchors were placed at 1 o’clock, 11 o’clock, and 10 o’clock. As in the studies by Chan and colleagues7 and Koh and colleagues,8 14.5-mm knotted anchors were used. One anterior anchor (10%) placed through an ASL portal penetrated the cortex by 1 mm, and 2 anterior anchors (20%) placed through anterior portals penetrated the cortex (1 was completely out of the bone). Overall, 65% of 11 o’clock anchors and 100% of 10 o’clock anchors violated the glenoid vault. With the 11 o’clock anchors, mean distance to SSN was 6 mm for ASL portals and 4.2 mm for anterior portals; with the 10 o’clock anchors, mean distance to SSN was 8 mm for ASL portals and 2.1 mm for anterior portals.

Overall, the results of these 3 studies suggest that, with use of ASL portals, placement of SLAP anchors anterior to the biceps tendon is safe. Using the same portals, however, anchors placed posterior to the tendon are at higher risk for glenoid vault penetration. Supporting these findings are our study’s penetration rates: 66.7% for anchors placed through ASL portals and 16.7% for anchors placed through percutaneous PW portals. The different rates are not surprising given that the coracoid process projects anterior to the glenoid and provides additional bone stock for placement of anchors anteriorly vs posteriorly. Therefore, with percutaneous PW portals, the approach angle directs the anchor toward the bone of the coracoid base. Furthermore, the SSN passes nearest the posterior aspect of the glenoid. In a study by Shishido and Kikuchi,12 the distance from the posterior rim of the glenoid to the SSN was 18 mm, and from the superior rim was 29 mm. Therefore, anchors placed with an anterior approach naturally are directed toward the SSN.

Figure 3.
Given these findings, we think surgeons who repair posterior SLAP tears should place anchors through percutaneous PW portals, not ASL portals, in order to minimize the risks for glenoid vault penetration and SSN injury (Figures 3, 4A-4B).

In addition to portal placement and approach angle, anchor length likely affects the risks for glenoid vault penetration and SSN injury.
Figure 4.
Koh and colleagues8 found a mean distance of 14.2 mm from the glenoid rim to the medial cortex for anchors placed anterior to the biceps tendon and a mean distance of 20.7 mm from the glenoid rim to the SSN. Morgan and colleagues9 also evaluated the shortest distance from the glenoid rim to the SSN. Mean distance was 17.9 mm for 10 o’clock anchors and 20.9 mm for 11 o’clock anchors. Whereas the 3 cadaveric studies discussed earlier7-9 examined 14.5-mm knotted anchors with drill depths of 20 mm, we examined 12.5-mm knotless anchors with drill depths of 18 mm. Even with the 1 anchor penetration that occurred with a percutaneous portal in our study, the SSN was 20 mm from the 11 o’clock portal and 8 mm from the 10 o’clock portal. It is important to note that, for SLAP repair, the biomechanical characteristics of knotless anchors are equivalent to those of knotted anchors.13 In addition, knotless anchors offer the advantage of avoiding knot impingement and migration.14 On that basis, and given the anatomy mentioned, we primarily use short knotless anchors for SLAP repair and think that, as long as biomechanically supported, the trend should be to use shorter anchors for SLAP repair in order to minimize the risks for glenoid vault penetration and SSN injury.

One limitation of this study was the small number of cadavers, all of which were male. Female cadavers and cadavers of other ethnic origins likely have smaller glenoid vaults, and thus their inclusion would have altered our results. This issue was well described in studies mentioned in this article, and our goal was simply to compare ASL portals with percutaneous PW portals, so we think it does not change the fact that the risks for glenoid vault penetration and SSN injury are reduced with use of PW portals for anchors placed posterior to the biceps tendon.

 

 

Conclusion

This study was the first to examine glenoid vault penetration and SSN proximity with short anchors for SLAP repair. The risk for glenoid vault penetration during repair of SLAP tears posterior to the biceps tendon was reduced by anchor placement with a percutaneous posterior approach. The percutaneous posterior approach also directs the anchor away from the SSN.

Am J Orthop. 2017;46(1):E60-E64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

  • Anchors placed posterior to the biceps during SLAP repair are at risk for glenoid vault penetration and/or suprascapular nerve (SSN) injury.
  • Vault penetration and SSN injury are avoided by using a Port of Wilmington (PW) portal instead of an anterior portal.
  • A percutaneous PW portal is safe and passes through the rotator cuff muscle only.

Since being classified by Snyder and colleagues,1 various arthroscopic techniques have been used to repair superior labrum anterior and posterior (SLAP) tears, particularly type II tears. Despite being commonly performed, repairs of SLAP lesions remain challenging. There is high variability in the rate of good/excellent functional outcomes and athletes’ return to previous level of play after SLAP repairs.2,3 Furthermore, the rate of complications after SLAP repair is as high as 5%.4

One of the most common complications of repair of a type II SLAP tear is nerve injury.4 In particular, suprascapular nerve (SSN) injury has occurred after arthroscopic repair of SLAP tears.5,6 Three cadaveric studies have demonstrated that glenoid vault penetration is common during placement of knotted anchors for SLAP repair and that the SSN is at risk during placement of these anchors.7-9 However, 2 of the 3 studies used only an anterior portal in their evaluation of anchor placement. Safety of anchor placement posterior to the biceps tendon may be improved with a percutaneous approach using a Port of Wilmington (PW) portal.10,11 No studies have evaluated the risk of glenoid vault penetration and SSN injury with shorter knotless anchors.

We conducted a study to compare a standard anterosuperolateral (ASL) portal with a percutaneous PW portal for knotless anchors placed posterior to the biceps tendon during repair of SLAP tears. We hypothesized that anchors placed through the PW portal would be less likely to penetrate the glenoid vault and would be farther from the SSN in the event of bone penetration.

Materials and Methods

Six matched pairs of fresh human cadaveric shoulders were used in this study. Each specimen included the scapula, the clavicle, and the humerus. All 6 specimens were male, and their mean age was 41.2 years (range, 23-59 years). Shoulder arthroscopy was performed for placement of SLAP anchors, and open dissection followed.

Anchor Placement

The scapula was clamped and the shoulder placed in the lateral decubitus position with 30° of abduction, 20° of forward flexion, and neutral rotation.10 A standard posterior glenohumeral viewing portal was established and a 30° arthroscope inserted. Both shoulders of each matched pair were randomly assigned to anchor placement through either an ASL portal or a PW portal. Two anchors were placed in the superior glenoid to simulate repair of a posterior SLAP tear.11 Each was a 2.9-mm short (12.5-mm) knotless anchor (BioComposite PushLock; Arthrex) that included a polyetheretherketone (PEEK) eyelet for threading sutures before anchor placement. A drill guide was inserted according to manufacturer guidelines, and a 2.9-mm drill was used to make a bone socket 18 mm deep. The anchor eyelet was loaded with suture tape (Labral Tape; Arthrex), and the anchor and suture were inserted into the socket. The sutures were left uncut to aid in anchor visualization during open dissection. On a right shoulder, the first anchor was placed just posterior to the biceps tendon, at 11 o’clock, and the second anchor about 1 cm posterior to the first, at 10 o’clock. All anchors were placed by an arthroscopy fellowship–trained shoulder surgeon. Before placement, anchor location was confirmed by another arthroscopy fellowship–trained shoulder surgeon.

The ASL portal was created, with an 18-gauge spinal needle and an outside-in technique, about 1 cm lateral to the anterolateral corner of the acromion.

Figure 1.
The portal was established through the rotator interval just anterior to the leading edge of the supraspinatus tendon and posterior to the long head of the biceps tendon. In this portal, an 8.25-mm threaded cannula was inserted for anchor placement (Figure 1).

In the opposite shoulder, the PW portal was created, with a percutaneous technique, about 1 cm anterior and 1 cm lateral to the posterolateral corner of the acromion. An 18-gauge spinal needle was inserted to allow a 45° angle of approach to the posterosuperior glenoid.11
Figure 2.
A guide wire was threaded through the needle, and the needle was removed. Then the portal was dilated, and a 4.5-mm metal cannula was inserted for anchor placement (Figure 2).

Cadaveric Dissection

After anchor placement, another shoulder surgeon performed the dissection. Skin, subcutaneous tissue, deltoid, and clavicle were removed. In the percutaneous specimens, PW portal location relative to rotator cuff was recorded before cuff removal. After overlying soft tissues were removed from a specimen, the anchors were examined for glenoid vault penetration. In the setting of vault penetration, digital calipers were used to measure the shortest distance from anchor to SSN.

 

 

Results

In the ASL portal group, 8 (66.7%) of 12 anchors (4/6 at 11 o’clock, 4/6 at 10 o’clock) penetrated the medial glenoid vault.

Table.
In the 8 penetration cases, mean distance to SSN was 6.8 mm (range, 0-14 mm) for 11 o’clock anchors and 4.8 mm (range, 0-14 mm) for 10 o’clock anchors (Table).

In the PW portal group, 2 (16.7%) of 12 anchors (1/6 at 11 o’clock, 1/6 at 10 o’clock, both from a single specimen) penetrated the medial glenoid vault. Actually, in each case the eyelet and not the anchor penetrated the vault. In the penetration cases, distance to SSN was 20 mm for the 11 o’clock anchor and 8 mm for the 10 o’clock anchor (Table). Of the 6 portals, 3 passed through the supraspinatus muscle, 2 through the infraspinatus musculotendinous junction, and 1 through the infraspinatus muscle.

Discussion

Our study findings support the hypothesis that SLAP repair anchors placed posterior to the biceps tendon are more likely to remain in bone with use of a percutaneous approach relative to an ASL approach. Our findings also support the growing body of evidence that such anchors placed with an anterior approach increase the risk for SSN injury.

Three other cadaveric studies have evaluated anchor placement for SLAP repair. Chan and colleagues7 evaluated drill penetration during bone socket preparation for SLAP repair in 21 matched pairs of formalin-embalmed cadavers. A 20-mm drill was used for correspondence to a 14.5-mm anchor, though no anchors were inserted, and sockets were created in an open manner. Through a mimicked ASL portal, 1 socket was made anterior to the biceps tendon, at 1 o’clock; then, through a mimicked PW portal, 2 sockets were made posterior to the tendon, at 11 o’clock and 9 to 10 o’clock. Glenoid vault penetration occurred in 29% of the 42 anterior sockets, but only 1 anchor (2.4%) touched the SSN. Penetration did not occur with the 11 o’clock anchors. The 9 to 10 o’clock anchor was at highest risk for SSN injury (9.5%, 4 cases). The study was limited by lack of anchor placement and open creation of bone sockets in embalmed cadavers.

Koh and colleagues8 evaluated arthroscopic placement of anterior SLAP anchors in 6 matched pairs of fresh-frozen cadavers. Through an ASL portal, each 14.5-mm knotted anchor was placed anterior to the biceps tendon, at 1 o’clock. As in the study by Chan and colleagues,7 drill depth was 20 mm. Notably, anchors were seated 2 mm beyond manufacturer recommendations, and the cadavers were of Asian origin, likely indicating smaller glenoids compared to specimens from North America or Europe. All 12 anchors penetrated the glenoid vault; mean distance to SSN was 3.1 mm.

Morgan and colleagues9 compared anterior and ASL portals created for SLAP repairs in 10 matched-pair cadavers. Anchors were placed at 1 o’clock, 11 o’clock, and 10 o’clock. As in the studies by Chan and colleagues7 and Koh and colleagues,8 14.5-mm knotted anchors were used. One anterior anchor (10%) placed through an ASL portal penetrated the cortex by 1 mm, and 2 anterior anchors (20%) placed through anterior portals penetrated the cortex (1 was completely out of the bone). Overall, 65% of 11 o’clock anchors and 100% of 10 o’clock anchors violated the glenoid vault. With the 11 o’clock anchors, mean distance to SSN was 6 mm for ASL portals and 4.2 mm for anterior portals; with the 10 o’clock anchors, mean distance to SSN was 8 mm for ASL portals and 2.1 mm for anterior portals.

Overall, the results of these 3 studies suggest that, with use of ASL portals, placement of SLAP anchors anterior to the biceps tendon is safe. Using the same portals, however, anchors placed posterior to the tendon are at higher risk for glenoid vault penetration. Supporting these findings are our study’s penetration rates: 66.7% for anchors placed through ASL portals and 16.7% for anchors placed through percutaneous PW portals. The different rates are not surprising given that the coracoid process projects anterior to the glenoid and provides additional bone stock for placement of anchors anteriorly vs posteriorly. Therefore, with percutaneous PW portals, the approach angle directs the anchor toward the bone of the coracoid base. Furthermore, the SSN passes nearest the posterior aspect of the glenoid. In a study by Shishido and Kikuchi,12 the distance from the posterior rim of the glenoid to the SSN was 18 mm, and from the superior rim was 29 mm. Therefore, anchors placed with an anterior approach naturally are directed toward the SSN.

Figure 3.
Given these findings, we think surgeons who repair posterior SLAP tears should place anchors through percutaneous PW portals, not ASL portals, in order to minimize the risks for glenoid vault penetration and SSN injury (Figures 3, 4A-4B).

In addition to portal placement and approach angle, anchor length likely affects the risks for glenoid vault penetration and SSN injury.
Figure 4.
Koh and colleagues8 found a mean distance of 14.2 mm from the glenoid rim to the medial cortex for anchors placed anterior to the biceps tendon and a mean distance of 20.7 mm from the glenoid rim to the SSN. Morgan and colleagues9 also evaluated the shortest distance from the glenoid rim to the SSN. Mean distance was 17.9 mm for 10 o’clock anchors and 20.9 mm for 11 o’clock anchors. Whereas the 3 cadaveric studies discussed earlier7-9 examined 14.5-mm knotted anchors with drill depths of 20 mm, we examined 12.5-mm knotless anchors with drill depths of 18 mm. Even with the 1 anchor penetration that occurred with a percutaneous portal in our study, the SSN was 20 mm from the 11 o’clock portal and 8 mm from the 10 o’clock portal. It is important to note that, for SLAP repair, the biomechanical characteristics of knotless anchors are equivalent to those of knotted anchors.13 In addition, knotless anchors offer the advantage of avoiding knot impingement and migration.14 On that basis, and given the anatomy mentioned, we primarily use short knotless anchors for SLAP repair and think that, as long as biomechanically supported, the trend should be to use shorter anchors for SLAP repair in order to minimize the risks for glenoid vault penetration and SSN injury.

One limitation of this study was the small number of cadavers, all of which were male. Female cadavers and cadavers of other ethnic origins likely have smaller glenoid vaults, and thus their inclusion would have altered our results. This issue was well described in studies mentioned in this article, and our goal was simply to compare ASL portals with percutaneous PW portals, so we think it does not change the fact that the risks for glenoid vault penetration and SSN injury are reduced with use of PW portals for anchors placed posterior to the biceps tendon.

 

 

Conclusion

This study was the first to examine glenoid vault penetration and SSN proximity with short anchors for SLAP repair. The risk for glenoid vault penetration during repair of SLAP tears posterior to the biceps tendon was reduced by anchor placement with a percutaneous posterior approach. The percutaneous posterior approach also directs the anchor away from the SSN.

Am J Orthop. 2017;46(1):E60-E64. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

References

1. Snyder SJ, Banas MP, Karzel RP. An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg. 1995;4(4):243-248.

2. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.

3. Gorantla K, Gill C, Wright RW. The outcome of type II SLAP repair: a systematic review. Arthroscopy. 2010;26(4):537-545.

4. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

5. Kim SH, Koh YG, Sung CH, Moon HK, Park YS. Iatrogenic suprascapular nerve injury after repair of type II SLAP lesion. Arthroscopy. 2010;26(7):1005-1008.

6. Yoo JC, Lee YS, Ahn JH, Park JH, Kang HJ, Koh KH. Isolated suprascapular nerve injury below the spinoglenoid notch after SLAP repair. J Shoulder Elbow Surg. 2009;18(4):e27-e29.

7. Chan H, Beaupre LA, Bouliane MJ. Injury of the suprascapular nerve during arthroscopic repair of superior labral tears: an anatomic study. J Shoulder Elbow Surg. 2010;19(5):709-715.

8. Koh KH, Park WH, Lim TK, Yoo JC. Medial perforation of the glenoid neck following SLAP repair places the suprascapular nerve at risk: a cadaveric study. J Shoulder Elbow Surg. 2011;20(2):245-250.

9. Morgan RT, Henn RF 3rd, Paryavi E, Dreese J. Injury to the suprascapular nerve during superior labrum anterior and posterior repair: is a rotator interval portal safer than an anterosuperior portal? Arthroscopy. 2014;30(11):1418-1423.

10. Lo IK, Lind CC, Burkhart SS. Glenohumeral arthroscopy portals established using an outside-in technique: neurovascular anatomy at risk. Arthroscopy. 2004;20(6):596-602.

11. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.

12. Shishido H, Kikuchi S. Injury of the suprascapular nerve in shoulder surgery: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):372-376.

13. Uggen C, Wei A, Glousman RE, et al. Biomechanical comparison of knotless anchor repair versus simple suture repair for type II SLAP lesions. Arthroscopy. 2009;25(10):1085-1092.

14. Kim SH, Crater RB, Hargens AR. Movement-induced knot migration after anterior stabilization in the shoulder. Arthroscopy. 2013;29(3):485-490.

References

1. Snyder SJ, Banas MP, Karzel RP. An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg. 1995;4(4):243-248.

2. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.

3. Gorantla K, Gill C, Wright RW. The outcome of type II SLAP repair: a systematic review. Arthroscopy. 2010;26(4):537-545.

4. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.

5. Kim SH, Koh YG, Sung CH, Moon HK, Park YS. Iatrogenic suprascapular nerve injury after repair of type II SLAP lesion. Arthroscopy. 2010;26(7):1005-1008.

6. Yoo JC, Lee YS, Ahn JH, Park JH, Kang HJ, Koh KH. Isolated suprascapular nerve injury below the spinoglenoid notch after SLAP repair. J Shoulder Elbow Surg. 2009;18(4):e27-e29.

7. Chan H, Beaupre LA, Bouliane MJ. Injury of the suprascapular nerve during arthroscopic repair of superior labral tears: an anatomic study. J Shoulder Elbow Surg. 2010;19(5):709-715.

8. Koh KH, Park WH, Lim TK, Yoo JC. Medial perforation of the glenoid neck following SLAP repair places the suprascapular nerve at risk: a cadaveric study. J Shoulder Elbow Surg. 2011;20(2):245-250.

9. Morgan RT, Henn RF 3rd, Paryavi E, Dreese J. Injury to the suprascapular nerve during superior labrum anterior and posterior repair: is a rotator interval portal safer than an anterosuperior portal? Arthroscopy. 2014;30(11):1418-1423.

10. Lo IK, Lind CC, Burkhart SS. Glenohumeral arthroscopy portals established using an outside-in technique: neurovascular anatomy at risk. Arthroscopy. 2004;20(6):596-602.

11. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.

12. Shishido H, Kikuchi S. Injury of the suprascapular nerve in shoulder surgery: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):372-376.

13. Uggen C, Wei A, Glousman RE, et al. Biomechanical comparison of knotless anchor repair versus simple suture repair for type II SLAP lesions. Arthroscopy. 2009;25(10):1085-1092.

14. Kim SH, Crater RB, Hargens AR. Movement-induced knot migration after anterior stabilization in the shoulder. Arthroscopy. 2013;29(3):485-490.

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The American Journal of Orthopedics - 46(1)
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The American Journal of Orthopedics - 46(1)
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Safety of Superior Labrum Anterior and Posterior (SLAP) Repair Posterior to Biceps Tendon Is Improved With a Percutaneous Approach
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