Shoulder & Elbow

Glenohumeral internal rotation deficit (GIRD) can be observed in overhead athletes and is thought to play a role in generating pain and rotator cuff weakness in the dominant shoulder with sport. It is unclear what is an acceptable value of GIRD in a population of overhead athletes and whether it should be based solely on internal rotation deficit or should include total range of motion (ROM) deficit.^1,2 Acquired GIRD in the athlete’s throwing shoulder has been thoroughly documented in the literature as a loss of internal rotation relative to the nonthrowing shoulder, with etiologies including bony adaptations (increased humeral retroversion), muscular tightness, and posterior capsular tightness.^1,3-11 In particular, the repetitive torsional stresses acting on the throwing shoulder of baseball players is thought to produce, over the long term, structural adaptations such as increased humeral retroversion.^5,12-14 Further, for shoulders with posterior-inferior capsular tightness, cadaveric studies have shown increased contact pressure at the coracoacromial arch during simulated follow-through.¹⁵ Athletes of other overhead and throwing sports, such as football, softball, tennis, and volleyball, may show similar adaptations in overhead motion.^9,16,17

GIRD has been associated with a variety of pathologic conditions, including scapular dyskinesis, internal and secondary impingement, partial articular-sided rotator cuff tears, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^10,12,18-22

Restriction from engaging in exacerbating activities (eg, throwing) and compliance with a specific stretching program reduces or eliminates GIRD in the majority of cases.^1,23-28 In the few cases in which conservative management fails, operative intervention may be indicated.^1,23,29,30 Few investigators have detailed an operative technique for selective arthroscopic capsular release of the posterior-inferior capsule or evaluated the ability of athletes to return to sport after such surgery.

In this article, we present our technique for arthroscopic posterior-inferior capsular release and report the results of applying this technique in a population of athletes with symptomatic GIRD that was unresponsive to nonoperative treatment and was preventing them from returning to sport.

We hypothesized that selective arthroscopic surgical release of the posterior-inferior capsule would improve symptomatic GIRD and result in a return to sport in the majority of cases unresponsive to nonoperative treatment.

Materials and Methods

Patients

After obtaining institutional review board approval, we retrospectively reviewed patient charts and collected data. Study inclusion criteria were arthroscopic selective posterior-inferior capsular release between 2004 and 2008; failure to resume sport after minimum 3 months of physical therapy, including use of sleeper stretch, active joint mobilization by licensed physical therapist, and sport-specific restriction from exacerbating activities (eg, throwing for baseball players); and active participation in overhead sport.^1,27 Exclusion criteria were generalized adhesive capsulitis, labral pathology producing glenohumeral joint instability (Bankart or reverse Bankart lesion), high-grade or full-thickness tearing of rotator cuff, and clinically significant partial-thickness tearing or instability of long head of biceps tendon.

Assessment

One of 3 authors (Dr. Buss, Dr. Codding, or Dr. Dahm) used a bubble goniometer to measure passive internal rotation. Patients were positioned supine with 90° of thoracohumeral abduction and 90° of elbow flexion. The examiner’s hand stabilized the scapula against the examination table, in accordance with published techniques.^1,26 Active internal rotation was measured at 0° of thoracohumeral abduction by noting the most superior spinal segment reached. Before and after surgery, passive internal rotation measurements were taken on both arms. GIRD was determined by the difference between dominant and nondominant arm measurements; segmental differences were obtained by subtracting segments achieved between the dominant and nondominant arms.

Before surgery and at minimum 2-year follow-up after surgery, patients completed a subjective questionnaire, which included the American Shoulder and Elbow Surgeons (ASES) Standardized Shoulder Assessment Form, for assessment of both arms. ASES scores are reliable, valid, and responsive in evaluating shoulder pain and function.^15,31 Patients also answered questions about their ability to return to play, their level of play after surgery, and whether they would undergo the procedure again.

Surgical Technique

After induction of general anesthesia and standard preparation and draping, the patient is placed in a standard beach-chair position and examined. Diagnostic arthroscopy is then performed. In all patients, intra-articular evaluation revealed a thickened, contracted posterior band of the inferior glenohumeral ligament. This finding is consistent with other studies of patients with significant GIRD.^1,14,22,30

On completion of the diagnostic portion of the arthroscopy, attention is turned to the selective posterior-inferior capsular release. Key to proper execution of the release is establishing a posterior-inferior accessory portal. This is accomplished while viewing from a standard posterior (“soft spot”) portal and determining the appropriate location and angle of entry by spinal needle localization. Typically, an entry point is selected about 4 cm distal and 1 cm lateral to the standard posterior portal. An 18-gauge spinal needle introduced at this location is angled about 15° superiorly and about 20° medially. Once the appropriate vector is determined, a skin incision is made, and a Wissinger rod is introduced, over which a small-diameter cannula is passed. A hooked-tip electrocautery device is used to divide the posterior capsule from the glenoid labrum between the 8- and 6-o’clock positions in the right shoulder (Figure). Care is taken to perform the release immediately adjacent to the glenoid labrum and using short bursts of cautery in order to minimize risk of injury to the teres minor branch of the axillary nerve. Adequate release is confirmed by reassessing passive internal rotation under anesthesia. Additional procedures are performed, if necessary, after completion of the capsular release.

Postoperative rehabilitation consists initially of pendulum exercises and scapular retraction starting on postoperative day 1. Once the swelling from the surgical procedure subsides, typically within 1 week, passive and active-assisted ROM and gentle posterior capsular mobilization are initiated under the direction of a licensed physical therapist. Active ROM is allowed once the patient regains normal scapulothoracic rhythm. Strengthening consists initially of isometrics followed by light resistance strengthening for the rotator cuff and scapular stabilizers once active ROM and scapulothoracic rhythm return to normal. Passive internal rotation stretching, including use of the sleeper stretch, is implemented as soon as tolerated and continues throughout the rehabilitation process.³²

Statistical Analysis

Statistical analysis was performed with Stata Release 11 (StataCorp, College Station, Texas). Paired t tests were used to assess preoperative and postoperative mean differences in ASES scores, in passive glenohumeral internal rotation, and in active glenohumeral internal rotation; independent-samples t tests were used to assess side-to-side differences. Significance was set at P < .05.

Results

Fifteen overhead athletes met the study inclusion criteria. Two were lost to follow-up. Of the remaining 13 patients, 6 underwent isolated arthroscopic posterior-inferior capsular release, and 7 had concomitant procedures (6 subacromial decompressions, 1 superior labrum anterior-posterior [SLAP] repair). There were 11 male athletes and 2 female athletes. Twelve of the 13 patients were right-hand–dominant. Mean age at time of surgery was 21 years (range, 16-33 years). There were 10 baseball players (6 pitchers, 4 position players); the other 3 patients played softball (1), volleyball (1), or tennis (1). Six patients played at high school level, 5 at college level, 1 at professional level, and 1 at amateur level. All 13 patients underwent a minimum of 3 months of comprehensive rehabilitation, which included use of the sleeper stretch, active joint mobilization by a licensed physical therapist, and sport-specific restriction from exacerbating activities. Mean duration of symptoms before surgery was 18 months (range, 4-48 months). Mean postoperative follow-up was 31 months (range, 24-59 months). Mean ASES score was 71.5 (range, 33-95) before surgery and 86.9 (range, 60-100) after surgery (P < .001). Mean GIRD improved from 43.1° (range, 30°-60°) before surgery to 9.7° (range, –7° to 40°) after surgery (P < .001). Mean active internal rotation difference improved from 3.8 vertebral segments before surgery to 2.6 vertebral segments after surgery; this difference was not statistically significant (P = .459). Ten (77%) of the 13 patients returned to their preoperative level of play or a higher level; the other 3 (23%) did not return to their preoperative level of play but continued to compete in a different position (Table). Eleven patients (85%) stated they would repeat the procedure. One of the 2 patients who would not repeat the procedure was in the isolated posterior-inferior capsular release group; the other was in the concomitant-procedure group (subacromial decompression). Total glenohumeral ROM of dominant arm was 122° before surgery and 136° after surgery (P = .04). There was no significant difference in total ROM between dominant and nondominant arms after surgery (136° and 141°; P = .12), but the preoperative difference was significant (122° vs 141°; P = .022).

Discussion

GIRD has been associated with various pathologic conditions of the upper extremity. In 1991, Verna²⁸ found that a majority of 39 professional baseball pitchers with significant GIRD had shoulder problems that affected playing time. More recently, GIRD has been associated with a progression of injuries, including scapular dyskinesia, internal and secondary impingement, articular-sided partial rotator cuff tears, rotator cuff weakness, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^12,18-22 In a cadaveric study of humeral head translation, Harryman and colleagues³³ noted an anterosuperior migration of the humeral head during flexion and concluded it resulted from a loose anterior and tight posterior glenohumeral capsule, leading to loss of glenohumeral internal rotation. More recently, posterosuperior migration of the humeral head has been postulated, with GIRD secondary to an essential posterior capsular contracture.¹ Tyler and colleagues³⁴ clinically linked posterior capsular tightness with GIRD, and both cadaveric and magnetic resonance imaging studies have supported the finding that posterior capsular contracture leads to posterosuperior humeral head migration in association with GIRD.^14,20 Such a disruption in normal glenohumeral joint mechanics could produce phenomena of internal or secondary acromiohumeral impingement and pain.

More recently, in a large cohort of professional baseball pitchers, a significant correlation was found between the incidence of rotator cuff strength deficits and GIRD.³⁵ More than 40% of the pitchers with GIRD of at least 35° had a measureable rotator cuff strength deficit in the throwing shoulder.

Burkhart and colleagues²³ concluded that the shoulder most at risk for developing “dead arm” has GIRD and an advanced form of scapular dyskinesia known as SICK scapula (the phenomenon involves Scapula malposition, Inferior medial border prominence, Coracoid pain and malposition, and dysKinesis of scapular movement).

Most athletes with symptoms attributed to GIRD respond to conservative management. A posterior-inferior capsular stretching program focused on regaining internal rotation in the throwing arm has been shown to return about 90% of athletes to play.¹ Numerous studies have indicated that enrollment in a compliant stretching program reduces GIRD.^1,23-27 However, nonoperative treatment fails in a reported 10% of patients with GIRD; these patients may respond to operative treatment.¹

More specifically, for patients who do not respond to conservative treatment, a posterior-inferior capsular release may be indicated.^1,29 Ticker and colleagues²² identified 9 patients who had lost internal rotation and had a posterior capsular contracture at arthroscopy. That study, however, was not performed on overhead or throwing athletes. Yoneda and colleagues³⁰ followed 16 overhead throwing athletes after arthroscopic posterior-inferior capsular release and found favorable preliminary clinical results. Eleven of the 16 patients returned to their preinjury level of performance; the other 5 returned to a lower level. In addition, all 4 patients who underwent isolated arthroscopic capsular release had throwing power restored to between 90% and 100%.

In the present study, 10 of 13 patients who underwent arthroscopic posterior-inferior capsular release returned to their preoperative level of play or a higher level. Mean passive GIRD improved significantly from before surgery to after surgery. ASES scores likewise were significantly improved from before surgery to after surgery. The active internal rotation difference as measured by vertebral segment level was not significantly changed after surgery. This lack of improvement may stem from the more complex musculoligamentous interactions governing active internal rotation versus isolated, passive internal rotation. Another possible explanation for lack of improvement is that the interobserver and intraobserver reliability of this method is lower.³⁶

At 2-year follow-up, the patient who had undergone concomitant SLAP repair demonstrated a 23% improvement in ASES score and more internal rotation on the dominant arm relative to the nondominant arm. This patient returned to a level of play at least as good as his preoperative level. Although we could not determine its statistical significance, this patient’s improvement suggests that the SLAP repair did not reduce the efficacy of the posterior-inferior capsular release.

Limitations of this study include its relatively small cohort (precluded statistical comparisons between groups), the proportion of patients (7/13) who had concomitant surgeries, and the limited options for patient outcome scores. Although the ASES score is a validated outcome score, the Kerlan-Jobe Orthopaedic Clinic Shoulder and Elbow (KJOC) score or the Disabilities of the Arm, Shoulder, and Hand (DASH) score may be more appropriate in an athletic population. In addition, although all study patients had GIRD that was unresponsive to a concerted trial of nonoperative management, we did not have a control group (nonoperatively treated patients) for comparison. Finally, we did not obtain computed tomography scans or account for the potential contribution of humeral retroversion to GIRD in this group of patients.

Conclusion

Selective arthroscopic posterior-inferior capsular release can be recommended as a reasonable operative solution for overhead athletes with symptomatic GIRD that has not responded to conservative management. In the present study, ASES scores improved significantly, and 77% of our athlete-patients returned to sport at their preoperative level of play or a higher level.

Glenohumeral internal rotation deficit (GIRD) can be observed in overhead athletes and is thought to play a role in generating pain and rotator cuff weakness in the dominant shoulder with sport. It is unclear what is an acceptable value of GIRD in a population of overhead athletes and whether it should be based solely on internal rotation deficit or should include total range of motion (ROM) deficit.^1,2 Acquired GIRD in the athlete’s throwing shoulder has been thoroughly documented in the literature as a loss of internal rotation relative to the nonthrowing shoulder, with etiologies including bony adaptations (increased humeral retroversion), muscular tightness, and posterior capsular tightness.^1,3-11 In particular, the repetitive torsional stresses acting on the throwing shoulder of baseball players is thought to produce, over the long term, structural adaptations such as increased humeral retroversion.^5,12-14 Further, for shoulders with posterior-inferior capsular tightness, cadaveric studies have shown increased contact pressure at the coracoacromial arch during simulated follow-through.¹⁵ Athletes of other overhead and throwing sports, such as football, softball, tennis, and volleyball, may show similar adaptations in overhead motion.^9,16,17

GIRD has been associated with a variety of pathologic conditions, including scapular dyskinesis, internal and secondary impingement, partial articular-sided rotator cuff tears, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^10,12,18-22

Restriction from engaging in exacerbating activities (eg, throwing) and compliance with a specific stretching program reduces or eliminates GIRD in the majority of cases.^1,23-28 In the few cases in which conservative management fails, operative intervention may be indicated.^1,23,29,30 Few investigators have detailed an operative technique for selective arthroscopic capsular release of the posterior-inferior capsule or evaluated the ability of athletes to return to sport after such surgery.

In this article, we present our technique for arthroscopic posterior-inferior capsular release and report the results of applying this technique in a population of athletes with symptomatic GIRD that was unresponsive to nonoperative treatment and was preventing them from returning to sport.

We hypothesized that selective arthroscopic surgical release of the posterior-inferior capsule would improve symptomatic GIRD and result in a return to sport in the majority of cases unresponsive to nonoperative treatment.

Materials and Methods

Patients

After obtaining institutional review board approval, we retrospectively reviewed patient charts and collected data. Study inclusion criteria were arthroscopic selective posterior-inferior capsular release between 2004 and 2008; failure to resume sport after minimum 3 months of physical therapy, including use of sleeper stretch, active joint mobilization by licensed physical therapist, and sport-specific restriction from exacerbating activities (eg, throwing for baseball players); and active participation in overhead sport.^1,27 Exclusion criteria were generalized adhesive capsulitis, labral pathology producing glenohumeral joint instability (Bankart or reverse Bankart lesion), high-grade or full-thickness tearing of rotator cuff, and clinically significant partial-thickness tearing or instability of long head of biceps tendon.

Assessment

One of 3 authors (Dr. Buss, Dr. Codding, or Dr. Dahm) used a bubble goniometer to measure passive internal rotation. Patients were positioned supine with 90° of thoracohumeral abduction and 90° of elbow flexion. The examiner’s hand stabilized the scapula against the examination table, in accordance with published techniques.^1,26 Active internal rotation was measured at 0° of thoracohumeral abduction by noting the most superior spinal segment reached. Before and after surgery, passive internal rotation measurements were taken on both arms. GIRD was determined by the difference between dominant and nondominant arm measurements; segmental differences were obtained by subtracting segments achieved between the dominant and nondominant arms.

Before surgery and at minimum 2-year follow-up after surgery, patients completed a subjective questionnaire, which included the American Shoulder and Elbow Surgeons (ASES) Standardized Shoulder Assessment Form, for assessment of both arms. ASES scores are reliable, valid, and responsive in evaluating shoulder pain and function.^15,31 Patients also answered questions about their ability to return to play, their level of play after surgery, and whether they would undergo the procedure again.

Surgical Technique

After induction of general anesthesia and standard preparation and draping, the patient is placed in a standard beach-chair position and examined. Diagnostic arthroscopy is then performed. In all patients, intra-articular evaluation revealed a thickened, contracted posterior band of the inferior glenohumeral ligament. This finding is consistent with other studies of patients with significant GIRD.^1,14,22,30

On completion of the diagnostic portion of the arthroscopy, attention is turned to the selective posterior-inferior capsular release. Key to proper execution of the release is establishing a posterior-inferior accessory portal. This is accomplished while viewing from a standard posterior (“soft spot”) portal and determining the appropriate location and angle of entry by spinal needle localization. Typically, an entry point is selected about 4 cm distal and 1 cm lateral to the standard posterior portal. An 18-gauge spinal needle introduced at this location is angled about 15° superiorly and about 20° medially. Once the appropriate vector is determined, a skin incision is made, and a Wissinger rod is introduced, over which a small-diameter cannula is passed. A hooked-tip electrocautery device is used to divide the posterior capsule from the glenoid labrum between the 8- and 6-o’clock positions in the right shoulder (Figure). Care is taken to perform the release immediately adjacent to the glenoid labrum and using short bursts of cautery in order to minimize risk of injury to the teres minor branch of the axillary nerve. Adequate release is confirmed by reassessing passive internal rotation under anesthesia. Additional procedures are performed, if necessary, after completion of the capsular release.

Postoperative rehabilitation consists initially of pendulum exercises and scapular retraction starting on postoperative day 1. Once the swelling from the surgical procedure subsides, typically within 1 week, passive and active-assisted ROM and gentle posterior capsular mobilization are initiated under the direction of a licensed physical therapist. Active ROM is allowed once the patient regains normal scapulothoracic rhythm. Strengthening consists initially of isometrics followed by light resistance strengthening for the rotator cuff and scapular stabilizers once active ROM and scapulothoracic rhythm return to normal. Passive internal rotation stretching, including use of the sleeper stretch, is implemented as soon as tolerated and continues throughout the rehabilitation process.³²

Statistical Analysis

Statistical analysis was performed with Stata Release 11 (StataCorp, College Station, Texas). Paired t tests were used to assess preoperative and postoperative mean differences in ASES scores, in passive glenohumeral internal rotation, and in active glenohumeral internal rotation; independent-samples t tests were used to assess side-to-side differences. Significance was set at P < .05.

Results

Fifteen overhead athletes met the study inclusion criteria. Two were lost to follow-up. Of the remaining 13 patients, 6 underwent isolated arthroscopic posterior-inferior capsular release, and 7 had concomitant procedures (6 subacromial decompressions, 1 superior labrum anterior-posterior [SLAP] repair). There were 11 male athletes and 2 female athletes. Twelve of the 13 patients were right-hand–dominant. Mean age at time of surgery was 21 years (range, 16-33 years). There were 10 baseball players (6 pitchers, 4 position players); the other 3 patients played softball (1), volleyball (1), or tennis (1). Six patients played at high school level, 5 at college level, 1 at professional level, and 1 at amateur level. All 13 patients underwent a minimum of 3 months of comprehensive rehabilitation, which included use of the sleeper stretch, active joint mobilization by a licensed physical therapist, and sport-specific restriction from exacerbating activities. Mean duration of symptoms before surgery was 18 months (range, 4-48 months). Mean postoperative follow-up was 31 months (range, 24-59 months). Mean ASES score was 71.5 (range, 33-95) before surgery and 86.9 (range, 60-100) after surgery (P < .001). Mean GIRD improved from 43.1° (range, 30°-60°) before surgery to 9.7° (range, –7° to 40°) after surgery (P < .001). Mean active internal rotation difference improved from 3.8 vertebral segments before surgery to 2.6 vertebral segments after surgery; this difference was not statistically significant (P = .459). Ten (77%) of the 13 patients returned to their preoperative level of play or a higher level; the other 3 (23%) did not return to their preoperative level of play but continued to compete in a different position (Table). Eleven patients (85%) stated they would repeat the procedure. One of the 2 patients who would not repeat the procedure was in the isolated posterior-inferior capsular release group; the other was in the concomitant-procedure group (subacromial decompression). Total glenohumeral ROM of dominant arm was 122° before surgery and 136° after surgery (P = .04). There was no significant difference in total ROM between dominant and nondominant arms after surgery (136° and 141°; P = .12), but the preoperative difference was significant (122° vs 141°; P = .022).

Discussion

GIRD has been associated with various pathologic conditions of the upper extremity. In 1991, Verna²⁸ found that a majority of 39 professional baseball pitchers with significant GIRD had shoulder problems that affected playing time. More recently, GIRD has been associated with a progression of injuries, including scapular dyskinesia, internal and secondary impingement, articular-sided partial rotator cuff tears, rotator cuff weakness, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^12,18-22 In a cadaveric study of humeral head translation, Harryman and colleagues³³ noted an anterosuperior migration of the humeral head during flexion and concluded it resulted from a loose anterior and tight posterior glenohumeral capsule, leading to loss of glenohumeral internal rotation. More recently, posterosuperior migration of the humeral head has been postulated, with GIRD secondary to an essential posterior capsular contracture.¹ Tyler and colleagues³⁴ clinically linked posterior capsular tightness with GIRD, and both cadaveric and magnetic resonance imaging studies have supported the finding that posterior capsular contracture leads to posterosuperior humeral head migration in association with GIRD.^14,20 Such a disruption in normal glenohumeral joint mechanics could produce phenomena of internal or secondary acromiohumeral impingement and pain.

More recently, in a large cohort of professional baseball pitchers, a significant correlation was found between the incidence of rotator cuff strength deficits and GIRD.³⁵ More than 40% of the pitchers with GIRD of at least 35° had a measureable rotator cuff strength deficit in the throwing shoulder.

Burkhart and colleagues²³ concluded that the shoulder most at risk for developing “dead arm” has GIRD and an advanced form of scapular dyskinesia known as SICK scapula (the phenomenon involves Scapula malposition, Inferior medial border prominence, Coracoid pain and malposition, and dysKinesis of scapular movement).

Most athletes with symptoms attributed to GIRD respond to conservative management. A posterior-inferior capsular stretching program focused on regaining internal rotation in the throwing arm has been shown to return about 90% of athletes to play.¹ Numerous studies have indicated that enrollment in a compliant stretching program reduces GIRD.^1,23-27 However, nonoperative treatment fails in a reported 10% of patients with GIRD; these patients may respond to operative treatment.¹

More specifically, for patients who do not respond to conservative treatment, a posterior-inferior capsular release may be indicated.^1,29 Ticker and colleagues²² identified 9 patients who had lost internal rotation and had a posterior capsular contracture at arthroscopy. That study, however, was not performed on overhead or throwing athletes. Yoneda and colleagues³⁰ followed 16 overhead throwing athletes after arthroscopic posterior-inferior capsular release and found favorable preliminary clinical results. Eleven of the 16 patients returned to their preinjury level of performance; the other 5 returned to a lower level. In addition, all 4 patients who underwent isolated arthroscopic capsular release had throwing power restored to between 90% and 100%.

In the present study, 10 of 13 patients who underwent arthroscopic posterior-inferior capsular release returned to their preoperative level of play or a higher level. Mean passive GIRD improved significantly from before surgery to after surgery. ASES scores likewise were significantly improved from before surgery to after surgery. The active internal rotation difference as measured by vertebral segment level was not significantly changed after surgery. This lack of improvement may stem from the more complex musculoligamentous interactions governing active internal rotation versus isolated, passive internal rotation. Another possible explanation for lack of improvement is that the interobserver and intraobserver reliability of this method is lower.³⁶

At 2-year follow-up, the patient who had undergone concomitant SLAP repair demonstrated a 23% improvement in ASES score and more internal rotation on the dominant arm relative to the nondominant arm. This patient returned to a level of play at least as good as his preoperative level. Although we could not determine its statistical significance, this patient’s improvement suggests that the SLAP repair did not reduce the efficacy of the posterior-inferior capsular release.

Limitations of this study include its relatively small cohort (precluded statistical comparisons between groups), the proportion of patients (7/13) who had concomitant surgeries, and the limited options for patient outcome scores. Although the ASES score is a validated outcome score, the Kerlan-Jobe Orthopaedic Clinic Shoulder and Elbow (KJOC) score or the Disabilities of the Arm, Shoulder, and Hand (DASH) score may be more appropriate in an athletic population. In addition, although all study patients had GIRD that was unresponsive to a concerted trial of nonoperative management, we did not have a control group (nonoperatively treated patients) for comparison. Finally, we did not obtain computed tomography scans or account for the potential contribution of humeral retroversion to GIRD in this group of patients.

Conclusion

Selective arthroscopic posterior-inferior capsular release can be recommended as a reasonable operative solution for overhead athletes with symptomatic GIRD that has not responded to conservative management. In the present study, ASES scores improved significantly, and 77% of our athlete-patients returned to sport at their preoperative level of play or a higher level.

Glenohumeral internal rotation deficit (GIRD) can be observed in overhead athletes and is thought to play a role in generating pain and rotator cuff weakness in the dominant shoulder with sport. It is unclear what is an acceptable value of GIRD in a population of overhead athletes and whether it should be based solely on internal rotation deficit or should include total range of motion (ROM) deficit.^1,2 Acquired GIRD in the athlete’s throwing shoulder has been thoroughly documented in the literature as a loss of internal rotation relative to the nonthrowing shoulder, with etiologies including bony adaptations (increased humeral retroversion), muscular tightness, and posterior capsular tightness.^1,3-11 In particular, the repetitive torsional stresses acting on the throwing shoulder of baseball players is thought to produce, over the long term, structural adaptations such as increased humeral retroversion.^5,12-14 Further, for shoulders with posterior-inferior capsular tightness, cadaveric studies have shown increased contact pressure at the coracoacromial arch during simulated follow-through.¹⁵ Athletes of other overhead and throwing sports, such as football, softball, tennis, and volleyball, may show similar adaptations in overhead motion.^9,16,17

GIRD has been associated with a variety of pathologic conditions, including scapular dyskinesis, internal and secondary impingement, partial articular-sided rotator cuff tears, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^10,12,18-22

Restriction from engaging in exacerbating activities (eg, throwing) and compliance with a specific stretching program reduces or eliminates GIRD in the majority of cases.^1,23-28 In the few cases in which conservative management fails, operative intervention may be indicated.^1,23,29,30 Few investigators have detailed an operative technique for selective arthroscopic capsular release of the posterior-inferior capsule or evaluated the ability of athletes to return to sport after such surgery.

In this article, we present our technique for arthroscopic posterior-inferior capsular release and report the results of applying this technique in a population of athletes with symptomatic GIRD that was unresponsive to nonoperative treatment and was preventing them from returning to sport.

We hypothesized that selective arthroscopic surgical release of the posterior-inferior capsule would improve symptomatic GIRD and result in a return to sport in the majority of cases unresponsive to nonoperative treatment.

Materials and Methods

Patients

After obtaining institutional review board approval, we retrospectively reviewed patient charts and collected data. Study inclusion criteria were arthroscopic selective posterior-inferior capsular release between 2004 and 2008; failure to resume sport after minimum 3 months of physical therapy, including use of sleeper stretch, active joint mobilization by licensed physical therapist, and sport-specific restriction from exacerbating activities (eg, throwing for baseball players); and active participation in overhead sport.^1,27 Exclusion criteria were generalized adhesive capsulitis, labral pathology producing glenohumeral joint instability (Bankart or reverse Bankart lesion), high-grade or full-thickness tearing of rotator cuff, and clinically significant partial-thickness tearing or instability of long head of biceps tendon.

Assessment

One of 3 authors (Dr. Buss, Dr. Codding, or Dr. Dahm) used a bubble goniometer to measure passive internal rotation. Patients were positioned supine with 90° of thoracohumeral abduction and 90° of elbow flexion. The examiner’s hand stabilized the scapula against the examination table, in accordance with published techniques.^1,26 Active internal rotation was measured at 0° of thoracohumeral abduction by noting the most superior spinal segment reached. Before and after surgery, passive internal rotation measurements were taken on both arms. GIRD was determined by the difference between dominant and nondominant arm measurements; segmental differences were obtained by subtracting segments achieved between the dominant and nondominant arms.

Before surgery and at minimum 2-year follow-up after surgery, patients completed a subjective questionnaire, which included the American Shoulder and Elbow Surgeons (ASES) Standardized Shoulder Assessment Form, for assessment of both arms. ASES scores are reliable, valid, and responsive in evaluating shoulder pain and function.^15,31 Patients also answered questions about their ability to return to play, their level of play after surgery, and whether they would undergo the procedure again.

Surgical Technique

After induction of general anesthesia and standard preparation and draping, the patient is placed in a standard beach-chair position and examined. Diagnostic arthroscopy is then performed. In all patients, intra-articular evaluation revealed a thickened, contracted posterior band of the inferior glenohumeral ligament. This finding is consistent with other studies of patients with significant GIRD.^1,14,22,30

On completion of the diagnostic portion of the arthroscopy, attention is turned to the selective posterior-inferior capsular release. Key to proper execution of the release is establishing a posterior-inferior accessory portal. This is accomplished while viewing from a standard posterior (“soft spot”) portal and determining the appropriate location and angle of entry by spinal needle localization. Typically, an entry point is selected about 4 cm distal and 1 cm lateral to the standard posterior portal. An 18-gauge spinal needle introduced at this location is angled about 15° superiorly and about 20° medially. Once the appropriate vector is determined, a skin incision is made, and a Wissinger rod is introduced, over which a small-diameter cannula is passed. A hooked-tip electrocautery device is used to divide the posterior capsule from the glenoid labrum between the 8- and 6-o’clock positions in the right shoulder (Figure). Care is taken to perform the release immediately adjacent to the glenoid labrum and using short bursts of cautery in order to minimize risk of injury to the teres minor branch of the axillary nerve. Adequate release is confirmed by reassessing passive internal rotation under anesthesia. Additional procedures are performed, if necessary, after completion of the capsular release.

Postoperative rehabilitation consists initially of pendulum exercises and scapular retraction starting on postoperative day 1. Once the swelling from the surgical procedure subsides, typically within 1 week, passive and active-assisted ROM and gentle posterior capsular mobilization are initiated under the direction of a licensed physical therapist. Active ROM is allowed once the patient regains normal scapulothoracic rhythm. Strengthening consists initially of isometrics followed by light resistance strengthening for the rotator cuff and scapular stabilizers once active ROM and scapulothoracic rhythm return to normal. Passive internal rotation stretching, including use of the sleeper stretch, is implemented as soon as tolerated and continues throughout the rehabilitation process.³²

Statistical Analysis

Statistical analysis was performed with Stata Release 11 (StataCorp, College Station, Texas). Paired t tests were used to assess preoperative and postoperative mean differences in ASES scores, in passive glenohumeral internal rotation, and in active glenohumeral internal rotation; independent-samples t tests were used to assess side-to-side differences. Significance was set at P < .05.

Results

Fifteen overhead athletes met the study inclusion criteria. Two were lost to follow-up. Of the remaining 13 patients, 6 underwent isolated arthroscopic posterior-inferior capsular release, and 7 had concomitant procedures (6 subacromial decompressions, 1 superior labrum anterior-posterior [SLAP] repair). There were 11 male athletes and 2 female athletes. Twelve of the 13 patients were right-hand–dominant. Mean age at time of surgery was 21 years (range, 16-33 years). There were 10 baseball players (6 pitchers, 4 position players); the other 3 patients played softball (1), volleyball (1), or tennis (1). Six patients played at high school level, 5 at college level, 1 at professional level, and 1 at amateur level. All 13 patients underwent a minimum of 3 months of comprehensive rehabilitation, which included use of the sleeper stretch, active joint mobilization by a licensed physical therapist, and sport-specific restriction from exacerbating activities. Mean duration of symptoms before surgery was 18 months (range, 4-48 months). Mean postoperative follow-up was 31 months (range, 24-59 months). Mean ASES score was 71.5 (range, 33-95) before surgery and 86.9 (range, 60-100) after surgery (P < .001). Mean GIRD improved from 43.1° (range, 30°-60°) before surgery to 9.7° (range, –7° to 40°) after surgery (P < .001). Mean active internal rotation difference improved from 3.8 vertebral segments before surgery to 2.6 vertebral segments after surgery; this difference was not statistically significant (P = .459). Ten (77%) of the 13 patients returned to their preoperative level of play or a higher level; the other 3 (23%) did not return to their preoperative level of play but continued to compete in a different position (Table). Eleven patients (85%) stated they would repeat the procedure. One of the 2 patients who would not repeat the procedure was in the isolated posterior-inferior capsular release group; the other was in the concomitant-procedure group (subacromial decompression). Total glenohumeral ROM of dominant arm was 122° before surgery and 136° after surgery (P = .04). There was no significant difference in total ROM between dominant and nondominant arms after surgery (136° and 141°; P = .12), but the preoperative difference was significant (122° vs 141°; P = .022).

Discussion

GIRD has been associated with various pathologic conditions of the upper extremity. In 1991, Verna²⁸ found that a majority of 39 professional baseball pitchers with significant GIRD had shoulder problems that affected playing time. More recently, GIRD has been associated with a progression of injuries, including scapular dyskinesia, internal and secondary impingement, articular-sided partial rotator cuff tears, rotator cuff weakness, damage to the biceps–labral complex, and ulnar collateral ligament insufficiency.^12,18-22 In a cadaveric study of humeral head translation, Harryman and colleagues³³ noted an anterosuperior migration of the humeral head during flexion and concluded it resulted from a loose anterior and tight posterior glenohumeral capsule, leading to loss of glenohumeral internal rotation. More recently, posterosuperior migration of the humeral head has been postulated, with GIRD secondary to an essential posterior capsular contracture.¹ Tyler and colleagues³⁴ clinically linked posterior capsular tightness with GIRD, and both cadaveric and magnetic resonance imaging studies have supported the finding that posterior capsular contracture leads to posterosuperior humeral head migration in association with GIRD.^14,20 Such a disruption in normal glenohumeral joint mechanics could produce phenomena of internal or secondary acromiohumeral impingement and pain.

More recently, in a large cohort of professional baseball pitchers, a significant correlation was found between the incidence of rotator cuff strength deficits and GIRD.³⁵ More than 40% of the pitchers with GIRD of at least 35° had a measureable rotator cuff strength deficit in the throwing shoulder.

Burkhart and colleagues²³ concluded that the shoulder most at risk for developing “dead arm” has GIRD and an advanced form of scapular dyskinesia known as SICK scapula (the phenomenon involves Scapula malposition, Inferior medial border prominence, Coracoid pain and malposition, and dysKinesis of scapular movement).

Most athletes with symptoms attributed to GIRD respond to conservative management. A posterior-inferior capsular stretching program focused on regaining internal rotation in the throwing arm has been shown to return about 90% of athletes to play.¹ Numerous studies have indicated that enrollment in a compliant stretching program reduces GIRD.^1,23-27 However, nonoperative treatment fails in a reported 10% of patients with GIRD; these patients may respond to operative treatment.¹

More specifically, for patients who do not respond to conservative treatment, a posterior-inferior capsular release may be indicated.^1,29 Ticker and colleagues²² identified 9 patients who had lost internal rotation and had a posterior capsular contracture at arthroscopy. That study, however, was not performed on overhead or throwing athletes. Yoneda and colleagues³⁰ followed 16 overhead throwing athletes after arthroscopic posterior-inferior capsular release and found favorable preliminary clinical results. Eleven of the 16 patients returned to their preinjury level of performance; the other 5 returned to a lower level. In addition, all 4 patients who underwent isolated arthroscopic capsular release had throwing power restored to between 90% and 100%.

In the present study, 10 of 13 patients who underwent arthroscopic posterior-inferior capsular release returned to their preoperative level of play or a higher level. Mean passive GIRD improved significantly from before surgery to after surgery. ASES scores likewise were significantly improved from before surgery to after surgery. The active internal rotation difference as measured by vertebral segment level was not significantly changed after surgery. This lack of improvement may stem from the more complex musculoligamentous interactions governing active internal rotation versus isolated, passive internal rotation. Another possible explanation for lack of improvement is that the interobserver and intraobserver reliability of this method is lower.³⁶

At 2-year follow-up, the patient who had undergone concomitant SLAP repair demonstrated a 23% improvement in ASES score and more internal rotation on the dominant arm relative to the nondominant arm. This patient returned to a level of play at least as good as his preoperative level. Although we could not determine its statistical significance, this patient’s improvement suggests that the SLAP repair did not reduce the efficacy of the posterior-inferior capsular release.

Limitations of this study include its relatively small cohort (precluded statistical comparisons between groups), the proportion of patients (7/13) who had concomitant surgeries, and the limited options for patient outcome scores. Although the ASES score is a validated outcome score, the Kerlan-Jobe Orthopaedic Clinic Shoulder and Elbow (KJOC) score or the Disabilities of the Arm, Shoulder, and Hand (DASH) score may be more appropriate in an athletic population. In addition, although all study patients had GIRD that was unresponsive to a concerted trial of nonoperative management, we did not have a control group (nonoperatively treated patients) for comparison. Finally, we did not obtain computed tomography scans or account for the potential contribution of humeral retroversion to GIRD in this group of patients.

Conclusion

Selective arthroscopic posterior-inferior capsular release can be recommended as a reasonable operative solution for overhead athletes with symptomatic GIRD that has not responded to conservative management. In the present study, ASES scores improved significantly, and 77% of our athlete-patients returned to sport at their preoperative level of play or a higher level.

Rotator cuff tears (RCTs) are common tendon injuries that can cause chronic pain and severe functional disability. Massive RCTs do not heal spontaneously and, in many cases, result in poor clinical outcomes. Specifically, muscle atrophy and fatty infiltration correlate with poor outcomes after surgical repair.¹ Fatty infiltration of the rotator cuff is a common phenomenon that can lead to permanent structural alterations within the tendon. It has been suggested that changes in muscle fiber orientation (the pennation angle) can cause mesenchymal stem cells to migrate to the interface between muscle fibers and the region of fatty infiltration of the muscle.² Understanding the factors involved in muscle degeneration and atrophy, and in fatty infiltration, may lead to treatments that improve outcomes for patients with massive RCTs. One proposed treatment involves placing continuous mechanical traction on the ends of the torn tendon.² Findings from this research have indicated that acute tears that become chronic tears are typified by inelasticity and poor function of the muscle­–tendon unit. It is therefore important to develop a method that speeds tendon healing without causing the muscle fiber atrophy and pennation angle changes that lead to fatty atrophy, which appears to be an irreversible structural change.

On the basis of the theory that adding mesenchymal cells may improve tendon healing, investigators have studied use of transcription factors (eg, scleraxis) specific to tendogenesis in the embryonal stage.^3,4 Nevertheless, certain transcription factors are associated with formation of fibrocartilage in higher concentrations.⁴ Moreover, decalcified bone matrix increases cartilage formation when added to the tendon repair site.⁵ Cartilage formation, however, is associated with poorer functional results.⁶ Thus, there is a need for a method that facilitates faster tendon healing with higher quality tissue formation and less muscle atrophy.

Chitosan, a linear polysaccharide, is associated with scarless healing of soft tissues and prevention of adhesion formation both intraperitoneally and during tendon healing after surgery.^7,8 Chitosan tends to precipitate in physiologic pH, thereby mitigating its potency. Fortunately, a chitosan solution that does not precipitate in physiologic conditions was recently developed.⁹ The solution’s lack of precipitation, coupled with its in situ gelling, allows it to adhere to the repair site long enough to take effect. These characteristics could allow for intimate contact between gel and tendon, facilitating guided-tissue regeneration and preventing adhesion of the rotator cuff to surrounding tissue. By contrast, other biological agents (eg, platelet-rich plasma) are administered as fluid rather than gel and are therefore more susceptible to diffusing from the repair site, mitigating their effects. Thus, chitosan gel is fairly unique among agents.

In the study reported here, we histologically investigated whether a chitosan gel would help improve healing of rotator cuff tendon (acute supraspinatus) tears in a rat model.

Materials and Methods

Supraspinatus Surgical Model

Forty Wistar rats, each weighing between 300 and 400 g, were used in this study. All procedures were approved by the Institutional Animal Care and Use Committee at Rabin Medical Center in Petah Tikva, Israel. The rats were anesthetized with ketamine 90 mg/kg and xylazine 10 mg/kg, both administered intramuscularly, and anesthesia was prolonged as needed with 2% isoflurane, administered by nose cone. The skin was incised 5 cm along the upper back following the midline of the spine. The resulting skin flaps were retracted and the scapula exposed. Careful blunt dissection allowed visualization of the rotator cuff and the trans-scapular arch. A full-thickness incision of the supraspinatus tendon was then made 2 mm distal to the arch. This procedure was performed on both shoulders. For the right supraspinatus tendon, a bioabsorbable chitosan–hydrochloric acid solution (>70% de-acetylated chitosan, molecular weight of 600 kDa; Heppe Medical Chitosan GmbH, Halle, Germany) was sterilely applied to the ends of the tendon (total volume, 0.5 mL) and automatically gelled in situ by heating to about 37°C (rat’s internal body temperature). The tendon ends were subsequently approximated with a single 4-0 Prolene suture (Ethicon, Somerville, New Jersey). The left shoulder (tendon repaired with suture only) served as a control.

The rats were housed for a maximum of 12 weeks after surgery. They were sacrificed (in groups of 5 each) 2 hours, 3 days, 1 week, 2 weeks, 4 weeks, 6 weeks, 8 weeks, and 12 weeks after surgery. After each rat was sacrificed, both shoulder girdles were harvested, and the sutures were removed from the supraspinatus tendons.

Histologic Analysis

After routine fixation with 4% formalin for 48 hours and decalcification with 10% ethylenediaminetetraacetic acid (EDTA) for 3 weeks, the specimens were sectioned with a microtome blade. Care was taken to ensure the plane of the microtome blade was parallel with the longitudinal plane of the supraspinatus muscle and tendon to allow for evaluation of pennation angle. Hematoxylin-eosin staining and Masson trichrome staining were subsequently performed.

A variety of histologic measurements were obtained with use of ImageJ software (US National Institutes of Health). Percentage of fibrous tissue was determined by examining the slides at low magnification fields (×25) at the tendon healing site. Three such fields were evaluated per specimen. The fibrous tissue was circled manually, and percentage of tissue area was assessed and compared with total region of interest. Cellularity was carefully outlined and measured as percentage of total tendon area occupied by cells. Fatty atrophy was defined as either present or absent. Muscle fiber diameter was defined as average diameter of 10 muscle fibers measured within 2 mm of the tendon laceration site. Inflammatory cell collections were defined as either large (>100 µm in diameter) or small (<100 µm in diameter) and were dichotomized to either present or absent. Pennation angle was defined as average angle between muscle fibers and longitudinal axis of supraspinatus muscle and tendon unit. Ten fibers proximal to and within 2 mm of the laceration site were randomly selected, measured, and averaged.

Statistical Analysis

Statistical analysis was performed with Analyse-it 2.20 for Microsoft Excel 2010 (Analyse-it Software, Leeds, United Kingdom). Data were initially analyzed with the Kolmogorov-Smirnov test to assess for normality of distribution. The t test was used to compare continuous variables when the data were normally distributed and the Mann-Whitney test when the data were not normally distributed.

Results

All tendons (both groups) healed within 12 weeks. Generally, the tissue formed at the repair site exhibited a mixture of tenocyte-like cells (fibrotic tissue) and granulation tissue without clear orientation. As noted in Figure 1, the tendons treated with chitosan had more fibrotic tissue (overall mean, 21.5%) relative to the control group (mean, 12.3%), and the difference was significant (P = .003). The most notable differences were found at time points later than 1 week after surgery. In addition, amount of cellularity (Figure 2) was higher in chitosan-treated tendon and control tendon than in the normal, uninjured adjacent tendon at all time points (P < .001). Chitosan-treated tendons had significantly higher cellularity than untreated control tendons from 1 to 2 weeks (P < .001), and control tendons were significantly hypercellular compared with chitosan-treated tendons from 4 to 8 weeks (P < .001), but both groups exhibited similar cellularity by 12 weeks (P > .05). Fatty atrophy was found at significantly higher rates in control rats than in chitosan-treated rats (P = .001; Table). Furthermore, as noted in Figure 3, muscle fiber diameter decreased in both groups after injury (P < .001).

Figure 4 shows that the amount of inflammatory collections was significantly smaller in the chitosan-treated group than in the control group over the course of the study (P = .01). In addition, pennation angle steadily decreased in the control group throughout the study period, whereas it transiently decreased in the chitosan-treated group (until 2 weeks) before returning to its immediate postoperative level by 12 weeks (Figure 5). Overall, the chitosan-treated group maintained a higher pennation angle than the control group did (P < .001).

Discussion

RCTs affect more than 40% of patients over age 60 years and are a common cause of debilitating pain, reduced shoulder function, and weakness.¹⁰ Thirty thousand to 75,000 rotator cuff repairs are performed annually in the United States.¹¹ Although the best treatment for this disorder remains a topic of debate, arthroscopic and (when necessary) open surgical repair is the accepted gold standard for the treatment of tears that do not improve with conservative management. Despite advances in the surgical treatment of these tears, the surgical failure rates are high (range, 20%-90%), with failures attributed to factors beyond patient age, tear size and chronicity, muscle atrophy and degeneration, tendon quality, repair technique, and postoperative rehabilitation.^12,13 Repair strategies that biologically enhance the patient’s intrinsic healing potential are needed.

In tendon repair, choice of repair material (eg, graft) is crucial in determining the success of tissue engineering approaches. The ideal scaffold is biocompatible and does not elicit a host inflammatory response. The selected scaffold in its composition and fabricated form must be capable of holding and supporting cells. In addition, the scaffold should be biodegradable, serving as a temporary support for such cells and mechanically augmenting the repaired tendon while allowing for eventual replacement by matrix components. Moreover, the scaffold should have high porosity and a large surface area. Furthermore, the material should mimic the native tendon extracellular matrix (ECM) architecture to allow cells to be distributed throughout the scaffold and to facilitate diffusion of nutrients and factors that promote cellular proliferation and ECM production.

Given the importance of glycosaminoglycans (GAGs) in supporting the reticular structure of the matrix, use of GAGs or GAG-analogues as components of a tendon tissue scaffold for enhancing repair is well documented.¹⁴ One such candidate is chitosan, a partially de-acetylated derivative of chitin found in arthropod exoskeletons. Structurally, chitosan shares some characteristics with various GAGs and hyaluronic acid.¹⁵ More specifically, chitosan is a linear polysaccharide composed of glucosamine and N-acetyl glucosamine units linked by β-glycosidic bonds. Investigators have studied the properties of chitosan, including its biocompatibility, biodegradability, antibacterial activity, mucoadhesivity, and wound healing.^16,17

One of the most promising features of chitosan is that it can be processed into porous structures for use in cell transplantation and tissue regeneration.^18,19 Porous chitosan structures can be formed by freezing and lyophilizing chitosan-acetic acid solutions; chondrogenic cell adhesion and proliferation onto these structures have been reported.^20,21 This chitosan scaffolding method has also been used to test different composites with collagens, gelatins, GAGs, and hyaluronic acid, all of which have also been proposed as useful 3-dimensional materials for tissue repair.²²

In the present study, we used chitosan matrix in RCT repair. We hypothesized that chitosan matrix could enhance rotator cuff repair the same way it enhances repair in epidermal tissues.¹⁶ Histologic findings demonstrated that the percentage of fibrous tissue was significantly higher in the chitosan-treated group than in the control group. This improved fibroblastic response may be attributed to the ability of chitosan to enhance cell migration and serve as a scaffold for repair. Other studies have indicated that chitin, of which chitosan is the primary derivative, accelerated the healing of skin and subcutaneous tissues by increased cell migration.²³ Moreover, Okamoto and colleagues²⁴ reported that chitin implants stimulated abundant angiogenesis through the same mechanism.

Inadequate initial strength of a repair may lead to a recurrent cuff tear or a disability of rotator cuff function in the early healing stages. In our study, the chitosan matrix tended to be absorbed by 6 weeks after surgery. Its adherence to and ultimate absorption at the repair site may be challenged by the flow of irrigation fluid through the subacromial space in the setting of arthroscopic surgery. However, because the chitosan remains in a more robust gel form, it is better able to resist being washed from the repair site. For augmentation, it may be possible to apply a biocompatible patch over the gel to further protect it from being dislodged. In addition, histologic findings showed that the fibrous repair tissue gradually increased until reaching a peak 8 weeks after surgery—an indication that the absorption rate of the chitosan scaffold lags behind full recovery of the repair tissue. Given this relationship, further studies are needed to determine the mechanical strength of the repair between 6 and 8 weeks, which is important for avoiding recurrent tears.

This study had a few limitations. First, as with any animal model, the anatomy and function of the rat shoulder differ from those of the human shoulder. The acromial arch differs in quadruped animals, with less coverage of the supraspinatus and more of the subscapularis.²⁵ These anatomical differences could yield altered stress mechanics that could affect tendon repair. Furthermore, rats and humans differ in their RCT healing rates. Thus, the pathophysiology of muscle atrophy and fat infiltration in rats may slightly differ from that in humans. In addition, no mechanical testing was performed to compare chitosan-treated and untreated rotator cuff repairs, and such testing is needed to clarify the biomechanical importance of augmentation. Furthermore, no immunohistochemical analysis was performed for collagen. In the repair of rotator cuff tendons, surgeons must consider not only the number of cells but also the production of ECM. Although not directly confirmed in this study, chitosan induced fibrous tissue proliferation that mirrored production of a large amount of collagen fibers. Last, we used an open RTC model. As an arthroscopic model was not used, no definitive conclusions can be drawn regarding use of chitosan in arthroscopy.

Conclusion

Use of chitosan as an acellular matrix improved formation of healing fibrous tissue, increased the number of cells, and prevented fatty atrophy and inflammatory aggregates inside repair sites while facilitating recovery of the natural pennation angle of the tissue. These results demonstrate that chitosan can enhance tendon healing in the setting of acute RCT. Further research, including biomechanical testing of repaired tendons, is needed to further delineate the utility of chitosan in regenerating irreparable RCTs.

Rotator cuff tears (RCTs) are common tendon injuries that can cause chronic pain and severe functional disability. Massive RCTs do not heal spontaneously and, in many cases, result in poor clinical outcomes. Specifically, muscle atrophy and fatty infiltration correlate with poor outcomes after surgical repair.¹ Fatty infiltration of the rotator cuff is a common phenomenon that can lead to permanent structural alterations within the tendon. It has been suggested that changes in muscle fiber orientation (the pennation angle) can cause mesenchymal stem cells to migrate to the interface between muscle fibers and the region of fatty infiltration of the muscle.² Understanding the factors involved in muscle degeneration and atrophy, and in fatty infiltration, may lead to treatments that improve outcomes for patients with massive RCTs. One proposed treatment involves placing continuous mechanical traction on the ends of the torn tendon.² Findings from this research have indicated that acute tears that become chronic tears are typified by inelasticity and poor function of the muscle­–tendon unit. It is therefore important to develop a method that speeds tendon healing without causing the muscle fiber atrophy and pennation angle changes that lead to fatty atrophy, which appears to be an irreversible structural change.

On the basis of the theory that adding mesenchymal cells may improve tendon healing, investigators have studied use of transcription factors (eg, scleraxis) specific to tendogenesis in the embryonal stage.^3,4 Nevertheless, certain transcription factors are associated with formation of fibrocartilage in higher concentrations.⁴ Moreover, decalcified bone matrix increases cartilage formation when added to the tendon repair site.⁵ Cartilage formation, however, is associated with poorer functional results.⁶ Thus, there is a need for a method that facilitates faster tendon healing with higher quality tissue formation and less muscle atrophy.

Chitosan, a linear polysaccharide, is associated with scarless healing of soft tissues and prevention of adhesion formation both intraperitoneally and during tendon healing after surgery.^7,8 Chitosan tends to precipitate in physiologic pH, thereby mitigating its potency. Fortunately, a chitosan solution that does not precipitate in physiologic conditions was recently developed.⁹ The solution’s lack of precipitation, coupled with its in situ gelling, allows it to adhere to the repair site long enough to take effect. These characteristics could allow for intimate contact between gel and tendon, facilitating guided-tissue regeneration and preventing adhesion of the rotator cuff to surrounding tissue. By contrast, other biological agents (eg, platelet-rich plasma) are administered as fluid rather than gel and are therefore more susceptible to diffusing from the repair site, mitigating their effects. Thus, chitosan gel is fairly unique among agents.

In the study reported here, we histologically investigated whether a chitosan gel would help improve healing of rotator cuff tendon (acute supraspinatus) tears in a rat model.

Materials and Methods

Supraspinatus Surgical Model

Forty Wistar rats, each weighing between 300 and 400 g, were used in this study. All procedures were approved by the Institutional Animal Care and Use Committee at Rabin Medical Center in Petah Tikva, Israel. The rats were anesthetized with ketamine 90 mg/kg and xylazine 10 mg/kg, both administered intramuscularly, and anesthesia was prolonged as needed with 2% isoflurane, administered by nose cone. The skin was incised 5 cm along the upper back following the midline of the spine. The resulting skin flaps were retracted and the scapula exposed. Careful blunt dissection allowed visualization of the rotator cuff and the trans-scapular arch. A full-thickness incision of the supraspinatus tendon was then made 2 mm distal to the arch. This procedure was performed on both shoulders. For the right supraspinatus tendon, a bioabsorbable chitosan–hydrochloric acid solution (>70% de-acetylated chitosan, molecular weight of 600 kDa; Heppe Medical Chitosan GmbH, Halle, Germany) was sterilely applied to the ends of the tendon (total volume, 0.5 mL) and automatically gelled in situ by heating to about 37°C (rat’s internal body temperature). The tendon ends were subsequently approximated with a single 4-0 Prolene suture (Ethicon, Somerville, New Jersey). The left shoulder (tendon repaired with suture only) served as a control.

The rats were housed for a maximum of 12 weeks after surgery. They were sacrificed (in groups of 5 each) 2 hours, 3 days, 1 week, 2 weeks, 4 weeks, 6 weeks, 8 weeks, and 12 weeks after surgery. After each rat was sacrificed, both shoulder girdles were harvested, and the sutures were removed from the supraspinatus tendons.

Histologic Analysis

After routine fixation with 4% formalin for 48 hours and decalcification with 10% ethylenediaminetetraacetic acid (EDTA) for 3 weeks, the specimens were sectioned with a microtome blade. Care was taken to ensure the plane of the microtome blade was parallel with the longitudinal plane of the supraspinatus muscle and tendon to allow for evaluation of pennation angle. Hematoxylin-eosin staining and Masson trichrome staining were subsequently performed.

A variety of histologic measurements were obtained with use of ImageJ software (US National Institutes of Health). Percentage of fibrous tissue was determined by examining the slides at low magnification fields (×25) at the tendon healing site. Three such fields were evaluated per specimen. The fibrous tissue was circled manually, and percentage of tissue area was assessed and compared with total region of interest. Cellularity was carefully outlined and measured as percentage of total tendon area occupied by cells. Fatty atrophy was defined as either present or absent. Muscle fiber diameter was defined as average diameter of 10 muscle fibers measured within 2 mm of the tendon laceration site. Inflammatory cell collections were defined as either large (>100 µm in diameter) or small (<100 µm in diameter) and were dichotomized to either present or absent. Pennation angle was defined as average angle between muscle fibers and longitudinal axis of supraspinatus muscle and tendon unit. Ten fibers proximal to and within 2 mm of the laceration site were randomly selected, measured, and averaged.

Statistical Analysis

Statistical analysis was performed with Analyse-it 2.20 for Microsoft Excel 2010 (Analyse-it Software, Leeds, United Kingdom). Data were initially analyzed with the Kolmogorov-Smirnov test to assess for normality of distribution. The t test was used to compare continuous variables when the data were normally distributed and the Mann-Whitney test when the data were not normally distributed.

Results

All tendons (both groups) healed within 12 weeks. Generally, the tissue formed at the repair site exhibited a mixture of tenocyte-like cells (fibrotic tissue) and granulation tissue without clear orientation. As noted in Figure 1, the tendons treated with chitosan had more fibrotic tissue (overall mean, 21.5%) relative to the control group (mean, 12.3%), and the difference was significant (P = .003). The most notable differences were found at time points later than 1 week after surgery. In addition, amount of cellularity (Figure 2) was higher in chitosan-treated tendon and control tendon than in the normal, uninjured adjacent tendon at all time points (P < .001). Chitosan-treated tendons had significantly higher cellularity than untreated control tendons from 1 to 2 weeks (P < .001), and control tendons were significantly hypercellular compared with chitosan-treated tendons from 4 to 8 weeks (P < .001), but both groups exhibited similar cellularity by 12 weeks (P > .05). Fatty atrophy was found at significantly higher rates in control rats than in chitosan-treated rats (P = .001; Table). Furthermore, as noted in Figure 3, muscle fiber diameter decreased in both groups after injury (P < .001).

Figure 4 shows that the amount of inflammatory collections was significantly smaller in the chitosan-treated group than in the control group over the course of the study (P = .01). In addition, pennation angle steadily decreased in the control group throughout the study period, whereas it transiently decreased in the chitosan-treated group (until 2 weeks) before returning to its immediate postoperative level by 12 weeks (Figure 5). Overall, the chitosan-treated group maintained a higher pennation angle than the control group did (P < .001).

Discussion

RCTs affect more than 40% of patients over age 60 years and are a common cause of debilitating pain, reduced shoulder function, and weakness.¹⁰ Thirty thousand to 75,000 rotator cuff repairs are performed annually in the United States.¹¹ Although the best treatment for this disorder remains a topic of debate, arthroscopic and (when necessary) open surgical repair is the accepted gold standard for the treatment of tears that do not improve with conservative management. Despite advances in the surgical treatment of these tears, the surgical failure rates are high (range, 20%-90%), with failures attributed to factors beyond patient age, tear size and chronicity, muscle atrophy and degeneration, tendon quality, repair technique, and postoperative rehabilitation.^12,13 Repair strategies that biologically enhance the patient’s intrinsic healing potential are needed.

In tendon repair, choice of repair material (eg, graft) is crucial in determining the success of tissue engineering approaches. The ideal scaffold is biocompatible and does not elicit a host inflammatory response. The selected scaffold in its composition and fabricated form must be capable of holding and supporting cells. In addition, the scaffold should be biodegradable, serving as a temporary support for such cells and mechanically augmenting the repaired tendon while allowing for eventual replacement by matrix components. Moreover, the scaffold should have high porosity and a large surface area. Furthermore, the material should mimic the native tendon extracellular matrix (ECM) architecture to allow cells to be distributed throughout the scaffold and to facilitate diffusion of nutrients and factors that promote cellular proliferation and ECM production.

Given the importance of glycosaminoglycans (GAGs) in supporting the reticular structure of the matrix, use of GAGs or GAG-analogues as components of a tendon tissue scaffold for enhancing repair is well documented.¹⁴ One such candidate is chitosan, a partially de-acetylated derivative of chitin found in arthropod exoskeletons. Structurally, chitosan shares some characteristics with various GAGs and hyaluronic acid.¹⁵ More specifically, chitosan is a linear polysaccharide composed of glucosamine and N-acetyl glucosamine units linked by β-glycosidic bonds. Investigators have studied the properties of chitosan, including its biocompatibility, biodegradability, antibacterial activity, mucoadhesivity, and wound healing.^16,17

One of the most promising features of chitosan is that it can be processed into porous structures for use in cell transplantation and tissue regeneration.^18,19 Porous chitosan structures can be formed by freezing and lyophilizing chitosan-acetic acid solutions; chondrogenic cell adhesion and proliferation onto these structures have been reported.^20,21 This chitosan scaffolding method has also been used to test different composites with collagens, gelatins, GAGs, and hyaluronic acid, all of which have also been proposed as useful 3-dimensional materials for tissue repair.²²

In the present study, we used chitosan matrix in RCT repair. We hypothesized that chitosan matrix could enhance rotator cuff repair the same way it enhances repair in epidermal tissues.¹⁶ Histologic findings demonstrated that the percentage of fibrous tissue was significantly higher in the chitosan-treated group than in the control group. This improved fibroblastic response may be attributed to the ability of chitosan to enhance cell migration and serve as a scaffold for repair. Other studies have indicated that chitin, of which chitosan is the primary derivative, accelerated the healing of skin and subcutaneous tissues by increased cell migration.²³ Moreover, Okamoto and colleagues²⁴ reported that chitin implants stimulated abundant angiogenesis through the same mechanism.

Inadequate initial strength of a repair may lead to a recurrent cuff tear or a disability of rotator cuff function in the early healing stages. In our study, the chitosan matrix tended to be absorbed by 6 weeks after surgery. Its adherence to and ultimate absorption at the repair site may be challenged by the flow of irrigation fluid through the subacromial space in the setting of arthroscopic surgery. However, because the chitosan remains in a more robust gel form, it is better able to resist being washed from the repair site. For augmentation, it may be possible to apply a biocompatible patch over the gel to further protect it from being dislodged. In addition, histologic findings showed that the fibrous repair tissue gradually increased until reaching a peak 8 weeks after surgery—an indication that the absorption rate of the chitosan scaffold lags behind full recovery of the repair tissue. Given this relationship, further studies are needed to determine the mechanical strength of the repair between 6 and 8 weeks, which is important for avoiding recurrent tears.

This study had a few limitations. First, as with any animal model, the anatomy and function of the rat shoulder differ from those of the human shoulder. The acromial arch differs in quadruped animals, with less coverage of the supraspinatus and more of the subscapularis.²⁵ These anatomical differences could yield altered stress mechanics that could affect tendon repair. Furthermore, rats and humans differ in their RCT healing rates. Thus, the pathophysiology of muscle atrophy and fat infiltration in rats may slightly differ from that in humans. In addition, no mechanical testing was performed to compare chitosan-treated and untreated rotator cuff repairs, and such testing is needed to clarify the biomechanical importance of augmentation. Furthermore, no immunohistochemical analysis was performed for collagen. In the repair of rotator cuff tendons, surgeons must consider not only the number of cells but also the production of ECM. Although not directly confirmed in this study, chitosan induced fibrous tissue proliferation that mirrored production of a large amount of collagen fibers. Last, we used an open RTC model. As an arthroscopic model was not used, no definitive conclusions can be drawn regarding use of chitosan in arthroscopy.

Conclusion

Use of chitosan as an acellular matrix improved formation of healing fibrous tissue, increased the number of cells, and prevented fatty atrophy and inflammatory aggregates inside repair sites while facilitating recovery of the natural pennation angle of the tissue. These results demonstrate that chitosan can enhance tendon healing in the setting of acute RCT. Further research, including biomechanical testing of repaired tendons, is needed to further delineate the utility of chitosan in regenerating irreparable RCTs.

Rotator cuff tears (RCTs) are common tendon injuries that can cause chronic pain and severe functional disability. Massive RCTs do not heal spontaneously and, in many cases, result in poor clinical outcomes. Specifically, muscle atrophy and fatty infiltration correlate with poor outcomes after surgical repair.¹ Fatty infiltration of the rotator cuff is a common phenomenon that can lead to permanent structural alterations within the tendon. It has been suggested that changes in muscle fiber orientation (the pennation angle) can cause mesenchymal stem cells to migrate to the interface between muscle fibers and the region of fatty infiltration of the muscle.² Understanding the factors involved in muscle degeneration and atrophy, and in fatty infiltration, may lead to treatments that improve outcomes for patients with massive RCTs. One proposed treatment involves placing continuous mechanical traction on the ends of the torn tendon.² Findings from this research have indicated that acute tears that become chronic tears are typified by inelasticity and poor function of the muscle­–tendon unit. It is therefore important to develop a method that speeds tendon healing without causing the muscle fiber atrophy and pennation angle changes that lead to fatty atrophy, which appears to be an irreversible structural change.

On the basis of the theory that adding mesenchymal cells may improve tendon healing, investigators have studied use of transcription factors (eg, scleraxis) specific to tendogenesis in the embryonal stage.^3,4 Nevertheless, certain transcription factors are associated with formation of fibrocartilage in higher concentrations.⁴ Moreover, decalcified bone matrix increases cartilage formation when added to the tendon repair site.⁵ Cartilage formation, however, is associated with poorer functional results.⁶ Thus, there is a need for a method that facilitates faster tendon healing with higher quality tissue formation and less muscle atrophy.

Chitosan, a linear polysaccharide, is associated with scarless healing of soft tissues and prevention of adhesion formation both intraperitoneally and during tendon healing after surgery.^7,8 Chitosan tends to precipitate in physiologic pH, thereby mitigating its potency. Fortunately, a chitosan solution that does not precipitate in physiologic conditions was recently developed.⁹ The solution’s lack of precipitation, coupled with its in situ gelling, allows it to adhere to the repair site long enough to take effect. These characteristics could allow for intimate contact between gel and tendon, facilitating guided-tissue regeneration and preventing adhesion of the rotator cuff to surrounding tissue. By contrast, other biological agents (eg, platelet-rich plasma) are administered as fluid rather than gel and are therefore more susceptible to diffusing from the repair site, mitigating their effects. Thus, chitosan gel is fairly unique among agents.

In the study reported here, we histologically investigated whether a chitosan gel would help improve healing of rotator cuff tendon (acute supraspinatus) tears in a rat model.

Materials and Methods

Supraspinatus Surgical Model

Forty Wistar rats, each weighing between 300 and 400 g, were used in this study. All procedures were approved by the Institutional Animal Care and Use Committee at Rabin Medical Center in Petah Tikva, Israel. The rats were anesthetized with ketamine 90 mg/kg and xylazine 10 mg/kg, both administered intramuscularly, and anesthesia was prolonged as needed with 2% isoflurane, administered by nose cone. The skin was incised 5 cm along the upper back following the midline of the spine. The resulting skin flaps were retracted and the scapula exposed. Careful blunt dissection allowed visualization of the rotator cuff and the trans-scapular arch. A full-thickness incision of the supraspinatus tendon was then made 2 mm distal to the arch. This procedure was performed on both shoulders. For the right supraspinatus tendon, a bioabsorbable chitosan–hydrochloric acid solution (>70% de-acetylated chitosan, molecular weight of 600 kDa; Heppe Medical Chitosan GmbH, Halle, Germany) was sterilely applied to the ends of the tendon (total volume, 0.5 mL) and automatically gelled in situ by heating to about 37°C (rat’s internal body temperature). The tendon ends were subsequently approximated with a single 4-0 Prolene suture (Ethicon, Somerville, New Jersey). The left shoulder (tendon repaired with suture only) served as a control.

The rats were housed for a maximum of 12 weeks after surgery. They were sacrificed (in groups of 5 each) 2 hours, 3 days, 1 week, 2 weeks, 4 weeks, 6 weeks, 8 weeks, and 12 weeks after surgery. After each rat was sacrificed, both shoulder girdles were harvested, and the sutures were removed from the supraspinatus tendons.

Histologic Analysis

After routine fixation with 4% formalin for 48 hours and decalcification with 10% ethylenediaminetetraacetic acid (EDTA) for 3 weeks, the specimens were sectioned with a microtome blade. Care was taken to ensure the plane of the microtome blade was parallel with the longitudinal plane of the supraspinatus muscle and tendon to allow for evaluation of pennation angle. Hematoxylin-eosin staining and Masson trichrome staining were subsequently performed.

A variety of histologic measurements were obtained with use of ImageJ software (US National Institutes of Health). Percentage of fibrous tissue was determined by examining the slides at low magnification fields (×25) at the tendon healing site. Three such fields were evaluated per specimen. The fibrous tissue was circled manually, and percentage of tissue area was assessed and compared with total region of interest. Cellularity was carefully outlined and measured as percentage of total tendon area occupied by cells. Fatty atrophy was defined as either present or absent. Muscle fiber diameter was defined as average diameter of 10 muscle fibers measured within 2 mm of the tendon laceration site. Inflammatory cell collections were defined as either large (>100 µm in diameter) or small (<100 µm in diameter) and were dichotomized to either present or absent. Pennation angle was defined as average angle between muscle fibers and longitudinal axis of supraspinatus muscle and tendon unit. Ten fibers proximal to and within 2 mm of the laceration site were randomly selected, measured, and averaged.

Statistical Analysis

Statistical analysis was performed with Analyse-it 2.20 for Microsoft Excel 2010 (Analyse-it Software, Leeds, United Kingdom). Data were initially analyzed with the Kolmogorov-Smirnov test to assess for normality of distribution. The t test was used to compare continuous variables when the data were normally distributed and the Mann-Whitney test when the data were not normally distributed.

Results

All tendons (both groups) healed within 12 weeks. Generally, the tissue formed at the repair site exhibited a mixture of tenocyte-like cells (fibrotic tissue) and granulation tissue without clear orientation. As noted in Figure 1, the tendons treated with chitosan had more fibrotic tissue (overall mean, 21.5%) relative to the control group (mean, 12.3%), and the difference was significant (P = .003). The most notable differences were found at time points later than 1 week after surgery. In addition, amount of cellularity (Figure 2) was higher in chitosan-treated tendon and control tendon than in the normal, uninjured adjacent tendon at all time points (P < .001). Chitosan-treated tendons had significantly higher cellularity than untreated control tendons from 1 to 2 weeks (P < .001), and control tendons were significantly hypercellular compared with chitosan-treated tendons from 4 to 8 weeks (P < .001), but both groups exhibited similar cellularity by 12 weeks (P > .05). Fatty atrophy was found at significantly higher rates in control rats than in chitosan-treated rats (P = .001; Table). Furthermore, as noted in Figure 3, muscle fiber diameter decreased in both groups after injury (P < .001).

Figure 4 shows that the amount of inflammatory collections was significantly smaller in the chitosan-treated group than in the control group over the course of the study (P = .01). In addition, pennation angle steadily decreased in the control group throughout the study period, whereas it transiently decreased in the chitosan-treated group (until 2 weeks) before returning to its immediate postoperative level by 12 weeks (Figure 5). Overall, the chitosan-treated group maintained a higher pennation angle than the control group did (P < .001).

Discussion

RCTs affect more than 40% of patients over age 60 years and are a common cause of debilitating pain, reduced shoulder function, and weakness.¹⁰ Thirty thousand to 75,000 rotator cuff repairs are performed annually in the United States.¹¹ Although the best treatment for this disorder remains a topic of debate, arthroscopic and (when necessary) open surgical repair is the accepted gold standard for the treatment of tears that do not improve with conservative management. Despite advances in the surgical treatment of these tears, the surgical failure rates are high (range, 20%-90%), with failures attributed to factors beyond patient age, tear size and chronicity, muscle atrophy and degeneration, tendon quality, repair technique, and postoperative rehabilitation.^12,13 Repair strategies that biologically enhance the patient’s intrinsic healing potential are needed.

In tendon repair, choice of repair material (eg, graft) is crucial in determining the success of tissue engineering approaches. The ideal scaffold is biocompatible and does not elicit a host inflammatory response. The selected scaffold in its composition and fabricated form must be capable of holding and supporting cells. In addition, the scaffold should be biodegradable, serving as a temporary support for such cells and mechanically augmenting the repaired tendon while allowing for eventual replacement by matrix components. Moreover, the scaffold should have high porosity and a large surface area. Furthermore, the material should mimic the native tendon extracellular matrix (ECM) architecture to allow cells to be distributed throughout the scaffold and to facilitate diffusion of nutrients and factors that promote cellular proliferation and ECM production.

Given the importance of glycosaminoglycans (GAGs) in supporting the reticular structure of the matrix, use of GAGs or GAG-analogues as components of a tendon tissue scaffold for enhancing repair is well documented.¹⁴ One such candidate is chitosan, a partially de-acetylated derivative of chitin found in arthropod exoskeletons. Structurally, chitosan shares some characteristics with various GAGs and hyaluronic acid.¹⁵ More specifically, chitosan is a linear polysaccharide composed of glucosamine and N-acetyl glucosamine units linked by β-glycosidic bonds. Investigators have studied the properties of chitosan, including its biocompatibility, biodegradability, antibacterial activity, mucoadhesivity, and wound healing.^16,17

One of the most promising features of chitosan is that it can be processed into porous structures for use in cell transplantation and tissue regeneration.^18,19 Porous chitosan structures can be formed by freezing and lyophilizing chitosan-acetic acid solutions; chondrogenic cell adhesion and proliferation onto these structures have been reported.^20,21 This chitosan scaffolding method has also been used to test different composites with collagens, gelatins, GAGs, and hyaluronic acid, all of which have also been proposed as useful 3-dimensional materials for tissue repair.²²

In the present study, we used chitosan matrix in RCT repair. We hypothesized that chitosan matrix could enhance rotator cuff repair the same way it enhances repair in epidermal tissues.¹⁶ Histologic findings demonstrated that the percentage of fibrous tissue was significantly higher in the chitosan-treated group than in the control group. This improved fibroblastic response may be attributed to the ability of chitosan to enhance cell migration and serve as a scaffold for repair. Other studies have indicated that chitin, of which chitosan is the primary derivative, accelerated the healing of skin and subcutaneous tissues by increased cell migration.²³ Moreover, Okamoto and colleagues²⁴ reported that chitin implants stimulated abundant angiogenesis through the same mechanism.

Inadequate initial strength of a repair may lead to a recurrent cuff tear or a disability of rotator cuff function in the early healing stages. In our study, the chitosan matrix tended to be absorbed by 6 weeks after surgery. Its adherence to and ultimate absorption at the repair site may be challenged by the flow of irrigation fluid through the subacromial space in the setting of arthroscopic surgery. However, because the chitosan remains in a more robust gel form, it is better able to resist being washed from the repair site. For augmentation, it may be possible to apply a biocompatible patch over the gel to further protect it from being dislodged. In addition, histologic findings showed that the fibrous repair tissue gradually increased until reaching a peak 8 weeks after surgery—an indication that the absorption rate of the chitosan scaffold lags behind full recovery of the repair tissue. Given this relationship, further studies are needed to determine the mechanical strength of the repair between 6 and 8 weeks, which is important for avoiding recurrent tears.

This study had a few limitations. First, as with any animal model, the anatomy and function of the rat shoulder differ from those of the human shoulder. The acromial arch differs in quadruped animals, with less coverage of the supraspinatus and more of the subscapularis.²⁵ These anatomical differences could yield altered stress mechanics that could affect tendon repair. Furthermore, rats and humans differ in their RCT healing rates. Thus, the pathophysiology of muscle atrophy and fat infiltration in rats may slightly differ from that in humans. In addition, no mechanical testing was performed to compare chitosan-treated and untreated rotator cuff repairs, and such testing is needed to clarify the biomechanical importance of augmentation. Furthermore, no immunohistochemical analysis was performed for collagen. In the repair of rotator cuff tendons, surgeons must consider not only the number of cells but also the production of ECM. Although not directly confirmed in this study, chitosan induced fibrous tissue proliferation that mirrored production of a large amount of collagen fibers. Last, we used an open RTC model. As an arthroscopic model was not used, no definitive conclusions can be drawn regarding use of chitosan in arthroscopy.

Conclusion

Use of chitosan as an acellular matrix improved formation of healing fibrous tissue, increased the number of cells, and prevented fatty atrophy and inflammatory aggregates inside repair sites while facilitating recovery of the natural pennation angle of the tissue. These results demonstrate that chitosan can enhance tendon healing in the setting of acute RCT. Further research, including biomechanical testing of repaired tendons, is needed to further delineate the utility of chitosan in regenerating irreparable RCTs.

Anterior-inferior and posterior-inferior labral tears are common injuries treated with arthroscopic surgery¹ typically performed with beach-chair^2,3 or lateral decubitus^1,2 positioning and variable headrest positioning. Iatrogenic nerve damage that occurs after arthroscopic shoulder surgery—including damage to the suprascapular, axillary, musculocutaneous, subscapular, and spinal accessory nerves—has recently been reported to be more common than previously recognized.^2,4

Although iatrogenic nerve injuries are in general being recognized,^1,2,4 reports of greater auricular nerve injuries are limited. The greater auricular nerve is a superficial cutaneous nerve that arises from the cervical plexus at the C2 and C3 spinal nerves, obliquely crosses the sternocleidomastoid muscle, and splits into anterior and posterior portions that innervate the skin over the mastoid process and parotid gland.^5,6 In particular, as illustrated by Ginsberg and Eicher⁶ (Figure 1), its superficial anatomy lies very near where a headrest is positioned during arthroscopic surgery, and increased pressure on the nerve throughout arthroscopic shoulder surgery may lead to neurapraxia.^6,7 In 2 case series, authors reported on a total of 5 patients who had greater auricular nerve palsy after uncomplicated shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 The authors attributed these palsies to the horseshoe headrest, which they believed was compressing the greater auricular nerve during the entire surgery.^7,8 However, standard universal headrests, which are thought to distribute pressures that would theoretically place the greater auricular nerve at risk for palsy, previously had not been described as contributing to palsy of the greater auricular nerve.

In this article, we report on a case of greater auricular nerve palsy that occurred after the patient’s anterior-inferior and posterior-inferior labral tear was arthroscopically repaired using beach-chair positioning and a standard universal headrest. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

An 18-year-old right-hand–dominant high school American football player was referred for orthopedic evaluation of left chronic glenohumeral instability after 6 months of physical therapy. Physical examination revealed a positive apprehension test with the shoulder abducted and externally rotated at 90° and a positive relocation test. The patient complained of pain and instability when his arm was placed in a cross-chest adducted position and a posteroinferiorly directed axial load was applied. Magnetic resonance arthrogram showed an anterior-inferior labral Bankart tear with a small Hill-Sachs lesion to the humeral head but did not clearly reveal the posterior-inferior labral tear. Because of persistent left shoulder instability with most overhead activities and continued pain, the patient decided to undergo left shoulder arthroscopic Bankart repair with inferior capsular shift and posterior-inferior labral repair with capsulorraphy. He had no significant past medical history or known drug allergies.

The patient was placed in the standard beach-chair position: upright at 45° to the floor, hips flexed at 60°, knees flexed at 30°.¹ Pneumatic compression devices were placed on his lower extremities. His head was secured in neutral position to a standard universal headrest (model A-90026; Allen Medical Systems, Acton, Massachusetts) (Figures 2, 3). Care was taken to protect the deep neurovascular structures and bony prominences throughout. The patient was in this position for 122 minutes of the operation, from positioning and draping to wound closure and dressing application. Before draping, the anesthesiologist, head nurse, and circulating nurse ensured that head and neck were in neutral position. The anesthesiologist monitored positioning throughout the perioperative period to ensure head and neck were in neutral, and the head did not need to be repositioned during surgery. Standard preoperative intravenous antibiotics were given.

General anesthesia and postoperative interscalene block were used. Standard preparation and draping were performed. Three standard arthroscopic portal incisions were used: posterior, anterior, and anterosuperolateral. Findings included extensive labral pathology, small bony Hill-Sachs lesion to humeral head, small bony anterior glenoid deficiency, and deficient anterior-inferior and posterior-inferior labral remnant. These were repaired arthroscopically in a standard fashion using bioabsorbable suture anchors. There were no arthroscopic complications. After surgery, a standard well-fitted shoulder immobilizer was placed. The anesthesiologist provided interscalene regional analgesia (15 mL of bupivacaine 0.5%) in the recovery area after surgery.

Postoperative neurovascular examination in the recovery room revealed no discomfort. The patient was discharged the same day. At a scheduled 1-week follow-up, he complained of numbness and dysesthesia on the left side of the greater auricular nerve distribution. A diagnosis of greater auricular nerve palsy was made by physical examination; the symptoms were along the classic greater auricular nerve distribution affecting the lower face and ear (Figure 4). The patient had no pain, skin lesions, or soft-tissue swelling. Otolaryngology confirmed the diagnosis and recommended observation-only treatment of symptoms. Symptoms lessened over the next 3 months, and the altered sensation resolved without deficit by 6 months. In addition, by 6 months the patient had returned to full activities (including collision sports) pain-free and with normal left shoulder function. Because symptoms continued to improve, the patient was followed with clinical observation, and a formal work-up was not necessary.

Discussion

The most important finding in this case is the greater auricular nerve palsy that occurred after arthroscopic anterior-inferior and posterior-inferior labral repairs in beach-chair positioning. This greater auricular nerve palsy was the first encountered by Dr. Foad, who over 17 years in a primarily shoulder practice setting has used beach-chair positioning exclusively. Previous reports have described a palsy occurring after arthroscopic shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 Ng and Page⁷ discontinued and recommended against use of this headrest because of the complications of the palsy, and Park and Kim⁸ recommended a headrest redesign. We think the present case report is the first to describe a greater auricular nerve palsy that occurred after arthroscopic surgery using a standard universal headrest, which theoretically should prevent compression of the greater auricular nerve. Increased awareness of the possibility of greater auricular nerve palsy, even when proper precautions are taken,¹ is therefore warranted.

Based on the location of our patient’s palsy, we think his paralysis was most likely the result of nerve compression by the headrest during the shoulder surgery. Other factors, though unlikely, may have played a role. These include operative time (increases duration of nerve compression) and head positioning. However, 122 minutes is not unusually long for a patient’s head to be in this position during a procedure, and over the past 10 years the same anesthesiologist, head nurse, and circulating nurse have routinely used the same beach-chair positioning and headrest for Dr. Foad’s patients. Second, the postoperative interscalene block theoretically could have caused the palsy, but we think this is unlikely, as the block is placed lower on the neck, at the C6 level, and the greater auricular nerve branches off the C2–C3 spinal nerves. As described by Rains and colleagues,⁹ other authors have reported transient neuropathies to the brachial plexus, which originates in the C5–C8 region, but not to the greater auricular nerve. Last, it cannot be ruled out that a variant of the greater auricular nerve could have played a role, given the variation in the greater auricular nerve.^10,11 However, Brennan and colleagues¹⁰ reported that 2 of 25 neck dissections involved a variant in which the anterior division of the greater auricular nerve passed into the submandibular triangle and joined the mandibular region of the facial nerve. Stimulation of this nerve resulted in activity of the depressor of the lower lip, which was not the location of our patient’s palsy. In addition, our patient’s symptoms followed a classic nerve distribution of the greater auricular nerve (Figures 1, 4), which would seem to decrease the likelihood that a variant was the source of the palsy.

The superficial nature of the greater auricular nerve, which runs roughly parallel with the sternocleidomastoid muscle and innervates much of the superficial region of the skin over the mastoid, parotid gland, and mandible,^5-7 theoretically places the nerve at risk for compressive forces from the headrest during arthroscopic shoulder surgery. Skyhar and colleagues³ first described beach-chair positioning as an alternative to lateral decubitus positioning, which had been reported to result in neurologic injury in about 10% of surgical cases.⁹ The theoretical advantages of beach-chair positioning are lack of traction needed and ease of setup, which would therefore decrease the possibility of neuropathy.^1,3 However, as seen in this and other case reports,^7,8 greater auricular nerve neuropathy should still be considered a possible complication, even when using beach-chair positioning.

Besides neuropathy after arthroscopic shoulder surgery, as described in previous case reports^7,8 and in the present report, greater auricular nerve injury has been described as arising from other stimuli. Greater auricular nerve injury has arisen after perineural tumor metastasis,⁶ neuroma of greater auricular nerve after endolympathic shunt surgery,¹² internal fixation of mandibular condyle,¹³ and carotid endarterectomy.^14,15 Given the superficial nature of the greater auricular nerve, it may not be all that surprising that a palsy could also develop after headrest compression during arthroscopic shoulder surgery.

This case report brings to light a possible complication of greater auricular nerve palsy during arthroscopic shoulder surgery using beach-chair positioning and a standard universal headrest. Studies should now investigate whether greater auricular nerve palsy is more common than realized, especially with regard to specific headrests in beach-chair positioning. For now, though, Dr. Foad’s intention is not to change to a different headrest or discontinue beach-chair positioning but to draw attention to this rare complication. Additional attention should be given to the location of the headrest in relation to the greater auricular nerve, especially in cases in which operative time may be longer.

Conclusion

We have reported a greater auricular nerve palsy that occurred after arthroscopic shoulder surgery for an anterior-inferior and posterior-inferior labral tear. This is the first report of a greater auricular nerve palsy occurring with beach-chair positioning and a standard universal headrest. Symptoms resolved within 6 months. New studies should investigate the incidence of greater auricular nerve palsy after arthroscopic shoulder surgery.

Anterior-inferior and posterior-inferior labral tears are common injuries treated with arthroscopic surgery¹ typically performed with beach-chair^2,3 or lateral decubitus^1,2 positioning and variable headrest positioning. Iatrogenic nerve damage that occurs after arthroscopic shoulder surgery—including damage to the suprascapular, axillary, musculocutaneous, subscapular, and spinal accessory nerves—has recently been reported to be more common than previously recognized.^2,4

Although iatrogenic nerve injuries are in general being recognized,^1,2,4 reports of greater auricular nerve injuries are limited. The greater auricular nerve is a superficial cutaneous nerve that arises from the cervical plexus at the C2 and C3 spinal nerves, obliquely crosses the sternocleidomastoid muscle, and splits into anterior and posterior portions that innervate the skin over the mastoid process and parotid gland.^5,6 In particular, as illustrated by Ginsberg and Eicher⁶ (Figure 1), its superficial anatomy lies very near where a headrest is positioned during arthroscopic surgery, and increased pressure on the nerve throughout arthroscopic shoulder surgery may lead to neurapraxia.^6,7 In 2 case series, authors reported on a total of 5 patients who had greater auricular nerve palsy after uncomplicated shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 The authors attributed these palsies to the horseshoe headrest, which they believed was compressing the greater auricular nerve during the entire surgery.^7,8 However, standard universal headrests, which are thought to distribute pressures that would theoretically place the greater auricular nerve at risk for palsy, previously had not been described as contributing to palsy of the greater auricular nerve.

In this article, we report on a case of greater auricular nerve palsy that occurred after the patient’s anterior-inferior and posterior-inferior labral tear was arthroscopically repaired using beach-chair positioning and a standard universal headrest. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

An 18-year-old right-hand–dominant high school American football player was referred for orthopedic evaluation of left chronic glenohumeral instability after 6 months of physical therapy. Physical examination revealed a positive apprehension test with the shoulder abducted and externally rotated at 90° and a positive relocation test. The patient complained of pain and instability when his arm was placed in a cross-chest adducted position and a posteroinferiorly directed axial load was applied. Magnetic resonance arthrogram showed an anterior-inferior labral Bankart tear with a small Hill-Sachs lesion to the humeral head but did not clearly reveal the posterior-inferior labral tear. Because of persistent left shoulder instability with most overhead activities and continued pain, the patient decided to undergo left shoulder arthroscopic Bankart repair with inferior capsular shift and posterior-inferior labral repair with capsulorraphy. He had no significant past medical history or known drug allergies.

The patient was placed in the standard beach-chair position: upright at 45° to the floor, hips flexed at 60°, knees flexed at 30°.¹ Pneumatic compression devices were placed on his lower extremities. His head was secured in neutral position to a standard universal headrest (model A-90026; Allen Medical Systems, Acton, Massachusetts) (Figures 2, 3). Care was taken to protect the deep neurovascular structures and bony prominences throughout. The patient was in this position for 122 minutes of the operation, from positioning and draping to wound closure and dressing application. Before draping, the anesthesiologist, head nurse, and circulating nurse ensured that head and neck were in neutral position. The anesthesiologist monitored positioning throughout the perioperative period to ensure head and neck were in neutral, and the head did not need to be repositioned during surgery. Standard preoperative intravenous antibiotics were given.

General anesthesia and postoperative interscalene block were used. Standard preparation and draping were performed. Three standard arthroscopic portal incisions were used: posterior, anterior, and anterosuperolateral. Findings included extensive labral pathology, small bony Hill-Sachs lesion to humeral head, small bony anterior glenoid deficiency, and deficient anterior-inferior and posterior-inferior labral remnant. These were repaired arthroscopically in a standard fashion using bioabsorbable suture anchors. There were no arthroscopic complications. After surgery, a standard well-fitted shoulder immobilizer was placed. The anesthesiologist provided interscalene regional analgesia (15 mL of bupivacaine 0.5%) in the recovery area after surgery.

Postoperative neurovascular examination in the recovery room revealed no discomfort. The patient was discharged the same day. At a scheduled 1-week follow-up, he complained of numbness and dysesthesia on the left side of the greater auricular nerve distribution. A diagnosis of greater auricular nerve palsy was made by physical examination; the symptoms were along the classic greater auricular nerve distribution affecting the lower face and ear (Figure 4). The patient had no pain, skin lesions, or soft-tissue swelling. Otolaryngology confirmed the diagnosis and recommended observation-only treatment of symptoms. Symptoms lessened over the next 3 months, and the altered sensation resolved without deficit by 6 months. In addition, by 6 months the patient had returned to full activities (including collision sports) pain-free and with normal left shoulder function. Because symptoms continued to improve, the patient was followed with clinical observation, and a formal work-up was not necessary.

Discussion

The most important finding in this case is the greater auricular nerve palsy that occurred after arthroscopic anterior-inferior and posterior-inferior labral repairs in beach-chair positioning. This greater auricular nerve palsy was the first encountered by Dr. Foad, who over 17 years in a primarily shoulder practice setting has used beach-chair positioning exclusively. Previous reports have described a palsy occurring after arthroscopic shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 Ng and Page⁷ discontinued and recommended against use of this headrest because of the complications of the palsy, and Park and Kim⁸ recommended a headrest redesign. We think the present case report is the first to describe a greater auricular nerve palsy that occurred after arthroscopic surgery using a standard universal headrest, which theoretically should prevent compression of the greater auricular nerve. Increased awareness of the possibility of greater auricular nerve palsy, even when proper precautions are taken,¹ is therefore warranted.

Based on the location of our patient’s palsy, we think his paralysis was most likely the result of nerve compression by the headrest during the shoulder surgery. Other factors, though unlikely, may have played a role. These include operative time (increases duration of nerve compression) and head positioning. However, 122 minutes is not unusually long for a patient’s head to be in this position during a procedure, and over the past 10 years the same anesthesiologist, head nurse, and circulating nurse have routinely used the same beach-chair positioning and headrest for Dr. Foad’s patients. Second, the postoperative interscalene block theoretically could have caused the palsy, but we think this is unlikely, as the block is placed lower on the neck, at the C6 level, and the greater auricular nerve branches off the C2–C3 spinal nerves. As described by Rains and colleagues,⁹ other authors have reported transient neuropathies to the brachial plexus, which originates in the C5–C8 region, but not to the greater auricular nerve. Last, it cannot be ruled out that a variant of the greater auricular nerve could have played a role, given the variation in the greater auricular nerve.^10,11 However, Brennan and colleagues¹⁰ reported that 2 of 25 neck dissections involved a variant in which the anterior division of the greater auricular nerve passed into the submandibular triangle and joined the mandibular region of the facial nerve. Stimulation of this nerve resulted in activity of the depressor of the lower lip, which was not the location of our patient’s palsy. In addition, our patient’s symptoms followed a classic nerve distribution of the greater auricular nerve (Figures 1, 4), which would seem to decrease the likelihood that a variant was the source of the palsy.

The superficial nature of the greater auricular nerve, which runs roughly parallel with the sternocleidomastoid muscle and innervates much of the superficial region of the skin over the mastoid, parotid gland, and mandible,^5-7 theoretically places the nerve at risk for compressive forces from the headrest during arthroscopic shoulder surgery. Skyhar and colleagues³ first described beach-chair positioning as an alternative to lateral decubitus positioning, which had been reported to result in neurologic injury in about 10% of surgical cases.⁹ The theoretical advantages of beach-chair positioning are lack of traction needed and ease of setup, which would therefore decrease the possibility of neuropathy.^1,3 However, as seen in this and other case reports,^7,8 greater auricular nerve neuropathy should still be considered a possible complication, even when using beach-chair positioning.

Besides neuropathy after arthroscopic shoulder surgery, as described in previous case reports^7,8 and in the present report, greater auricular nerve injury has been described as arising from other stimuli. Greater auricular nerve injury has arisen after perineural tumor metastasis,⁶ neuroma of greater auricular nerve after endolympathic shunt surgery,¹² internal fixation of mandibular condyle,¹³ and carotid endarterectomy.^14,15 Given the superficial nature of the greater auricular nerve, it may not be all that surprising that a palsy could also develop after headrest compression during arthroscopic shoulder surgery.

This case report brings to light a possible complication of greater auricular nerve palsy during arthroscopic shoulder surgery using beach-chair positioning and a standard universal headrest. Studies should now investigate whether greater auricular nerve palsy is more common than realized, especially with regard to specific headrests in beach-chair positioning. For now, though, Dr. Foad’s intention is not to change to a different headrest or discontinue beach-chair positioning but to draw attention to this rare complication. Additional attention should be given to the location of the headrest in relation to the greater auricular nerve, especially in cases in which operative time may be longer.

Conclusion

We have reported a greater auricular nerve palsy that occurred after arthroscopic shoulder surgery for an anterior-inferior and posterior-inferior labral tear. This is the first report of a greater auricular nerve palsy occurring with beach-chair positioning and a standard universal headrest. Symptoms resolved within 6 months. New studies should investigate the incidence of greater auricular nerve palsy after arthroscopic shoulder surgery.

Anterior-inferior and posterior-inferior labral tears are common injuries treated with arthroscopic surgery¹ typically performed with beach-chair^2,3 or lateral decubitus^1,2 positioning and variable headrest positioning. Iatrogenic nerve damage that occurs after arthroscopic shoulder surgery—including damage to the suprascapular, axillary, musculocutaneous, subscapular, and spinal accessory nerves—has recently been reported to be more common than previously recognized.^2,4

Although iatrogenic nerve injuries are in general being recognized,^1,2,4 reports of greater auricular nerve injuries are limited. The greater auricular nerve is a superficial cutaneous nerve that arises from the cervical plexus at the C2 and C3 spinal nerves, obliquely crosses the sternocleidomastoid muscle, and splits into anterior and posterior portions that innervate the skin over the mastoid process and parotid gland.^5,6 In particular, as illustrated by Ginsberg and Eicher⁶ (Figure 1), its superficial anatomy lies very near where a headrest is positioned during arthroscopic surgery, and increased pressure on the nerve throughout arthroscopic shoulder surgery may lead to neurapraxia.^6,7 In 2 case series, authors reported on a total of 5 patients who had greater auricular nerve palsy after uncomplicated shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 The authors attributed these palsies to the horseshoe headrest, which they believed was compressing the greater auricular nerve during the entire surgery.^7,8 However, standard universal headrests, which are thought to distribute pressures that would theoretically place the greater auricular nerve at risk for palsy, previously had not been described as contributing to palsy of the greater auricular nerve.

In this article, we report on a case of greater auricular nerve palsy that occurred after the patient’s anterior-inferior and posterior-inferior labral tear was arthroscopically repaired using beach-chair positioning and a standard universal headrest. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

An 18-year-old right-hand–dominant high school American football player was referred for orthopedic evaluation of left chronic glenohumeral instability after 6 months of physical therapy. Physical examination revealed a positive apprehension test with the shoulder abducted and externally rotated at 90° and a positive relocation test. The patient complained of pain and instability when his arm was placed in a cross-chest adducted position and a posteroinferiorly directed axial load was applied. Magnetic resonance arthrogram showed an anterior-inferior labral Bankart tear with a small Hill-Sachs lesion to the humeral head but did not clearly reveal the posterior-inferior labral tear. Because of persistent left shoulder instability with most overhead activities and continued pain, the patient decided to undergo left shoulder arthroscopic Bankart repair with inferior capsular shift and posterior-inferior labral repair with capsulorraphy. He had no significant past medical history or known drug allergies.

The patient was placed in the standard beach-chair position: upright at 45° to the floor, hips flexed at 60°, knees flexed at 30°.¹ Pneumatic compression devices were placed on his lower extremities. His head was secured in neutral position to a standard universal headrest (model A-90026; Allen Medical Systems, Acton, Massachusetts) (Figures 2, 3). Care was taken to protect the deep neurovascular structures and bony prominences throughout. The patient was in this position for 122 minutes of the operation, from positioning and draping to wound closure and dressing application. Before draping, the anesthesiologist, head nurse, and circulating nurse ensured that head and neck were in neutral position. The anesthesiologist monitored positioning throughout the perioperative period to ensure head and neck were in neutral, and the head did not need to be repositioned during surgery. Standard preoperative intravenous antibiotics were given.

General anesthesia and postoperative interscalene block were used. Standard preparation and draping were performed. Three standard arthroscopic portal incisions were used: posterior, anterior, and anterosuperolateral. Findings included extensive labral pathology, small bony Hill-Sachs lesion to humeral head, small bony anterior glenoid deficiency, and deficient anterior-inferior and posterior-inferior labral remnant. These were repaired arthroscopically in a standard fashion using bioabsorbable suture anchors. There were no arthroscopic complications. After surgery, a standard well-fitted shoulder immobilizer was placed. The anesthesiologist provided interscalene regional analgesia (15 mL of bupivacaine 0.5%) in the recovery area after surgery.

Postoperative neurovascular examination in the recovery room revealed no discomfort. The patient was discharged the same day. At a scheduled 1-week follow-up, he complained of numbness and dysesthesia on the left side of the greater auricular nerve distribution. A diagnosis of greater auricular nerve palsy was made by physical examination; the symptoms were along the classic greater auricular nerve distribution affecting the lower face and ear (Figure 4). The patient had no pain, skin lesions, or soft-tissue swelling. Otolaryngology confirmed the diagnosis and recommended observation-only treatment of symptoms. Symptoms lessened over the next 3 months, and the altered sensation resolved without deficit by 6 months. In addition, by 6 months the patient had returned to full activities (including collision sports) pain-free and with normal left shoulder function. Because symptoms continued to improve, the patient was followed with clinical observation, and a formal work-up was not necessary.

Discussion

The most important finding in this case is the greater auricular nerve palsy that occurred after arthroscopic anterior-inferior and posterior-inferior labral repairs in beach-chair positioning. This greater auricular nerve palsy was the first encountered by Dr. Foad, who over 17 years in a primarily shoulder practice setting has used beach-chair positioning exclusively. Previous reports have described a palsy occurring after arthroscopic shoulder surgery using beach-chair positioning and a horseshoe headrest.^7,8 Ng and Page⁷ discontinued and recommended against use of this headrest because of the complications of the palsy, and Park and Kim⁸ recommended a headrest redesign. We think the present case report is the first to describe a greater auricular nerve palsy that occurred after arthroscopic surgery using a standard universal headrest, which theoretically should prevent compression of the greater auricular nerve. Increased awareness of the possibility of greater auricular nerve palsy, even when proper precautions are taken,¹ is therefore warranted.

Based on the location of our patient’s palsy, we think his paralysis was most likely the result of nerve compression by the headrest during the shoulder surgery. Other factors, though unlikely, may have played a role. These include operative time (increases duration of nerve compression) and head positioning. However, 122 minutes is not unusually long for a patient’s head to be in this position during a procedure, and over the past 10 years the same anesthesiologist, head nurse, and circulating nurse have routinely used the same beach-chair positioning and headrest for Dr. Foad’s patients. Second, the postoperative interscalene block theoretically could have caused the palsy, but we think this is unlikely, as the block is placed lower on the neck, at the C6 level, and the greater auricular nerve branches off the C2–C3 spinal nerves. As described by Rains and colleagues,⁹ other authors have reported transient neuropathies to the brachial plexus, which originates in the C5–C8 region, but not to the greater auricular nerve. Last, it cannot be ruled out that a variant of the greater auricular nerve could have played a role, given the variation in the greater auricular nerve.^10,11 However, Brennan and colleagues¹⁰ reported that 2 of 25 neck dissections involved a variant in which the anterior division of the greater auricular nerve passed into the submandibular triangle and joined the mandibular region of the facial nerve. Stimulation of this nerve resulted in activity of the depressor of the lower lip, which was not the location of our patient’s palsy. In addition, our patient’s symptoms followed a classic nerve distribution of the greater auricular nerve (Figures 1, 4), which would seem to decrease the likelihood that a variant was the source of the palsy.

The superficial nature of the greater auricular nerve, which runs roughly parallel with the sternocleidomastoid muscle and innervates much of the superficial region of the skin over the mastoid, parotid gland, and mandible,^5-7 theoretically places the nerve at risk for compressive forces from the headrest during arthroscopic shoulder surgery. Skyhar and colleagues³ first described beach-chair positioning as an alternative to lateral decubitus positioning, which had been reported to result in neurologic injury in about 10% of surgical cases.⁹ The theoretical advantages of beach-chair positioning are lack of traction needed and ease of setup, which would therefore decrease the possibility of neuropathy.^1,3 However, as seen in this and other case reports,^7,8 greater auricular nerve neuropathy should still be considered a possible complication, even when using beach-chair positioning.

Besides neuropathy after arthroscopic shoulder surgery, as described in previous case reports^7,8 and in the present report, greater auricular nerve injury has been described as arising from other stimuli. Greater auricular nerve injury has arisen after perineural tumor metastasis,⁶ neuroma of greater auricular nerve after endolympathic shunt surgery,¹² internal fixation of mandibular condyle,¹³ and carotid endarterectomy.^14,15 Given the superficial nature of the greater auricular nerve, it may not be all that surprising that a palsy could also develop after headrest compression during arthroscopic shoulder surgery.

This case report brings to light a possible complication of greater auricular nerve palsy during arthroscopic shoulder surgery using beach-chair positioning and a standard universal headrest. Studies should now investigate whether greater auricular nerve palsy is more common than realized, especially with regard to specific headrests in beach-chair positioning. For now, though, Dr. Foad’s intention is not to change to a different headrest or discontinue beach-chair positioning but to draw attention to this rare complication. Additional attention should be given to the location of the headrest in relation to the greater auricular nerve, especially in cases in which operative time may be longer.

Conclusion

We have reported a greater auricular nerve palsy that occurred after arthroscopic shoulder surgery for an anterior-inferior and posterior-inferior labral tear. This is the first report of a greater auricular nerve palsy occurring with beach-chair positioning and a standard universal headrest. Symptoms resolved within 6 months. New studies should investigate the incidence of greater auricular nerve palsy after arthroscopic shoulder surgery.

Complications with the use of anchor screws in shoulder surgery have been well-documented^1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.

Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.^3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.³ However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.

Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.

Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.

A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.

After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.

The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.

Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.

After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).

Discussion

Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.^3,4 Zuckerman and Matsen⁴ divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.⁵ In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.

Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues⁵ performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.

The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.

This case has shown the importance of obtaining post­operative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.¹

Conclusion

Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.^1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.

Complications with the use of anchor screws in shoulder surgery have been well-documented^1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.

Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.^3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.³ However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.

Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.

Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.

A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.

After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.

The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.

Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.

After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).

Discussion

Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.^3,4 Zuckerman and Matsen⁴ divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.⁵ In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.

Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues⁵ performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.

The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.

This case has shown the importance of obtaining post­operative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.¹

Conclusion

Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.^1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.

Complications with the use of anchor screws in shoulder surgery have been well-documented^1,2 and can be divided into 3 categories: insertion (eg, incomplete seating, inadequate insertion, and migration), biologic (eg, large tacks producing synovitis and bone reaction), and, less commonly, mechanical (eg, intra- and extra-articular bone pull-out with migration) complications.

Prominent hardware, including suture anchors, as a cause of arthritis and joint damage has been well-documented in shoulder surgery.^3,4 For example, anchors placed on the glenoid rim have been implicated in severe cartilage loss if they protrude above the level of the glenoid rim.³ However, to the authors’ knowledge, prominent anchor placement after rotator cuff repair has not been reported as a cause of arthritis unless the anchor dislodges into the glenohumeral joint. The authors present a case in which a suture anchor used for rotator cuff repair protruded through the humeral head, resulting in glenohumeral arthritis. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 61-year-old woman presented with complaints of persistent right shoulder pain for 5 months after a fall from a bicycle. She had taken nonsteroidal anti-inflammatory medication without pain relief. On presentation, she had no atrophy or deformity, was neurologically intact for sensation and reflexes, and had full range of motion (ROM) but a painful arc. She had tenderness over the greater tuberosity and positive Neer and Hawkins-Kennedy impingement signs. She had pain but no weakness to resisted abduction or to resisted external rotation with the arms at the sides.

Preoperative conventional radiographs of the shoulder were normal. A gadolinium-enhanced magnetic resonance arthrogram showed a high-grade articular partial tear of the supraspinatus, which was judged to be at least two-thirds of the tendon width. Because nonoperative methods had failed, the patient elected operative intervention for this tear.

Diagnostic arthroscopy (with the patient in a lateral decubitus position) showed a normal joint except for a high-grade, 8×8-mm, greater than 6 mm deep, partial tear of the articular side of the supraspinatus tendon. The subacromial space had moderate to severe bursal tissue inflammation but no full-thickness component to the rotator cuff tear. A bursectomy, coracoacromial ligament release, and partial anterolateral acromioplasty were performed.

A transtendinous technique was used to repair this high-grade tear. For an anatomically rigid repair, we used 3 suture anchors with a straight configuration because each metal anchor has only 1 suture. According to the standard arthroscopic transtendinous repair technique, the suture anchors were placed through the rotator cuff tendon (at the lateral articular margin at the medial extent of the footprint) after localization of the angle with a spinal needle. A shuttle relay was used to pass the sutures, and the knot was pulled into the subacromial space, cinching the rotator cuff on top of the suture anchors and reestablishing the contact of the tendon to the footprint. We used two 2.4-mm FASTak suture anchors (Arthrex, Naples, Florida) and one 3.5-mm Corkscrew suture anchor (Arthrex). This process was repeated for the remaining suture limbs. The placement of the suture anchors adequately reduced the articular part of the cuff to the footprint.

After surgery, the patient had no complications, and radiographs taken the next day suggested no abnormalities (Figure 1A). The shoulder was immobilized for 4 weeks after surgery, and passive, gentle ROM exercise was supervised by a physical therapist twice a week during this period. After the first 4 weeks, an active ROM program was begun. However, shortly after initiating motion in the shoulder, the patient complained of a recurrence of pain that she described as a sharp and grinding sensation.

The patient was reevaluated 8 weeks after surgery. Her pain was worsening, and she was having difficulty regaining ROM. Conventional radiographs showed the tip of the metal anchor protruding through the articular cartilage of the humeral head (Figure 1B). The patient was informed of the findings, and immediate surgery was performed to remove the anchor.

Arthroscopic examination showed extensive damage to the glenoid cartilage (Figure 1C) and an intra-articularly intact rotator cuff repair. The cartilage damage was located in the posterior and inferior half of the glenoid, which is related to the forward flexion of the arm; the depth of the cartilage defect was approximately 2 mm. Under the image intensifier, an empty suture anchor driver was inserted into the previous screw insertion hole, and the anchor was screwed back out and removed.

After surgery, the patient’s arm was placed in a sling, and an ROM program began 4 weeks later. The sensation of grinding was eliminated, and her pain gradually improved. Three years after surgery, she had no pain, no weakness, and full ROM without limitations (Figure 2).

Discussion

Protrusion and migration of suture anchors in shoulder surgery has been documented extensively.^3,4 Zuckerman and Matsen⁴ divided these complications into 4 groups: (1) incorrect placement, (2) migration after placement, (3) loosening, and (4) device breakage. These complications may be frequently related to surgical technique, and all these studies describe backward migration of the anchor out of the drill hole. In the current case, the anchor tip penetrated the articular surface of the humeral head, not because of anchor migration but because the anchor was inserted too far. To the authors’ knowledge, there is only 1 reported case of anchor protrusion through the humeral head; it involved a different type of anchor insertion system.⁵ In that case, there was only mild cartilage damage to the glenoid, and the patient recovered after removal of the anchors.

Several factors contributed to the improper insertion of the anchor in the current patient. First, repairing a high-grade articular side defect or partial articular supraspinatus tendon avulsion lesion can be technically challenging because rotator cuff tissue obscures the view when inserting the anchor. Second, the anchor was inserted too medially on the greater tuberosity, which made the distance from the tuberosity to the joint shorter. Wong and colleagues⁵ performed an analysis of the angle of insertion that would be safe using a PEEK PushLock SP system (Arthrex), but they emphasized that the angle depends on the configuration of the particular insertion system. The current case also shows that the surgeon should be cognizant of the fact that penetration of the humeral head by the anchor can occur if the surgeon is unaware of the distance from the anchor to the laser line on the insertion device or of the distance from the tuberosity to the articular surface of the humeral head.

The current case also shows that the type of anchor and delivery system may contribute to this complication. Double-loaded suture anchors can decrease the number of anchors needed for secure fixation. Bioabsorbable anchors can be used for this purpose, but they may be technically more difficult to use for repairing partial tears of the rotator cuff. Better visualization of the laser line on the anchor may be facilitated by using a probe from an anterior portal to hold the cuff up while the anchor is inserted.

This case has shown the importance of obtaining post­operative radiographic studies in patients who have metal anchors placed during shoulder surgery, especially if they complain of continued pain, new pain, crepitus, or grinding. When conventional radiography is insufficient for locating the anchor or its proximity to the joint line, computed tomography can be helpful.¹

Conclusion

Removing failed suture anchors can be challenging, especially when they protrude into the joint on the humeral side.^1,6 The best way to prevent this complication is through careful technique. The anchors should not be inserted beyond the depth of the laser line on the anchors, and every attempt should be made to make sure the laser line is visible at the time of anchor insertion. Postoperative radiographs should be considered for patients with metal anchors in the shoulder, especially if the patient continues to have symptoms or develops new symptoms in the shoulder after surgery.

Cautery and radiofrequency ablation (RFA) devices are commonly used in shoulder arthroscopic surgery for hemostasis and ablation of soft tissue. Although these devices are easily used and applied, complications (eg, extensive release of deltoid muscle,¹ nerve damage,² tendon damage,³ cartilage damage from heat transfer⁴) can occur during arthroscopic surgery. Radiofrequency devices can elevate fluid temperatures to unsafe levels and directly or indirectly injure surrounding tissue.^5,6 Skin complications from using these devices include direct burns to the subcutaneous tissues from the joint to the skin surface⁷ and skin burns related to overheated arthroscopic fluid.⁸

In our English-language literature review, however, we found no report of a skin burn secondary to contact between a RFA device and a spinal needle used in identifying structures during an arthroscopic acromioplasty. We report such a case here. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 51-year-old woman injured her left, nondominant shoulder when a descending garage door hit her directly on the superior aspect of the shoulder. She had immediate onset of pain on the top and lateral side of the shoulder and was evaluated by a primary care physician. Radiographs and magnetic resonance imaging (MRI) were normal. The patient was referred to an orthopedic surgeon for further evaluation.

The orthopedic surgeon found her to be in good health, with no history of diabetes, vascular conditions, or skin disorders. The initial diagnosis after history taking and physical examination was impingement syndrome with subacromial bursitis. The surgeon recommended nonoperative treatment: ice, nonsteroidal anti-inflammatory drugs, and physical therapy. After 3 months, the patient’s examination was unchanged, and there was no improvement in pain. Cortisone injected into the subacromial space helped for a few weeks, but the pain returned. After 2 more cortisone injections over 9 months failed, repeat MRI showed no tears of the rotator cuff or any other salient abnormalities. The treatment options were discussed with the patient, and, because the physical examination findings were consistent with impingement syndrome and nonoperative measures had failed, she consented to arthroscopic evaluation of the shoulder and arthroscopic partial anterior-lateral acromioplasty.

The procedure was performed 8 months after initial injury. With the patient under general anesthesia and in a lateral decubitus position, her arm was placed in an arm holder. Before the partial acromioplasty, two 18-gauge spinal needles were inserted from the skin surface into the subacromial space to help localize the anterolateral acromion and the acromioclavicular joint. The procedure was performed with a pump using saline bags kept at room temperature. A bipolar radiofrequency device (Stryker Energy Radiofrequency Ablation System; Stryker, Mahwah, New Jersey) was used to débride the subacromial bursa and the periosteum of the undersurface of the acromion. While the bursa was being débrided, the radiofrequency device inadvertently touched the anterior lateral needle probe, and a small skin burn formed around the needle on the surface of the shoulder (Figure). The radiofrequency device did not directly contact the skin, and the deltoid fascia was intact. The spinal needle was removed, and the skin around the burn was excised; the muscle beneath the skin was intact and showed no signs of thermal damage. The skin was mobilized and closed with interrupted simple sutures using a 4-0 nylon suture. The procedure was then completed with no other complications.

After surgery, the patient recovered without complications, and the skin lesion healed with no signs of infection and no skin or muscle defects. Some stiffness was treated with medication and physical therapy. Nine months after surgery, the patient reported mild shoulder stiffness and remained dissatisfied with the appearance of the skin in the area of the burn.

Discussion

Our patient’s case is a reminder that contact between a radiofrequency device and metal needles can transfer heat to tissues and cause skin burns. When using a radiofrequency device around metal needles or cannulas, surgeons should be sure to avoid prolonged contact with the metal. Our patient’s case is the first reported case of a thermal skin injury occurring when a spinal needle was heated by an arthroscopic ablater.

Other authors have reported indirect thermal skin injuries caused by radiofrequency devices during arthroscopic surgery, but the causes were postulated to be direct contact between device and skin⁷ and overheating of the arthroscopy fluid.^5,6,8 Huang and colleagues⁸ reported that full-thickness skin burns occurred when normal saline used during routine knee arthroscopy overheated from use of a radiofrequency device. Burn lesions, noted on their patient’s leg within 1 day after surgery, required subsequent débridement, a muscle flap, and split-skin grafting. Skin burns caused by overheated fluid have occurred irrespective of type of fluid used (eg, 1.5% glycine or lactated Ringer solution).⁶ There was no evidence that our patient’s burn resulted from extravasated overheated fluid, as the lesion was localized to the area immediately around the needle and was not geographic, as was described by Huang and colleagues.⁸

Other possible causes of skin burns during arthroscopic surgery have been described, but none applies in our patient’s case. Segami and colleagues⁷ described a burn resulting from direct transfer of heat from the radiofrequency device to the skin because of their proximity. This mechanism was not the cause in our patient’s case; there was no evidence of a defect or burned deltoid muscle at time of surgery. Lau and Dao⁹ reported 2 small full-thickness skin burns caused by a fiberoptic-light cable tip placed on a patient’s leg; in addition, the hot (>170°C) cables caused the paper drapes to combust.⁹ Skin burns secondary to use of skin antiseptics have been reported,¹⁰ but such lesions typically are located beneath tourniquets or in areas of friction from surgical drapes. In some cases, lesions described as skin burns may actually have been pressure lesions secondary to moist skin and friction.¹¹

Whether type of radiofrequency device contributes to the occurrence of heat-related lesions during arthroscopic surgery is unknown. Some investigators have suggested there is more potential for harm with bipolar RFA devices than with monopolar devices.^12,13 Monopolar devices pass energy between a probe and a grounding plate, whereas bipolar devices pass energy through 2 points on the probe.¹⁴ Because the heat for the monopolar probe derives from the frictional resistance of tissues to each other rather than from the probe itself, the bipolar probe theoretically allows for better temperature control. In addition, bipolar probes require less current to achieve the same heating effect. However, recent studies have suggested that, compared with monopolar radiofrequency devices, bipolar radiofrequency devices are associated with larger increases in temperature at equal depths after an equal number of applications.^12,13

To our knowledge, no one has specifically investigated the type of bipolar device used in the present case. This case report, the first to describe a thermal skin injury caused by direct contact between a radiofrequency device and a metal needle inserted in the skin, is a reminder that contact between radiofrequency devices and spinal needles or other metal cannulas used in arthroscopic surgery should be avoided.

Cautery and radiofrequency ablation (RFA) devices are commonly used in shoulder arthroscopic surgery for hemostasis and ablation of soft tissue. Although these devices are easily used and applied, complications (eg, extensive release of deltoid muscle,¹ nerve damage,² tendon damage,³ cartilage damage from heat transfer⁴) can occur during arthroscopic surgery. Radiofrequency devices can elevate fluid temperatures to unsafe levels and directly or indirectly injure surrounding tissue.^5,6 Skin complications from using these devices include direct burns to the subcutaneous tissues from the joint to the skin surface⁷ and skin burns related to overheated arthroscopic fluid.⁸

In our English-language literature review, however, we found no report of a skin burn secondary to contact between a RFA device and a spinal needle used in identifying structures during an arthroscopic acromioplasty. We report such a case here. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 51-year-old woman injured her left, nondominant shoulder when a descending garage door hit her directly on the superior aspect of the shoulder. She had immediate onset of pain on the top and lateral side of the shoulder and was evaluated by a primary care physician. Radiographs and magnetic resonance imaging (MRI) were normal. The patient was referred to an orthopedic surgeon for further evaluation.

The orthopedic surgeon found her to be in good health, with no history of diabetes, vascular conditions, or skin disorders. The initial diagnosis after history taking and physical examination was impingement syndrome with subacromial bursitis. The surgeon recommended nonoperative treatment: ice, nonsteroidal anti-inflammatory drugs, and physical therapy. After 3 months, the patient’s examination was unchanged, and there was no improvement in pain. Cortisone injected into the subacromial space helped for a few weeks, but the pain returned. After 2 more cortisone injections over 9 months failed, repeat MRI showed no tears of the rotator cuff or any other salient abnormalities. The treatment options were discussed with the patient, and, because the physical examination findings were consistent with impingement syndrome and nonoperative measures had failed, she consented to arthroscopic evaluation of the shoulder and arthroscopic partial anterior-lateral acromioplasty.

The procedure was performed 8 months after initial injury. With the patient under general anesthesia and in a lateral decubitus position, her arm was placed in an arm holder. Before the partial acromioplasty, two 18-gauge spinal needles were inserted from the skin surface into the subacromial space to help localize the anterolateral acromion and the acromioclavicular joint. The procedure was performed with a pump using saline bags kept at room temperature. A bipolar radiofrequency device (Stryker Energy Radiofrequency Ablation System; Stryker, Mahwah, New Jersey) was used to débride the subacromial bursa and the periosteum of the undersurface of the acromion. While the bursa was being débrided, the radiofrequency device inadvertently touched the anterior lateral needle probe, and a small skin burn formed around the needle on the surface of the shoulder (Figure). The radiofrequency device did not directly contact the skin, and the deltoid fascia was intact. The spinal needle was removed, and the skin around the burn was excised; the muscle beneath the skin was intact and showed no signs of thermal damage. The skin was mobilized and closed with interrupted simple sutures using a 4-0 nylon suture. The procedure was then completed with no other complications.

After surgery, the patient recovered without complications, and the skin lesion healed with no signs of infection and no skin or muscle defects. Some stiffness was treated with medication and physical therapy. Nine months after surgery, the patient reported mild shoulder stiffness and remained dissatisfied with the appearance of the skin in the area of the burn.

Discussion

Our patient’s case is a reminder that contact between a radiofrequency device and metal needles can transfer heat to tissues and cause skin burns. When using a radiofrequency device around metal needles or cannulas, surgeons should be sure to avoid prolonged contact with the metal. Our patient’s case is the first reported case of a thermal skin injury occurring when a spinal needle was heated by an arthroscopic ablater.

Other authors have reported indirect thermal skin injuries caused by radiofrequency devices during arthroscopic surgery, but the causes were postulated to be direct contact between device and skin⁷ and overheating of the arthroscopy fluid.^5,6,8 Huang and colleagues⁸ reported that full-thickness skin burns occurred when normal saline used during routine knee arthroscopy overheated from use of a radiofrequency device. Burn lesions, noted on their patient’s leg within 1 day after surgery, required subsequent débridement, a muscle flap, and split-skin grafting. Skin burns caused by overheated fluid have occurred irrespective of type of fluid used (eg, 1.5% glycine or lactated Ringer solution).⁶ There was no evidence that our patient’s burn resulted from extravasated overheated fluid, as the lesion was localized to the area immediately around the needle and was not geographic, as was described by Huang and colleagues.⁸

Other possible causes of skin burns during arthroscopic surgery have been described, but none applies in our patient’s case. Segami and colleagues⁷ described a burn resulting from direct transfer of heat from the radiofrequency device to the skin because of their proximity. This mechanism was not the cause in our patient’s case; there was no evidence of a defect or burned deltoid muscle at time of surgery. Lau and Dao⁹ reported 2 small full-thickness skin burns caused by a fiberoptic-light cable tip placed on a patient’s leg; in addition, the hot (>170°C) cables caused the paper drapes to combust.⁹ Skin burns secondary to use of skin antiseptics have been reported,¹⁰ but such lesions typically are located beneath tourniquets or in areas of friction from surgical drapes. In some cases, lesions described as skin burns may actually have been pressure lesions secondary to moist skin and friction.¹¹

Whether type of radiofrequency device contributes to the occurrence of heat-related lesions during arthroscopic surgery is unknown. Some investigators have suggested there is more potential for harm with bipolar RFA devices than with monopolar devices.^12,13 Monopolar devices pass energy between a probe and a grounding plate, whereas bipolar devices pass energy through 2 points on the probe.¹⁴ Because the heat for the monopolar probe derives from the frictional resistance of tissues to each other rather than from the probe itself, the bipolar probe theoretically allows for better temperature control. In addition, bipolar probes require less current to achieve the same heating effect. However, recent studies have suggested that, compared with monopolar radiofrequency devices, bipolar radiofrequency devices are associated with larger increases in temperature at equal depths after an equal number of applications.^12,13

To our knowledge, no one has specifically investigated the type of bipolar device used in the present case. This case report, the first to describe a thermal skin injury caused by direct contact between a radiofrequency device and a metal needle inserted in the skin, is a reminder that contact between radiofrequency devices and spinal needles or other metal cannulas used in arthroscopic surgery should be avoided.

Cautery and radiofrequency ablation (RFA) devices are commonly used in shoulder arthroscopic surgery for hemostasis and ablation of soft tissue. Although these devices are easily used and applied, complications (eg, extensive release of deltoid muscle,¹ nerve damage,² tendon damage,³ cartilage damage from heat transfer⁴) can occur during arthroscopic surgery. Radiofrequency devices can elevate fluid temperatures to unsafe levels and directly or indirectly injure surrounding tissue.^5,6 Skin complications from using these devices include direct burns to the subcutaneous tissues from the joint to the skin surface⁷ and skin burns related to overheated arthroscopic fluid.⁸

In our English-language literature review, however, we found no report of a skin burn secondary to contact between a RFA device and a spinal needle used in identifying structures during an arthroscopic acromioplasty. We report such a case here. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 51-year-old woman injured her left, nondominant shoulder when a descending garage door hit her directly on the superior aspect of the shoulder. She had immediate onset of pain on the top and lateral side of the shoulder and was evaluated by a primary care physician. Radiographs and magnetic resonance imaging (MRI) were normal. The patient was referred to an orthopedic surgeon for further evaluation.

The orthopedic surgeon found her to be in good health, with no history of diabetes, vascular conditions, or skin disorders. The initial diagnosis after history taking and physical examination was impingement syndrome with subacromial bursitis. The surgeon recommended nonoperative treatment: ice, nonsteroidal anti-inflammatory drugs, and physical therapy. After 3 months, the patient’s examination was unchanged, and there was no improvement in pain. Cortisone injected into the subacromial space helped for a few weeks, but the pain returned. After 2 more cortisone injections over 9 months failed, repeat MRI showed no tears of the rotator cuff or any other salient abnormalities. The treatment options were discussed with the patient, and, because the physical examination findings were consistent with impingement syndrome and nonoperative measures had failed, she consented to arthroscopic evaluation of the shoulder and arthroscopic partial anterior-lateral acromioplasty.

The procedure was performed 8 months after initial injury. With the patient under general anesthesia and in a lateral decubitus position, her arm was placed in an arm holder. Before the partial acromioplasty, two 18-gauge spinal needles were inserted from the skin surface into the subacromial space to help localize the anterolateral acromion and the acromioclavicular joint. The procedure was performed with a pump using saline bags kept at room temperature. A bipolar radiofrequency device (Stryker Energy Radiofrequency Ablation System; Stryker, Mahwah, New Jersey) was used to débride the subacromial bursa and the periosteum of the undersurface of the acromion. While the bursa was being débrided, the radiofrequency device inadvertently touched the anterior lateral needle probe, and a small skin burn formed around the needle on the surface of the shoulder (Figure). The radiofrequency device did not directly contact the skin, and the deltoid fascia was intact. The spinal needle was removed, and the skin around the burn was excised; the muscle beneath the skin was intact and showed no signs of thermal damage. The skin was mobilized and closed with interrupted simple sutures using a 4-0 nylon suture. The procedure was then completed with no other complications.

After surgery, the patient recovered without complications, and the skin lesion healed with no signs of infection and no skin or muscle defects. Some stiffness was treated with medication and physical therapy. Nine months after surgery, the patient reported mild shoulder stiffness and remained dissatisfied with the appearance of the skin in the area of the burn.

Discussion

Our patient’s case is a reminder that contact between a radiofrequency device and metal needles can transfer heat to tissues and cause skin burns. When using a radiofrequency device around metal needles or cannulas, surgeons should be sure to avoid prolonged contact with the metal. Our patient’s case is the first reported case of a thermal skin injury occurring when a spinal needle was heated by an arthroscopic ablater.

Other authors have reported indirect thermal skin injuries caused by radiofrequency devices during arthroscopic surgery, but the causes were postulated to be direct contact between device and skin⁷ and overheating of the arthroscopy fluid.^5,6,8 Huang and colleagues⁸ reported that full-thickness skin burns occurred when normal saline used during routine knee arthroscopy overheated from use of a radiofrequency device. Burn lesions, noted on their patient’s leg within 1 day after surgery, required subsequent débridement, a muscle flap, and split-skin grafting. Skin burns caused by overheated fluid have occurred irrespective of type of fluid used (eg, 1.5% glycine or lactated Ringer solution).⁶ There was no evidence that our patient’s burn resulted from extravasated overheated fluid, as the lesion was localized to the area immediately around the needle and was not geographic, as was described by Huang and colleagues.⁸

Other possible causes of skin burns during arthroscopic surgery have been described, but none applies in our patient’s case. Segami and colleagues⁷ described a burn resulting from direct transfer of heat from the radiofrequency device to the skin because of their proximity. This mechanism was not the cause in our patient’s case; there was no evidence of a defect or burned deltoid muscle at time of surgery. Lau and Dao⁹ reported 2 small full-thickness skin burns caused by a fiberoptic-light cable tip placed on a patient’s leg; in addition, the hot (>170°C) cables caused the paper drapes to combust.⁹ Skin burns secondary to use of skin antiseptics have been reported,¹⁰ but such lesions typically are located beneath tourniquets or in areas of friction from surgical drapes. In some cases, lesions described as skin burns may actually have been pressure lesions secondary to moist skin and friction.¹¹

Whether type of radiofrequency device contributes to the occurrence of heat-related lesions during arthroscopic surgery is unknown. Some investigators have suggested there is more potential for harm with bipolar RFA devices than with monopolar devices.^12,13 Monopolar devices pass energy between a probe and a grounding plate, whereas bipolar devices pass energy through 2 points on the probe.¹⁴ Because the heat for the monopolar probe derives from the frictional resistance of tissues to each other rather than from the probe itself, the bipolar probe theoretically allows for better temperature control. In addition, bipolar probes require less current to achieve the same heating effect. However, recent studies have suggested that, compared with monopolar radiofrequency devices, bipolar radiofrequency devices are associated with larger increases in temperature at equal depths after an equal number of applications.^12,13

To our knowledge, no one has specifically investigated the type of bipolar device used in the present case. This case report, the first to describe a thermal skin injury caused by direct contact between a radiofrequency device and a metal needle inserted in the skin, is a reminder that contact between radiofrequency devices and spinal needles or other metal cannulas used in arthroscopic surgery should be avoided.