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Position of Immobilization After Dislocation of the Shoulder. A Cadaveric Study*

EIJI ITOI, M.D., YUJI HATAKEYAMA, M.D., MASAKAZU URAYAMA, M.D., RABINDRA L. PRADHAN, M.D., TADATO KIDO, M.D. and KOZO SATO, M.D., AKITA, JAPAN

Investigation performed at the Department of Orthopedic Surgery, Akita University School of Medicine, Akita

	Abstract

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Background: After reduction of a shoulder dislocation, the torn edges of a Bankart lesion need to be approximated for healing during immobilization. The position of immobilization has traditionally been adduction and internal rotation, but there is little direct evidence to support or discredit the use of this position. The purpose of the present study was to determine the relationship between the position of the arm and the coaptation of the edges of a simulated Bankart lesion created in cadaveric shoulders. Methods: Ten thawed fresh-frozen cadaveric shoulders were used for experimentation. All of the muscles were removed to expose the joint capsule. A simulated Bankart lesion was created by sectioning the anteroinferior aspect of the capsule from the labrum. With linear transducers attached to the anteroinferior and inferior portions of the Bankart lesion, the opening and closing of the lesion were recorded with the arm in 0, 30, 45, and 60 degrees of elevation in the coronal and sagittal planes as well as with the arm in rotation from full internal to full external rotation in 10-degree increments. Results: With the arm in adduction, the edges of the simulated Bankart lesion were coapted in the range from full internal rotation to 30 degrees of external rotation. With the arm in 30 degrees of flexion or abduction, the edges of the lesion were coapted in neutral and internal rotation but were separated in external rotation. At 45 and 60 degrees of flexion or abduction, the edges were separated regardless of rotation. Conclusions: The present study demonstrated that, in the cadaveric shoulder, there was a so-called coaptation zone in which the edges of a simulated Bankart lesion were kept approximated without the surrounding muscles. Clinical Relevance: Recent clinical data indicate that tight anterior soft tissue helps to keep the lesion approximated. Thus, choosing a position of immobilization (within the so-called coaptation zone) that increases tension in the anterior soft tissue (such as adduction and external rotation or abduction and neutral rotation) may be better than immobilizing the shoulder in the conventional position.

	Introduction

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The basic principle that must be followed to promote the healing process of a ruptured ligament or tendon is that the torn edges must be approximated and kept in place. The standard method of treatment of acute dislocation of the shoulder has been to immobilize the arm to the trunk after reduction^5,8,10,13,16. With the arm in this position, the shoulder is in adduction and internal rotation. Although many studies have been performed to assess different durations^4,5,13,14,17 and methods^3-5,13 of immobilization, we have found no experimental data that support immobilization of the arm to the trunk. Despite the lack of such experimental evidence, this position has been favored simply because the trunk is the only splint that is constantly available. However, we hypothesized that, in the conventional position of immobilization, the edges of a Bankart lesion are not coapted. There were two reasons for this hypothesis: the rate of recurrence of dislocation after immobilization in a conventional position is relatively high (ranging from forty-eight [47 percent] of 102 to twenty-one of twenty-one) among young patients^4,9,13,14,19, and no consensus has been obtained regarding the optimum period of immobilization^4,5,13,14,17. In order to test our hypothesis, we needed to know how the coaptation of the edges of a Bankart lesion changes with alterations in the position of the arm. This study was specifically designed to determine the relationship between the position of the arm and the coaptation of the edges of a simulated Bankart lesion created in cadaveric shoulders.

	Materials and Methods

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Preparation of Specimens
Ten fresh-frozen cadaveric shoulders from donors who were fifty-three to eighty-two years old (mean, sixty-four years old) at the time of death were thawed overnight at room temperature. None of the shoulders had roentgenographic evidence of osteoarthritis. Each specimen was disarticulated at the scapulothoracic joint proximally and was dissected at the mid-part of the humerus distal to the deltoid attachment distally. All of the muscles were removed except for those of the rotator cuff, which were elevated from the scapula and were carefully dissected from the capsule distally until they could not be dissected bluntly any further. The tendons were then sectioned, and cables were attached to the remnant portions of the subscapularis and infraspinatus tendons to apply load. With this technique, the medial half of the capsule (the glenoid side) was fully exposed. An acrylic plate was attached to the medial border of the scapula parallel to the border and was fixed with screws and polymethylmethacrylate. An intramedullary rod (ten millimeters in diameter) was inserted into the proximal aspect of the humerus and was fixed with polymethylmethacrylate. The scapula was attached to a custom shoulder-positioner that allowed the humerus to be placed in a given plane of elevation (such as the coronal or sagittal plane), a given angle of glenohumeral elevation (0 to 110 degrees), and a given angle of humeral rotation.

The anteroinferior aspect of the capsule was incised at its junction with the labrum, from the 2:00 position to the 7:00 position in the right shoulder and from the 5:00 position to the 10:00 position in the left shoulder, to simulate a Bankart lesion. This procedure removed the normal negative intra-articular pressure in the glenohumeral joint. After we confirmed that the humeral head overrode the anterior rim of the glenoid, the humeral head was reduced into the glenoid socket. A force of twenty-two newtons was applied to the humeral head against the glenoid fossa through the cables attached to the subscapularis and infraspinatus tendons to keep the humeral head centered in the glenoid fossa during the test²⁰. The specimen was kept moist with a spray of saline solution every five to ten minutes during the test, which was performed at room temperature (24 degrees Celsius).

Measurement Device
With the arm in adduction and neutral rotation (the reference position), two three-millimeter stroke differential variable reluctance transducers (MicroStrain, Burlington, Vermont) were attached to the anteroinferior and inferior portions of the capsule (at the 4:30 and 6:00 positions in the right shoulder and at the 7:30 and 6:00 positions in the left shoulder), bridging the lesion (Figs. 1-A and 1-B). The differential variable reluctance transducer has two stainless-steel barbed points; one was inserted into the capsulolabral tissue medially and the other was inserted into the capsule laterally, within five millimeters of the incised edge. The attachment of the device was strengthened by suturing it to the adjacent tissues around the points. The transducers were used to record the amount of opening of the lesion with the arm in various positions. This device provided an analog voltage that was linearly proportional to the displacement of the magnetic core. Because the core slid freely within the tube, the transducers had little influence on the opening and closing of the Bankart lesion being tested. Each transducer was calibrated to linear displacement by the manufacturer. The resolution of the device was 1.5 micrometers, the repeatability was ±1 micrometer, and the range of measurement was six millimeters. The transducers were connected to a four-channel chart-recorder (MB-STD-4; MicroStrain) to record the displacement data during the test.

View larger version (139K): [in this window] [in a new window]   FIG1-A: Figs. 1-A and 1-B: Photographs showing the positions of the differential variable reluctance transducers with the arm in 30 degrees of abduction. One transducer is at the anteroinferior portion (the 4:30 position) of the simulated Bankart lesion, and the other is at the inferior portion (the 6:00 position). Fig. 1-A: The edges of the lesion (arrow) were approximated with the arm in neutral rotation.

View larger version (145K): [in this window] [in a new window]   FIG1-B: Fig. 1-B The edges of the lesion (arrow) were separated with the arm in external rotation.

Positions of the Arm
The humerus was elevated in the coronal and sagittal planes to simulate abduction and flexion. Elevation angles were 0, 30, 45, and 60 degrees relative to the scapula, simulating 0, 30, 60, and 90 degrees of elevation of the arm relative to the trunk¹². At each elevated position, the arm was manually rotated from neutral rotation to full internal rotation, back to neutral rotation, and then to full external rotation in 10-degree increments.

Collection and Analysis of Data
We collected displacement data at each elevated position through the full range of rotation unless the separation of the edges of the gap of the Bankart lesion was wider than the range of measurement of the transducer. With elevation and rotation of the humerus as within-group factors, one-way repeated-measures analysis of variance was used to determine the effect of these factors on the displacement data. When the analysis of variance revealed a significant effect, the Newman-Keuls multiple-comparisons procedure was used to further characterize the angles at which there were significant differences. Significance was set at the 5 percent level.

	Results

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During the test, internal rotation of more than 50 degrees caused lengthening of the transducers in some of the specimens because of folding of the redundant capsule, although the edges of the Bankart lesion were tightly approximated. External rotation of more than 40 degrees in elevated positions and any rotation with the arm elevated 60 degrees caused opening of the Bankart lesion beyond the six-millimeter measurement capacity of the transducers in all of the specimens. Thus, only the data obtained with the arm elevated 0, 30, and 45 degrees and rotated from 40 degrees of internal rotation to 30 degrees of external rotation were analyzed.

Anteroinferior Portion of the Bankart Lesion During Abduction (Fig. 2)
With the arm abducted 0 degrees, we found no significant displacement of the transducer attached to the anteroinferior portion of the Bankart lesion through the entire arc of rotation, although there was a trend toward opening of the lesion at greater degrees of external rotation (p = 0.057). With the arm abducted 30 degrees, external rotation caused displacement of the edges of the Bankart lesion; the displacement at 30 degrees of external rotation was significantly larger than that at 0, 10, and 20 degrees of internal rotation (p = 0.013). At 45 degrees of abduction, displacement at 10, 20, and 30 degrees of external rotation was significantly larger than that at 0 to 40 degrees of internal rotation (p < 0.0001).

View larger version (28K): [in this window] [in a new window]   FIG2: Fig. 2 Graph showing displacement at the anteroinferior portion of the Bankart lesion during abduction. External rotation of the arm significantly increased displacement at 30 (p = 0.013) and 45 (p < 0.0001) degrees of abduction, but no significant increase was detected in adduction. The effect of abduction of the arm was significant as well (p < 0.049). The values are given as the mean and the standard deviation. IR = internal rotation, and ER = external rotation.

Inferior Portion of the Bankart Lesion During Abduction (Fig. 3)
The displacement data were similar for the inferior portion of the Bankart lesion. We were unable to detect a significant effect of rotation of the arm when the arm was in adduction (p = 0.08). However, external rotation significantly increased the displacement at 30 (p < 0.0001) and 45 (p = 0.0006) degrees of abduction. The displacement at 30 degrees of abduction was larger than that at 0 degrees of abduction with the arm in 20 (p = 0.049) and 30 (p = 0.0052) degrees of external rotation. The displacement at 45 degrees of abduction was larger than that at 0 degrees of abduction through the entire arc of rotation (p < 0.023).

View larger version (27K): [in this window] [in a new window]   FIG3: Fig. 3 Graph showing displacement at the inferior portion of the simulated Bankart lesion during abduction. External rotation of the arm significantly increased displacement at 30 (p < 0.0001) and 45 (p = 0.0006) degrees of abduction. The displacement at 30 degrees of abduction was significantly larger than that at 0 degrees of abduction with the arm in 20 (p = 0.049) and 30 (p = 0.0052) degees of external rotation, and the displacement at 45 degees of abduction was significantly larger than that at 0 degrees of abduction through the entire arc of rotation (p < 0.023). The values are given as the mean and the standard deviation. IR = internal rotation, and ER = external rotation.

Anteroinferior Portion of the Bankart Lesion During Flexion (Fig. 4)

View larger version (27K): [in this window] [in a new window]   FIG4: Fig. 4 Graph showing displacement at the anteroinferior portion of the simulated Bankart lesion during flexion. External rotation of the arm significantly increased displacement at 30 degrees of flexion (p = 0.0005). The displacement at 30 degrees of flexion was larger than that at 0 degrees of flexion with the arm in 30 degrees of external rotation (p = 0.033), and the displacement at 45 degrees of flexion was larger than that at 0 degrees of flexion through the entire arc of rotation (p < 0.046). The values are given as the mean and the standard deviation. IR = internal rotation, and ER = external rotation.

Inferior Portion of the Bankart Lesion During Flexion (Fig. 5)
The inferior portion of the Bankart lesion showed the same trend during flexion. External rotation significantly increased the displacement at 0 (p = 0.033), 30 (p = 0.015), and 45 (p < 0.0001) degrees of flexion. The displacement at 45 degrees of flexion was significantly larger than that at 0 (p < 0.028) and 30 (p < 0.040) degrees of flexion through the entire arc of rotation.

View larger version (27K): [in this window] [in a new window]   FIG5: Fig. 5 Graph showing displacement at the inferior portion of the simulated Bankart lesion during flexion. External rotation of the arm significantly increased displacement at 0 (p = 0.033), 30 (p = 0.015), and 45 (p < 0.0001) degrees of flexion. The displacement at 45 degrees of flexion was significantly larger than that at 0 (p < 0.028) and 30 (p < 0.040) degrees of flexion through the entire arc of rotation. The values are given as the mean and the standard deviation. IR = internal rotation, and ER = external rotation.

	Discussion

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Our study showed that coaptation of the edges of the Bankart lesion was maintained within a certain range of positions of the arm (what we call the coaptation zone). The conventional position of immobilization with the arm in adduction and internal rotation is surely within this coaptation zone. Thus, our hypothesis that the edges of a Bankart lesion are not coapted in the conventional position for splinting is not supported by our findings.

The coaptation zone, however, was much larger than we had expected. For example, the edges of the lesion were always in contact, even in external rotation, when the arm was adducted. The question is whether one position within this zone is preferable to another for the healing of the lesion.

Coaptation of the edges of the lesion in vivo may depend not only on the position of the arm but also on the amount of hematoma formation and the resulting tension of the anterior soft tissue. Various amounts of hematoma have been identified in the glenohumeral joint after dislocation^1,15,18. Large amounts may increase the size of the gap created by the lesion or elevate the capsulolabral complex off the glenoid rim, which could prevent healing of the lesion. Ishikawa et al.⁶ used a modified clavicular harness to compress the anterior aspect of the shoulder in order to avoid expansion of the capsule and consequent detachment of the site of the Bankart lesion due to hemarthrosis after dislocation. In their study, none of forty-one shoulders treated with the harness redislocated, whereas twenty-two (29 percent) of seventy-five shoulders immobilized with a Desault bandage redislocated.

The apposition of the subscapularis to the anterior aspect of the capsule may be another factor that influences healing. The tension of the subscapularis, which increases in external rotation⁷, may prevent separation of the site of the lesion from the glenoid. With kinematic magnetic resonance imaging, Bonutti et al.² showed that the tense subscapularis kept the capsule in contact with the underlying bone structures in external rotation, whereas in internal rotation the subscapularis became redundant and the labrum and the capsule folded into the joint in some unstable shoulders. As long as the arm is within the coaptation zone, a position that increases soft-tissue tension (such as adduction and external rotation or abduction and neutral rotation) may be preferable to the conventional position of adduction and internal rotation, in which the anterior structures are lax.

Perugia et al.¹¹ presented clinical data that strongly support this idea. They divided 112 shoulders that had an initial anterior dislocation into two groups. In one group fifty-six shoulders were immobilized with a Desault bandage for three weeks, and in the other the remaining fifty-six shoulders were immobilized in a shoulder spica with the arm in 60 degrees of abduction. At 4.2 years, the recurrence rate was 74 percent (of fifty-six) in the group treated with a Desault bandage and 21 percent (of fifty-six) in the group treated with a shoulder spica with the arm in 60 degrees of abduction. Thus, healing of the Bankart lesion was affected by the position of immobilization.

Without soft-tissue tension, hematoma formation, and intra-articular pressure, the model that we used is quite different from a shoulder in vivo. It is difficult to simulate a Bankart lesion with subperiosteal stripping of the capsulolabral complex from the glenoid. Also, the anterior aspect of the capsule may sometimes be elongated permanently in vivo and the posterior aspect may be damaged after dislocation. Our experiment was performed at room temperature, which might have affected the material properties of the capsule and, accordingly, the results of the study. In addition, constant application of force to the humeral head might have had some influence on the results, although we confirmed that the cables were not in contact with the capsule and, thus, did not have a direct effect on the condition of the simulated Bankart lesion. The cadaver model that we used lacked physiological dynamic muscle forces. Furthermore, the method of attaching the measuring device to the capsulolabral complex, which was by means of barbed points as well as reinforcement by suturing the device to the adjacent soft tissues, may have had some influence on the results. Because of micromovement of the device at the site of attachment as well as the material properties of the capsulolabral complex, there might have been a discrepancy between the measured gap and the real gap, although, as far as could be observed with the naked eye, such a discrepancy was negligible. For these reasons, direct application of our results to the clinical setting may be difficult. For example, because the lesion was more susceptible to opening without surrounding soft tissues, the in vivo coaptation zone may be even larger than the zone defined in the present study. However, the important finding in this study was that, even in shoulders without muscles, the edges of the Bankart lesion were kept approximated within a certain range of positions of the arm.

In conclusion, we found that, for cadaveric shoulders in which all of the muscles had been removed, there was a so-called coaptation zone that encompassed the usual position of immobilization. Recent reports have indicated that tight anterior soft tissue helps to approximate the lesion^2,11. Therefore, within the coaptation zone, a position of immobilization that increases anterior soft-tissue tension may be better than the conventional position, in which the anterior soft tissue is lax.

	Footnotes

 
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

Department of Orthopedic Surgery, Akita University School of Medicine, Hondo 1-1-1, Akita 010-8543, Japan. E-mail address for Dr. Itoi: itoi@med.akita-u.ac.jp.

	References

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