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Repair of the rotator cuff usually eliminates pain and improves the over-all function of the shoulder. Good function of the shoulder depends on the patient regaining a nearly normal passive and active range of motion with sufficient strength to perform activities of daily living, work, and sports13. Failure of procedures for repair of the rotator cuff usually is ascribed to disruption of the repair itself and may be associated with both pain and loss of active motion. However, loss of motion may occur with or without disruption of the repair and may be due to postoperative adhesions and actual capsular contracture. The prevalence of loss of motion has not been clearly reported in previous studies of the results of repair of the rotator cuff. A review of series of such procedures that were performed over the previous two decades revealed that, of 500 patients, twenty-one (4 per cent) had loss of motion that was believed to be due to postoperative adhesions2,5,6,8,14,15,17,21,24,31,32,39. Many reports have not included quantitative measurements of postoperative motion compared with preoperative motion; thus, it is difficult to arrive at an accurate appraisal of the prevalence of shoulder stiffness after repair of the rotator cuff. The senior one of us (J. J. P. W.) has found that loss of passive motion is not uncommon after repair of the rotator cuff, and although the patient may not always be symptomatic treatment may be necessary. The purpose of the current paper is to review the variables involved in loss of motion after repair of the rotator cuff and to describe an approach for its evaluation and treatment.
Some loss of motion after repair of a large tear of the rotator cuff may be inevitable, as dissection of the subscapularis and infraspinatus tendons free from surrounding tissue and local transposition of the tendons to repair the defect of the rotator cuff may result in limitation of the over-all passive excursion of portions of the cuff. For example, repair of a chronic rupture of the subscapularis often is associated with some loss of external rotation42. This is because of the shortening resulting from the repair of the tendon-muscle unit, as there is actual loss of tendon tissue. Furthermore, some patients may not be bothered by painless loss of motion as long as function and strength are improved. Symptomatic loss of motion after repair of the rotator cuff can have a variety of causes. One possible etiology is failure of a motor unit of the shoulderthat is, a tear of a rotator-cuff tendon, muscle failure (avulsion of the deltoid or disuse atrophy), or injury of the axillary nerve, the brachial plexus, or the suprascapular nerve. Shoulder stiffness can also be caused by soft-tissue contracture, which can be intra-articular (capsular contracture or tendon-shortening) or extra-articular (subacromial or subdeltoid scarring or scarring of the subscapularis-conjoined tendon region). Other causes are intrinsic disease or abnormality of the glenohumeral joint, such as osteoarthrosis or an osseous deformity, and a pain complex. These factors may occur in isolation or in combination. The history given by the patient is very important, as it may provide insight into the cause or causes of the loss of motion. For example, prolonged immobilization of the shoulder without any passive motion might be expected to lead to adhesions between tissue planes and thus to stiffness after a repair of the rotator cuff. An inappropriate load on the repair, such as that caused by a fall or by the initiation of an active range of motion during the first few weeks after the procedure, might lead to disruption of the repair. Additional patient-related factors of importance are a history of insulin-dependent diabetes mellitus and the formation of keloid scars28. These factors appear to be associated with a predisposition to loss of motion of the shoulder in the postoperative setting1. The most important observation to make during an evaluation of stiffness after a repair of the rotator cuff is whether the loss of motion is active or passive, or both11. Motion must always be compared with that of the contralateral, asymptomatic shoulder, if possible. Elimination of pain with use of a subacromial injection of ten milliliters of 1 per cent Xylocaine (lidocaine) can allow the physician to discriminate between loss of active motion due to pain and that due to a tear or contracture of the rotator cuff3. Testing should include not only flexion but also abduction in the scapular plane, internal and external rotation, and horizontal flexion (cross-chest adduction)1,9. The presence of pain with any of these motions also should be evaluated. Any differences between the arcs of active and passive motion should be noted. Careful measurements of isolated glenohumeral motion should be made with a goniometer, as patients who have shoulder stiffness often have scapulothoracic substitution (compensatory movement of the scapula on the thorax) and tilting of the trunk, which may give the appearance of more motion at the glenohumeral joint than is really present. Active motion is measured with the patient seated, and passive motion is measured with the patient supine. When the patient is supine, scapulothoracic substitution and tilting of the trunk are reduced, allowing more accurate measurement of glenohumeral rotation1. Loss of active motion but preservation of passive motion indicates failure of the repair of the rotator cuff or an injury of the axillary or suprascapular nerve, or both. In most patients, the location of the tear can be predicted on the basis of the pattern of lag between the arcs of active and passive motion25. For example, greater passive than active internal rotation indicates a tear of the subscapularis, while greater passive than active external rotation when the shoulder is abducted indicates a tear of the infraspinatus. Loss of passive motion and an equivalent limitation of active motion, with good strength, after a repair may or may not indicate a repeat tear; however, such findings do indicate postoperative adhesions and, sometimes, capsular contractures that limit motion. In some patients, articular incongruity, as might occur with osteoarthrosis, also may contribute to loss of motion. The pattern of motion loss is a particularly important indicator of the location or locations of adhesions. For example, loss of external rotation with the upper extremity at the side may be associated with contracture of the rotator-interval region of the anterosuperior portion of the glenohumeral joint, whereas limited abduction and external rotation usually indicates contracture of the inferior aspect of the capsule1,19,20,22. Loss of internal rotation is usually associated with a contracture of the posterior aspect of the capsule1,22. Persistent loss of motion after a repair of the rotator cuff often can be attributed to one of three causes: a pre-existing comorbid condition, such as osteoarthrosis or shoulder stiffness, in addition to the tear of the rotator cuff; the operative technique; or the technique used for postoperative rehabilitation. Some patients who have loss of motion caused by osteoarthrosis may be managed, incorrectly, for a tear of the rotator cuff. Furthermore, some degree of passive motion loss may not have been recognized or treated effectively before the repair of the rotator cuff. The result will be shoulder stiffness after the repair. This situation is analogous to performing a repair of the anterior cruciate ligament in a stiff knee. The result will be a healed ligament in a stiff knee. Therefore, it is preferable to recognize and treat shoulder stiffness adequately before performing a repair of the rotator cuff. Incorrect operative technique can lead directly to stiffness after a repair of the rotator cuff. For example, tight closure of the rotator-interval region with the upper extremity in internal rotation leads to loss of both external rotation and flexion (Fig. 1)35,38,40. In some patients, over-advancement of a tendon1,12,36 to close a tendon defect may lead to loss of motion by capturing the shoulder. However, most failures that are due to incorrect operative technique are caused by inadequate mobilization and repair of the torn tendon or by repair of the tendon under excessive tension.
Assuming that a technically adequate repair has been performed, the postoperative treatment has a direct bearing on the prevalence of shoulder stiffness after a repair of the rotator cuff. The aim during the initial phase of treatment (the first six weeks after the operation) is to protect the repair until it has healed while preserving passive motion. Thus, failure to begin a passive range of motion in the first week after the operation can lead to loss of motion. This loss of motion is usually due to adhesions between tissue planes, but it also may be due to capsular contracture. Some patients have a very low tolerance for pain during early passive motion, and this places them at risk for shoulder stiffness. Also, these patients tend to have a form of shoulder stiffness that is particularly resistant to non-operative therapy1,37,44. When a patient has loss of motion after a repair of the rotator cuff, additional important clinical observations include the presence of atrophy, which suggests a chronically torn tendon; painful flexion, which suggests residual impingement; tenderness over the acromioclavicular joint or the biceps tendon, which suggests an untreated pathological condition; weakness, which suggests an incomplete repair of the rotator cuff or a nerve injury; decreased skin sensation, which suggests an axillary-nerve injury; and a defect of the deltoid, which suggests an iatrogenic injury to the origin of the deltoid. Standard radiographs may be helpful for determining the extent of previous operative treatment for impingement and acromioclavicular disease. Our preference is to make a supraspinatus outlet radiograph, a 30-degree caudal tilt radiograph, a radiograph of the acromioclavicular joint, and an axillary radiograph4,7. These radiographs demonstrate the extent of the resection of the acromion and the acromioclavicular joint and provide information about the glenohumeral joint. Common problems that may be disclosed include failure to recognize and treat an os acromiale, excessive or inadequate resection of the acromion or the acromioclavicular joint, fracture of the os acromiale, and previously unrecognized osteoarthrosis of the glenohumeral joint. Additional adjuvant imaging that may be useful includes arthrography and magnetic resonance imaging. While the former will demonstrate a repeat tear after a repair, a watertight repair is not necessary for good function. Furthermore, arthrography does not directly show the degree and location of capsular contracture and adhesions27. Magnetic resonance imaging may provide additional useful information about the thickness of the tendon tissue as well as the degree of muscle atrophy and fatty degeneration16,26. This information can help the physician to decide on the treatment for stiffness of the shoulder and a repeat tear of the tendon repair. For example, thin tendon tissue might be expected to tear with closed manipulation, and a muscle with extensive atrophy and fatty degeneration would not be expected to function normally after a repair16. When all of the previously mentioned factors are taken into account, it appears that shoulder stiffness that might necessitate treatment is found in four types of patients: those who have stiffness without a tear after the repair, those who have both stiffness and a repeat tear after the repair, those who have stiffness in association with untreated osteoarthrosis of the glenohumeral joint, and those who have stiffness in combination with an injury of the deltoid or a nerve injury, or both, with or without a repeat tear after the repair. The treatment of each group of patients will be discussed.
Stiffness without a Tear of the Repaired Rotator Cuff Treatment options for these patients include intensive physical therapy, closed manipulation, and arthroscopic or open release of adhesions. All patients should be managed with stretching techniques by a physical therapist for at least three to six months after the repair, before other options for treatment are considered. During this period, the pain may subside and the patient's tolerance for stretching may improve. However, if no motion is gained during this period, it is neither clinically useful nor cost-effective to continue with this course of treatment. Closed manipulation, while appropriate for the treatment of idiopathic adhesive capsulitis, usually is not helpful for patients who have stiffness after a repair of the rotator cuff1,19,35,40,44. These patients usually have more extensive adhesions involving the tissue planes between the rotator cuff and the deltoid and the acromion, as well as actual capsular contractures. Furthermore, forceful manipulation after a repair of the rotator cuff may pose a risk to the integrity of the repair. Therefore, we usually do not attempt this form of treatment. Arthroscopic release of contracted capsule and adhesions is the method that we usually employ. This technique allows precise, selective release of adhesions between tissue planes as well as division of shortened, thickened capsular tissue1,19,40,43. Subsequently, gentle, controlled manipulation of the shoulder can restore motion with a reduced risk to the repair of the rotator cuff. Concomitant intra-articular and subacromial disease also may be detected and treated. For example, previously untreated disease of the biceps tendon can be managed with an arthroscopic tenotomy, and acromioclavicular disease and residual subacromial impingement also may be treated. An additional advantage of this technique is that it permits an immediate active range of motion without the need to await healing of repaired soft tissues. Contraindications to this technique are malunion of the tuberosity causing an osseous block to motion, articular incongruity due to osteoarthrosis, and extra-articular contractures such as entrapment or shortening of the subscapularis after a previous Putti-Platt or Bristow procedure, for example.
Arthroscopic Release When an interscalene catheter is used, a continuous infusion of 0.25 per cent bupivacaine is administered at a rate of six milliliters per hour for forty-eight hours. All of our patients also use a self-administered pain-relief system (patient-controlled analgesia) through an intravenous pump set to administer one milligram of morphine every eight minutes as needed, to a maximum of thirty milligrams in four hours.
Anterior Capsular Release We perform shoulder arthroscopy with the patient seated in the beach-chair position, without any traction on the arm41. The joint is distended with sterile saline solution through an 18-gauge spinal needle inserted into a posterior portal. The hydrostatic pressure tends to push the humeral head away from the glenoid and reduces the risk of injury to the cartilage as the arthroscope is inserted. The arthroscope is guided carefully over the humeral head. As the volume of the joint is usually small, retrograde flow of saline solution out of an open port in the arthroscopic sheath confirms the intra-articular placement of the arthroscope. Usually, only the anterosuperior region of the joint capsule can be visualized; no attempt should be made to force the arthroscope inferiorly into the joint (Fig. 2-A). The long head of the biceps tendon defines the region of the rotator interval, which is the area between the anterior edge of the supraspinatus tendon and the superior edge of the subscapularis tendon20. This region usually is contracted in individuals who lack external rotation of the adducted shoulder35,38.
An 18-gauge spinal needle is introduced from a superior and anterior location so that it enters the joint just underneath the long head of the biceps tendon. The needle then is withdrawn and is replaced with a seven-millimeter arthroscopic shoulder cannula (Linvatec, Concept Arthroscopy, Largo, Florida). A 4.5-millimeter motorized shaver (full radius resector; Linvatec, Concept Arthroscopy) is placed through the cannula, and the anterosuperior region of the joint is debrided of synovial tissue and adhesions. This allows the thick sheet of the scarred anterosuperior portion of the capsule to be clearly visualized (Fig. 2-A). An arthroscopic electrocautery device with a hooked tip (Linvatec, Concept Arthroscopy) is inserted through the anterior cannula, and the capsular scar is divided, beginning just anterior and inferior to the long head of the biceps and continuing inferiorly until the superior border of the subscapularis can be seen (Fig. 2-B). As this thick capsular tissue is divided, visualization of the joint improves, as the humeral head moves inferior and lateral to the glenoid with the release of this portion of the capsule (Fig. 2-C). This allows the arthroscope to be introduced farther anteriorly and inferiorly into the joint. If the anterior aspect of the capsule inferior to the superior border of the subscapularis is also thickened and contracted, it can be divided down to the inferior aspect of the glenoid. We never attempt to divide the capsule into the axillary pouch, as we believe that this creates a major risk of injury to the axillary nerve, which is in close proximity to that region of the capsule.
After the anterior capsular release, the arthroscope is withdrawn and gentle closed manipulation is performed, first to restore external rotation and then to restore flexion and internal rotation. Patients who continue to have marked limitation of internal rotation and cross-chest adduction have a posterior capsular contracture as well. In these individuals, a posterior capsular release is also necessary.
Posterior Capsular Release
Subacromial Arthroscopy Scarring in the subacromial space is common after a repair of the rotator cuff, especially if appropriate postoperative mobilization was not instituted (Figs. 4-A and 4-B). Subacromial bursoscopy and débridement is effective for freeing up extra-articular adhesions in the subacromial space. A lateral portal such as that used for routine subacromial decompression is made, and a motorized shaver is used to remove the tissue between the acromion and the rotator cuff. Débridement is carried out to the anterior aspect of the acromion but not into the fibers of the deltoid muscle. Additional anteroinferior acromial bone is removed arthroscopically if an incomplete or inadequate acromioplasty had been done previously. If loss of motion persists even after complete capsular release and subacromial débridement, then an open release usually is needed to address other extracapsular scarring and to permit tendon mobilization or z-plasty lengthening for the treatment of any residual loss of external rotation.
Stiffness with a Tear of the Repaired Rotator Cuff If closed manipulation does not improve motion, either an open or an arthroscopic release can be performed. If there is marked loss of passive motion and extensive scarring, it may be best to release the adhesions without revising the repaired rotator cuff at the same time, as the combination of both operations may increase the likelihood of subsequent shoulder stiffness. Instead, intensive postoperative physical therapy can be used to maintain the gains in motion, and several months later, when the shoulder is supple, a repeat repair of the tendon can be performed.
Open Release The open release can be accomplished through either an anterosuperior deltoid-splitting approach or a standard deltopectoral approach. Dissection and freeing up of the subscapularis muscle and tendon, however, should be performed through the latter approach so that the axillary nerve and the brachial plexus can be thoroughly visualized and protected1. Adhesions between the deltoid and the humerus are released first. This area may be densely scarred, and a combination of blunt and sharp dissection is needed to free up this interval. Care must be taken to avoid injury to the axillary nerve as it enters the deltoid through the quadrilateral space. If the muscle substance of the deltoid is violated as the dissection proceeds posteriorly, the axillary nerve can be injured. It is therefore important to keep the dissection on the humerus as it progresses posteriorly. The axillary nerve often can be identified three to five centimeters distal to the acromion, coursing from posteroinferior to anterosuperior and lying directly on the subdeltoid fascia. When the interval between the deltoid and the humerus has been developed, the dissection is carried superiorly into the subacromial space. Any scar or bursal tissue between the acromion and the superior aspect of the cuff should be excised, along with the coracoacromial ligament if it is present. Completion of this part of the dissection should leave the deltoid and the subacromial space free of the humeral head and rotator-cuff muscles. In order to free up the subscapularis, the interval between it and the conjoined tendon and coracoid must be dissected. The dissection should start at the coracoid and should proceed inferiorly along the lateral border of the conjoined tendon. The coracohumeral ligament is divided sharply, and the interval between the subscapularis and the conjoined tendon is dissected. Care is taken as the dissection proceeds medially so that the musculocutaneous nerve is not injured as it enters the muscle substance of the coracobrachialis and the biceps. If necessary, we identify the musculocutaneous nerve during this step in the dissection. The goal of this portion of the dissection is to free the subscapularis from adhesions in order to restore external rotation. In patients who have a marked loss of external rotation, the subscapularis must be completely released, beginning on its superficial surface, continuing around its superior and inferior borders, and finally releasing its inferior adhesion to the joint capsule and the scapula. During this procedure, the axillary nerve must be identified on the superficial surface of the muscle1. In order to do this, we detach the tendon of the subscapularis from its humeral insertion either by performing a z-plasty or by releasing the underlying capsule with the tendon. A humeral head retractor then can be used to displace the humeral head posteriorly, to facilitate the dissection of the subscapularis and the axillary nerve. A long, thin retractor placed over the subscapularis allows the brachial plexus and the axillary nerve to be visualized. The axillary nerve then is elevated with a right-angle clamp, and a vessel loupe is placed around it. Adhesions fixing the subscapularis to the inferior aspect of the capsule then can be released down to the axillary nerve. Adhesions between the subscapularis and the underlying capsule then are divided, and the interval between the subscapularis and the glenoid labrum also is developed. This complete release and freeing of the subscapularis usually restores enough mobility to the tendon so that it can be repaired to the lesser tuberosity, resulting in improved external rotation. However, if the tendon is still not mobile enough to allow external rotation of more than 30 degrees, a z-plasty lengthening of the subscapularis and the capsule in the coronal plane can be performed23,29,33,34. The subscapularis and the scarred capsule initially are dissected with some of the scarred tendon and capsule left attached to the lesser tuberosity. The subscapularis tendon then is repaired to this limb of tissue with the shoulder in external rotation, thus completing the z-plasty repair. Some patients who have severe loss of motion may have marked thickening and contracture of the inferior aspect of the capsule as well as contracture of the posterior aspect of the capsule. In these patients, the capsule can be released circumferentially with use of a humeral head retractor to displace the humeral head posteriorly and with the axillary nerve dissected away from the inferior aspect of the capsule. Next, a blunt retractor is placed along the inferior aspect of the capsule, which may then be sharply divided. As the inferior aspect of the capsule is divided, the humeral head can be moved farther away from the glenoid with the humeral head retractor, allowing access to the scarred posterior aspect of the capsule. This portion of the capsule can be divided by placing a small knife-blade on a long handle through the joint. The posterior aspect of the capsule should be divided along the glenoid labrum in order to avoid injury to the posterior rotator-cuff tendon, which attaches to the posterior aspect of the capsule in a more lateral location. After these releases, the subscapularis and the capsule are closed as described earlier.
Postoperative Treatment After an open release or a repeat repair of the rotator cuff, or both, passive motion only is permitted within the safe limits defined by the soft-tissue repair. When an arthroscopic release has been performed, both active motion and passive motion are permitted. Narcotic analgesics are used during the first several days after the procedure, and physical therapy is initiated immediately on an outpatient basis. Physical-therapy sessions are conducted five times a week for the first two weeks and three times a week for the next two weeks. In current managed-care insurance plans, it is important to advise the primary-care physician of this mandatory and essential aspect of postoperative treatment. Patients who have had an arthroscopic release also perform a home program using a pulley and self-assisted stretching, while those who have had an open release or a tendon repair, or both, continue with passive motion only for six weeks after the operation.
Stiffness with Untreated Osteoarthrosis
Stiffness with Deltoid or Nerve Injury While disruption of the deltoid origin is infrequent after a repair of the rotator cuff, it is a devastating complication18. The senior one of us has found that, if it is recognized within the first three weeks after the repair of the rotator cuff, it can be repaired satisfactorily, provided that excessive acromial bone has not been removed. In this procedure, all adhesions are released and the deltoid is mobilized and repaired. If a nerve injury has occurred, it should be determined whether it is a neurapraxic injury caused by a retractor or a direct axonotmesis caused by operative trauma. Most of these injuries are of the former type and will resolve; therefore, shoulder stiffness and disruption of the tendon repair should be treated according to the methods described previously.
The senior one of us has treated five cases of shoulder stiffness after a total of 221 repairs of the rotator cuff. An additional five patients were referred to us for treatment of stiffness associated with an intact repair following a repair of the rotator cuff that had been done elsewhere. The indication for the treatment of shoulder stiffness was painful limitation of motion in all planes that affected the ability of the patient to perform activities of daily living. Although no specific loss of motion was used as an absolute indication, all patients had marked shoulder stiffness after more than six months of postoperative therapy. Eight patients were managed with an arthroscopic capsular release and release of subacromial adhesions, with a satisfactory outcome (Figs. 5A and 5-B), whereas two needed an open release because of extra-articular scarring of the subscapularis. All patients had improved motion and relief of pain.
We concluded that, although symptomatic stiffness after a repair of the rotator cuff is a relatively uncommon problem, it can be well treated with either an arthroscopic or an open technique. After the operation, intensive supervised physical therapy is essential. Occasionally, a repeat repair of the rotator cuff should be delayed until passive motion has been restored.
*Printed with permission of The American Academy of Orthopaedic Surgeons. This article will appear in Instructional Course Lectures, Volume 47, The American Academy of Orthopaedic Surgeons, Rosemont, Illinois, March 1998.
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