Shoulder instability constitutes a spectrum of disorders that includes laxity, subluxation, and dislocation.
Immobilization has little effect on outcome after traumatic dislocation.
The prognosis for nonoperative management of patients younger than 30 years of age after traumatic dislocation is poor.
Rehabilitation is preferred over operative management in those with atraumatic instability.
Controlling the rate at which range of motion is regained is important to adequately protect capsulolabral repairs of the shoulder from undue stress during the early and middle postoperative periods.
The term shoulder instability constitutes a spectrum of disorders that includes laxity, subluxation, and dislocation. One of the most important concepts to be understood for any joint is distinguishing between laxity and instability. All joints are constrained in certain directions by how the bones interdigitate and by the ligaments that attach bone to bone. The amount that two bones can slide or rotate upon each other depends on the position of the ligaments between the bones, their architecture, and their length. This amount of movement is the laxity of the joint and is the normal motion that is necessary for its function.
Subluxation of the glenohumeral joint occurs when partial dissociation of the humerus and glenoid occurs. Glenohumeral instability is defined as abnormal symptomatic translation of the humeral head relative to the glenoid. Historically, a definition of instability for measurement purposes has been based on three philosophies: subluxation of the joint, rotation of the joint, or strain/tension in joint structures.
The bony configuration of the proximal humerus and the glenoid contribute to stability of the shoulder joint. However, the humeral head is much larger than the glenoid, much like a golf ball on a tee turned on its side. In the absence of significant bony restraint, stability to the glenohumeral joint is provided by the articulating surfaces, capsular and ligamentous structures, and the synchronous activity of the rotator cuff, deltoid, and scapular muscle groups. The glenohumeral joint stabilizers are commonly categorized as either static or dynamic. The static stabilizers refer to bony, cartilaginous, capsular, and ligamentous structures. The dynamic stabilizers include all the musculature around the shoulder. At the extreme ranges of motion (ROMs), the capsuloligamentous structures become taut and laxity decreases. In the mid-ROMs, none of these structures are taut, and their contribution to stability therefore is limited. Instead, dynamic stabilizers and the configuration of articular surfaces, labrum, and intra-articular pressure play a role in stabilization in the midrange. The mechanisms of dynamic stabilization by the muscles are (1) the concavity compression effect, (2) the barrier effect, and (3) the passive tension effect.
Disruption to either the static or dynamic glenohumeral restraints can manifest itself in a spectrum of clinical pathologies ranging from subtle subluxation to shoulder dislocation. Classification of the pathology of shoulder instability is important to tailor an individualized treatment program for patients. A system based on four factors is commonly used: the degree of instability, the frequency of occurrence, the etiology, and the direction of the instability.
The degree of instability is proportional to the level of injury to the capsulolabral structures. Subluxation is symptomatic instability without complete dislocation of the articular surfaces. These patients may complain of pain and/or a sense of instability. In many cases, the instability is atraumatic in nature. Pain may be present because the dynamic stabilizers need to work harder when the static stabilizers are not functioning optimally. Subluxation may develop initially due to microtrauma, then progress to dislocation, or the converse may occur. Dislocation is defined as complete separation of the articular surfaces, often requiring a reduction maneuver to restore joint alignment.
The frequency of instability is described as acute or chronic. An acute episode of glenohumeral instability generally refers to the primary dislocation and in which the patient is seen in the first few hours or days of the injury. Chronic instability refers to either recurrent episodes of acute instability or dislocations that remain unreduced for prolonged periods of time.
The etiology of instability may be categorized as traumatic, atraumatic, microtraumatic, congenital, or neuromuscular. Thomas and Matsen originally introduced the acronyms TUBS and AMBRI to help us think about the etiology and treatment of most patients who have shoulder instability. TUBS describes the patient with a T raumatic dislocation, U nidirectional, associated with B ankart’s lesion, and typically responds well to S urgery. Bankart’s lesion refers to the detachment of the anterior–inferior glenohumeral ligament complex and labrum from the glenoid rim. AMBRI describes a patient with A traumatic M ultidirectional instability (MDI) that is often B ilateral and responds to R ehabilitation; rarely, I nferior capsular shift is indicated.
The direction of instability can be anterior, posterior, inferior, or any combination of these. Unidirectional instability occurs in only one of these directions. MDI may demonstrate all three directions of instability in addition to generalized ligamentous laxity. The most common (up to 98%) direction of instability is anterior.
This chapter discusses the pathologies associated with shoulder instability as well as the nonoperative rehabilitation approaches for each. In many cases, surgical management is warranted, and postoperative rehabilitation is also discussed.
Traumatic instability can result from a high-velocity uncontrolled end-range force causing a breach in the capsulolabrum–bone interface. Glenohumeral instability affects approximately 2% of the population. Of all traumatic shoulder dislocations, between 85% and 95% are anterior. Injuries occur equally between dominant (56%) and nondominant (44%) extremities. Baker and colleagues found 75% of injuries to occur during athletics in the traditionally accepted position of abduction and external rotation. Other described mechanisms of injury include elevation with external rotation, direct blows, and falls on the outstretched arm. As patients age, a higher incidence of rotator cuff tears may be seen. It is common (84%–100%) for the anteroinferior portion of the labrum to be detached from the glenoid rim (Bankart’s lesion). Bankart’s lesion disrupts the concavity–compression effect during rotator cuff contraction and decreases the depth of the socket by 50% with detachment of the capsuloligamentous structures. Some authors have suggested that Bankart’s lesion is the “essential lesion” leading to recurrent anterior instability.
Traumatic glenoid and humeral head fractures can occur with an anterior shoulder dislocation. The Hill–Sachs lesion is found on the humerus and is an impression fracture caused by the humeral head impacting the anterior glenoid. The lesion is generally located at the posterosuperior portion of the humeral head. Two types of fractures occur involving the anteroinferior glenoid: the glenoid rim fracture and the avulsion fracture. The glenoid rim fracture is secondary to compression of the anteroinferior rim by the humeral head. An avulsion of the glenoid rim may occur as a result of tension failure of the inferior glenohumeral ligament.
Various nonoperative treatments, including shoulder immobilization, activity restriction, and exercise have been advocated in the management of primary traumatic anterior shoulder dislocation. The prognosis for young patients aged 15 to 25 years is generally considered to be poor. Surgical stabilization is recommended as the treatment of choice in patients who are younger than 30 years and who are athletic. Burkhead and Rockwood conducted a prospective study of 74 shoulders in 68 patients after traumatic dislocation. Patients performed a progressive strengthening exercise program emphasizing the rotator cuff, deltoid, and scapular stabilizers. Only 16% of the patients in this group had a good or excellent result.
The length of time of immobilization in internal rotation does not have much of an effect on recurrence in first-time dislocators. Hovelius and colleagues reported the results of their landmark work, a prospective study of 255 patients (257 shoulders) with primary anterior shoulder dislocation at 2, 5, 10, and 25 years. Patients in this cohort were treated with 3 to 4 weeks of strict immobilization or immobilization in a sling until comfortable with unrestricted use of the arm. Regardless of the immobilization period, redislocation occurred in 47% of patients aged 12 to 22 years, in 34% of patients from 23 to 29 years, and in 13% of patients aged 30 to 40 years for the 2-year duration of the initial study. At the 5-year follow-up study, two or more recurrences of dislocation had occurred in 55%, 37%, and 12% of patients in each age group, respectively. These authors recently reported a 25-year follow-up of the patients in this cohort. In total, regardless of immobilization, 38% of shoulders in those patients who had been 12 to 25 years of age at the time of the original dislocation and 18% of patients who had been 26 to 40 years of age had undergone surgical stabilization. These authors also concluded that a biological predisposition and age are important factors to consider with respect to recurrence after primary dislocation of the glenohumeral joint.
Itoi and colleagues demonstrated by using MRI that Bankart’s lesion is separated from the bone with the arm in internal rotation and is apposed to the bone with the arm in 30 degrees of external rotation. An initial study revealed that patients were not comfortable with the arm in 30 degrees of external rotation. So the immobilization was modified to 10 degrees of external rotation for a clinical trial. After 3 weeks of immobilization, the external rotation group had a recurrence rate of 26%, whereas the recurrence rate for those in the internal rotation group was 42%. A limitation of this study is that the average age of the patients was older than 30 and may not be generalized to a younger athletic population.
Robinson and colleagues reported the results of a prospective cohort study of 252 patients ranging in age from 15 to 35 years old who sustained an anterior glenohumeral dislocation and were treated with sling immobilization, followed by a physical therapy program. The rehabilitation program consisted of immobilization in a sling for 4 weeks. During this time, pendulum exercises and elbow ROM exercises were permitted three times daily. After sling removal at 4 weeks, patients were referred for a physical therapy rehabilitation program consisting of active-assisted shoulder ROM with limits of 90 degrees elevation or abduction and 30 degrees of external rotation. After 6 weeks, patients were allowed unrestricted ROM except for terminal stretching. Isometric rotator cuff strengthening was performed at week 6, progressing to isotonic exercises at 12 weeks. Return to general fitness and noncontact sports was allowed at 12 weeks and return to competitive sports after 16 weeks.
Of the original cohort of 252 patients, 150 (59.5%) patients had experienced a repeat dislocation or subluxation by the end of the study period. The mean time for the development of recurrent instability was 13.3 months. On survival analysis, recurrent instability had developed in 55.7% of the cohort by the end of 2 years, and in 86.7% of all the patients known to have recurrence, the complication had developed within this time period.
The athlete who sustains a dislocation during a competitive season poses a unique clinical dilemma. Buss and colleagues reviewed 30 athletes who sustained an anterior dislocation during their sport season. They showed that a program of early ROM and a shoulder brace limiting abduction and external rotation allowed 26 athletes to return and complete the season. However, 16 of these athletes required surgical stabilization at the end of the season. Therefore, the athlete needs to be made fully aware of the risks and benefits of returning to play during the season in which he or she sustained an anterior dislocation.
Clinicians must be aware that axillary nerve injury after glenohumeral dislocation has been documented in the literature. The reported incidence of axillary nerve injury after dislocation ranges from 5% to 54%, depending on the age of the patient studied and the extent of the diagnostic workup after dislocation. Neurologic complications after shoulder dislocation occur more frequently in patients 50 years of age and older, and if the shoulder remains dislocated for longer than 12 hours, the risk of brachial plexus and axillary nerve injury increases dramatically. The mechanism of injury in glenohumeral dislocations is one of traction and compression as the axillary nerve becomes stretched across the humerus as it dislocates anteriorly and inferiorly. Patients with axillary nerve injury are rehabilitated in the same way as all patients after traumatic glenohumeral dislocation. In most cases, the injury is a neurapraxia, and deltoid function will return over the course of 2 to 4 months.
Authors’ Preferred Rehabilitation after Anterior Shoulder Dislocation
After anterior shoulder dislocation, patients are typically immobilized in a sling for comfort and support. Approximately 2 to 4 weeks after dislocation, patients begin therapy and exercises. The main goal during this phase of rehabilitation is to allow functional healing of the soft tissues surrounding the shoulder. Patients begin with hand squeezes, elbow active ROM, and pendulum exercises. Some patients may experience apprehension, muscle guarding, and/or pain when initially performing pendulums. In these cases, it is prudent to “unload” the arm by performing closed chain exercises such as dusting or a chair stretch (see Figure 88-15 ) to allow for support of the extremity while achieving the desired improvement in ROM. These exercises can be progressed to using a large exercise ball or an Upper Extremity Ranger (Rehab Innovations, Inc., Omaha, NE) ( Fig. 92-1 ). At 4 to 6 weeks after dislocation, patients may begin active assisted forward elevation with the opposite hand or stick and external rotation with the arm supported in 45 degrees of abduction. Patients are cautioned to exercise only to tolerance and to not overstretch. External rotation ROM is limited to 30 degrees. After 6 weeks, patients may begin posterior capsule stretching to include extension, internal rotation up the back, and cross-body adduction. Rotator cuff strengthening with elastic bands or dumbbells with the arm in adduction can also begin at this time. Strengthening is gradually progressed to more functional positions with abduction and forward elevation below shoulder height, as well as supported external rotation. Scapular strengthening exercises are also important and begin with scapular retraction at waist level with elastic resistance. Scapular retraction with the band fixed overhead and near the floor can be performed to recruit most of the scapular muscles. Scapular strengthening exercises can be progressed to horizontal abduction with scapular retraction at 90 degrees of elevation (backhand) and horizontal adduction also at 90 degrees of elevation (forehand), both with elastic resistance. In the later stages of rehabilitation, exercises that have demonstrated a high level of electromyographic activity can be used. Although these exercises elicit a high level of electromyographic activity in the rotator cuff, deltoid, and scapular muscles, they are also highly provocative and should be added to the program with appropriate caution. They include prone horizontal abduction with external rotation at 90 degrees and 135 degrees, standing horizontal abduction with external rotation at 90 degrees of abduction with elastic resistance, and scaption with external rotation.
Manual resistance is also very effective in this population to promote co-contraction of the rotator cuff, deltoid, and scapular muscles. Rhythmic stabilization, alternating isometrics, and short arc ROMs can all be used. Manual resistance typically begins with the arm supported and performing alternating internal and external rotation ( Fig. 92-2A ). Progression is made to unsupported alternating abduction/external rotation and adduction/internal rotation ( Fig. 92-2B ).
Plyometric training using weighted balls can be used to enhance neuromuscular control, strength, and proprioception by reproducing the physiologic stretch-shortening cycle of muscle in multiple shoulder positions. By catching and then throwing a weighted ball, the adductors/internal rotators are eccentrically loaded and elongated, followed by concentric shortening phase. Plyometric exercise creates a fast muscle contraction, simulating athletic activity. For a patient undergoing rehabilitation after an anterior shoulder dislocation, we typically start with the arm in adduction and elbow bent to 90 degrees. The patient can simply toss the ball from one hand to the other. The exercise is progressed by gradually increasing shoulder external rotation and then by increasing the abduction angle, culminating in 90 degrees of abduction ( Fig. 92-3 ). If an athlete is unable to tolerate this increased activity, he or she most likely will not be able to return to his or her sport.
To further enhance strength, dynamic control, proprioception, and endurance, we like to use the Bodyblade (Hymanson, Inc., Playa Del Ray, CA). With this fiberglass rod, patients must sustain oscillations for various time intervals. The exercise can be performed with the arm in various positions starting in nonprovocative positions at the side and working into more functional positions away from the body ( Fig. 92-4 ). Controlling the oscillation of the blade requires co-contraction of the rotator cuff, deltoid, biceps, triceps, and scapular muscles. Buteau and colleagues reported a success using the Bodyblade in a patient after traumatic anterior shoulder dislocation.
The exact incidence of atraumatic instability is unknown because the etiology is, by definition, atraumatic, and there is a broad spectrum of pathology ranging from mild pain to dislocations. Patients with atraumatic instability have increased joint volume; the joint capsule is enlarged, the glenohumeral ligament is lax and thin, or the dynamic stabilizers (rotator cuff, deltoid, scapular muscles) may be weak or uncoordinated. Some individuals may present with collagen disorders, such as Ehlers–Danlos syndrome, in which minor injuries often precede the development of instabilities. Atraumatic instability is commonly referred to as MDI. However, there is currently a wide variation in the definition of MDI of the shoulder in the literature.
MDI has been defined as instability in two or three directions. In some studies, the diagnosis of MDI was based on the examiner’s ability to subluxate the shoulder anteriorly or posteriorly, even if the patient did not have symptomatic instability in one or both of those directions. Several studies suggested that it is possible to have MDI and still have Bankart’s lesion, which is typically thought to be a sign of traumatic, unidirectional instability.
Patients with MDI typically have symptoms of instability in more than one plane of motion. Commonly, MDI results from repetitive stress on a loose or hyperlax shoulder. MDI may also be present in patients without excess laxity of the shoulder. Instability may develop in individuals who sustain multiple traumatic events or repetitive microtrauma to the shoulder.
Although most people with MDI experience involuntary subluxations and dislocations, a select and unusual group may have the ability to voluntarily subluxate or dislocate their shoulder. Some individuals may be able to voluntarily subluxate, but are asymptomatic and do not require intervention. However, the symptomatic group may subluxate for secondary gain or psychiatric reasons, and an unconscious coordinated muscle firing sequence resulting in instability appears to have developed in some individuals. Electromyographic and biofeedback studies have identified several different abnormal firing patterns involving a combination of increased activation of the anterior deltoid and pectoralis major in conjunction with decreased activation of the posterior rotator cuff and serratus anterior.
There are several characteristic findings on physical examination to aid in the diagnosis of MDI. Patients will have excessive passive ROM in several directions. In addition, they may exhibit increased laxity of other joints including hyperextension at the elbows and/or the metacarpophalangeal joints. A positive sulcus sign may be present with application of a downward traction on the humerus. It is also important to examine the position and movement of the scapulae. Many patients with MDI will exhibit scapular dyskinesia.
The most commonly recommended treatment for MDI is nonoperative, with emphasis on rehabilitation and activity modification. Functional exercises that require coordination among multiple muscle groups have been recommended for retraining normal patterns of muscle activity in the patient with shoulder instability. However, there have been few reports pertaining to exercise rehabilitation in the nonoperative management of atraumatic shoulder instability. In a prospective study of 66 patients with atraumatic instability, a strengthening exercise program emphasizing the rotator cuff, deltoid, and scapular stabilizers yielded a good or excellent result in 80% of the patients. Surgery is reserved for patients in whom an extensive course of a well-designed rehabilitation program has failed and who continue to have shoulder symptoms.
Author’s Preferred Rehabilitation of Atraumatic Instability
Patients with MDI lack stability provided by the static stabilizers of the glenohumeral joint (i.e., ligaments and capsule). Therefore, the dynamic stabilizers (i.e., rotator cuff, deltoid, scapular muscles) need to be improved and integrated to allow functional movement. The examination of a patient with MDI should include an assessment of both active and passive ROM. Excessive passive ROM is a typical finding in this patient population. However, recognize that in some cases, active ROM may be limited due to apprehension or pain. Often these patients will have much greater passive ROM than active ROM. An assessment of posture and resting position of the scapula should be made. A depressed and downwardly rotated scapula may predispose the glenohumeral joint to instability. Scapular motion during active movement in flexion and abduction should also be assessed. Scapular winging during either of these motions indicates poor scapular muscle integration, and this should be addressed during rehabilitation. See Chapter 93 for more information on assessment and management of scapular dysfunction.
In extreme cases of instability, especially inferior subluxation, patients may be apprehensive about movement. In these cases, it is important to first find positions to allow for movement and, second, to restore the patient’s confidence in moving the extremity. In a patient with inferior instability, external rotation in adduction will tighten the superior glenohumeral ligament complex and allow the patient to begin moving in functional positions with confidence. , This can be achieved with the patient in the supine position and holding a towel in both hands with the forearms in supination. The patient is asked to pull the towel taught and then raise his or her arms overhead. Gravity can be gradually added by increasing the angle of the table or adding pillows under the patient’s head. Eventually the patient will be able to perform this activity in the erect position. Additional strategies to achieve functional movement include using the Upper Extremity Ranger at waist level (see Fig. 92-1 ) or an exercise ball. These exercises allow support for the extremity while reeducating the patient on functional movement patterns and progression to overhead activities.
Rotator cuff strengthening should begin in nonprovocative positions beginning with the arm at the side and gradually working into more provocative and functional positions of abduction and elevation. Resistance can be supplied by an elastic band and performed standing or with a dumbbell and performed in a side-lying position for internal and external rotation. At this stage, we also include scapular retraction exercises with elastic resistance at waist level to engage the scapular muscles. Once sufficient strength is achieved with the arm at the side, exercises are progressed away from the body including abduction and forward elevation to 45 degrees and external rotation supported at 45 degrees of elevation in the plane of the scapula.
Inman and colleagues proposed a theory of subjecting the shoulder to certain motions and positions promoting instability during treatment to elicit a reflexive muscular protective response during unstable events. Manual resistance is extremely effective in this patient population to help reestablish strength and proprioception. Rhythmic stabilization, alternating isometrics, and short arc ROMs can all be used. Manual resistance typically begins with the arm supported and performing alternating internal and external rotation (see Fig. 92-2A ). Progression is made to unsupported alternating abduction/external rotation and adduction/internal rotation (see Fig. 92-2B ). Rhythmic stabilization at a variety of glenohumeral angles, progressing from known to random patterns, from resistance applied proximal to distal to the glenohumeral joint, and from submaximal to maximal efforts, can be used to promote joint stability in functional positions.
Exercises are progressed to backhand and forehand movements at 90 degrees of elevation with elastic resistance. A useful functional exercise is horizontal abduction with external rotation at 90 degrees of elevation, which helps to integrate the rotator cuff, deltoid, and scapular muscles. To further enhance dynamic control and stability, plyometric training with weighted balls and the Bodyblade can be used in the same way as discussed for rehabilitation after traumatic dislocation. Individuals can gradually move into sport-specific activities with the eventual goal of full participation.
Superior Labral Anterior–Posterior (SLAP) Lesions
A symptomatic tear of the superior labrum at the origin of the biceps tendon has been established as a pathologic entity. Andrews and colleagues originally described detachment of the superior labrum in 73 throwing athletes with no history of a single episode of significant trauma and a mean age of 23 years. Snyder and colleagues later attached the acronym SLAP to these findings, indicating an injury in the superior labrum and extending anterior to posterior. In a later series, 140 injuries of the superior labrum represented 6% of shoulder procedures performed over an 8-year period. The average patient age was 38 years and 91% were men. The most common problem was pain, with 49% of all patients noting mechanical catching or grinding in their shoulders. The most common mechanism of injury (31%) was a fall or direct blow to the shoulder. The remainder arose from an episode of subluxation or dislocation (19%), pain when lifting a heavy object (16%), insidious onset of pain (14%), overhead racquet sports (6%), pain while throwing (6%), and no mechanism reported (8%). Repetitive overhead activity has also been hypothesized as a common mechanism for producing SLAP lesions. Andrews and colleagues first theorized that SLAP lesions in overhead throwing athletes was the result of the high eccentric activity of the biceps muscle, creating tension on the long head of the biceps tendon during the arm deceleration and follow-through phases of throwing.
Burkhart and colleagues hypothesized that a peel-back mechanism may produce a SLAP lesion in the overhead athlete. They believe that when the shoulder is placed in a position of abduction and maximal external rotation, the rotation causes a torsional force at the base of the biceps. Pradhan and colleagues reported increased superior labrum strain during the late cocking phase of throwing in a cadaveric study. Other authors have also demonstrated contact between the posterosuperior labrum and the rotator cuff when the arm is in an abducted and externally rotated position, which stimulates the late cocking phase of throwing.
SLAP lesions have been classified into four distinct categories based on the labral injury and the stability of the labrum–biceps complex found at arthroscopy. Subsequent authors added classification categories and specific subtypes. Type I lesions denote fraying and degeneration of the superior labrum with a normal biceps tendon anchor. Type II lesions may have fraying of the superior labrum, but their hallmark is a pathologic detachment of the labrum and biceps anchor from the superior glenoid. In type III SLAP lesions, the superior labrum has a vertical tear analogous to a bucket-handle tear in the meniscus of the knee. The remaining rim of labral tissue is well anchored to the glenoid, and the biceps anchor is intact. A type IV pattern involves a vertical tear of the superior labrum, but this superior labral tear extends to a variable amount up into the biceps tendon as well. The torn biceps tendon tends to displace with the labral flap into the joint, whereas the biceps anchor itself remains firmly attached to the superior glenoid. Last, a complex of two or more SLAP lesions may occur, with the most common presentation being types II and IV.
Several special tests have been described to help determine the presence of labral pathology, including the active compression test, the anterior slide test, the biceps load test, the clunk test, the crank test, the grind test, and the pain provocation test. However, it appears that each of these tests has limited diagnostic accuracy, and no single test is sensitive or specific enough to determine the presence of a SLAP lesion accurately. In addition, the studies that exist on their accuracy do not distinguish the type of SLAP lesion. Furthermore, many patients with SLAP lesions present with concomitant pathology, making diagnosis difficult. Therefore, it is important for the clinician to pay close attention to the mechanism of injury and the patient’s specific symptoms to make the diagnosis of a SLAP lesion.
Despite significant progress in shoulder diagnostic techniques, such as MRI or high-resolution ultrasound, imaging for disorders of the superior labrum is difficult and nonspecific. Although the long head of the biceps tendon and superior labrum can at times be well visualized by some of these methods, any finding must be strictly placed in the context of a history and physical examination. Magnetic resonance arthrography has been advocated to detect SLAP lesions and is currently the preferred imaging method to detect SLAP lesions.
Nonoperative management of SLAP lesions is often unsuccessful, particularly when there is a component of glenohumeral joint instability or when a concomitant rotator cuff tear is present. However, there is a subset of patients with lower demands, those older than 30 years of age, and those with type I lesions who may respond positively to nonoperative management. Patients typically present with pain brought on by their work or sport activity, reaching overhead, or reaching up the back. Clinical presentation includes decreased internal rotation and/or cross-body adduction ROM, rotator cuff strength, and altered scapular mechanics.
The initial phase of nonoperative management consists of rest from the pain-producing activity and anti-inflammatory medication. During this phase, we also begin stretching of the posterior capsule within the patient’s pain tolerance. These exercises include cross-body adduction and internal rotation up the back with either the opposite hand or a towel. These stretches are generally very effective at improving posterior capsule flexibility. Occasionally patients require a more aggressive stretch, and so the sleeper stretch is added (see Fig. 88-10 ). This stretch can be performed in a side-lying or standing position with the arm against a wall. The stretch can be extremely provocative, so patients must be cautioned to stretch to tolerance and not pain.
Once the pain begins to subside and ROM improves, we begin rotator cuff and scapular muscle strengthening as described earlier in this chapter. The same principle of starting with nonprovocative positions and working into more functional positions applies to the rehabilitation of patients with SLAP lesions. The exercise program is eventually progressed to include trunk, core, and kinetic chain exercises. We have found that many recreational athletes can return to their previous activity level by continuing a home program and with the knowledge that they may occasionally experience discomfort during or after activity.
Postoperative Rehabilitation of Capsulolabral Repair of the Shoulder
Optimal postoperative rehabilitation after capsulolabral repair of the shoulder requires the understanding and application of guiding rehabilitation principles while using guidelines that are specific to the surgical procedure performed and further individualized based on each patient’s unique pathology, comorbidities, and specific functional demands.
Specific patient variables such as their direction of instability, amount of natural laxity, severity of instability, comorbidities, and specific functional goals all affect postoperative rehabilitation. Postoperatively these factors influence rehabilitation by allowing a slightly quicker rehabilitation in patients with less severe pathology and fewer comorbidities. In patients with more severe pathology and more co-morbidities, a slightly slower and more gentle progression of rehabilitation is required.
Guiding Rehabilitation Principles
Success during rehabilitation after any orthopedic surgical procedure is dependent on the appropriate application of stress to the repaired structures. Initially minimal stress is required for beginning healing, followed by a progressive gradual increase in stress over several months to the surgical repair to protect it while the repair matures. Four principles are of critical importance for the rehabilitation professional to understand and successfully apply to be able to manipulate stress and facilitate healing in capsulolabral repairs of the shoulder and promote a safe return to function. Successful rehabilitation requires (1) a basic understanding of the surgical procedure; (2) an understanding of the anatomic structures that must be protected, how they are stressed, and the rate at which they heal; (3) the identification and skilled application of the methods used during rehabilitation to manipulate stress to the surgical repair; and (4) identifying the appropriate length of immobilization and rate of return to full ROM. These four principles form the foundation of the rationale for the specific rehabilitation guidelines, which are divided into three phases based on time since surgery (weeks 0–6, 6–12, and 12–24).
Guiding Principle I: Understanding the Surgical Procedure
Because each surgical repair is unique and affects rehabilitation, communication with the surgeon is important to become fully aware of the specifics of the surgical procedure and its impact on rehabilitation. Surgical management of symptomatic shoulder instability first involves a thorough examination of the glenohumeral joint at the time of operation with an assessment of the pathologic structures; then a game plan is developed for the instability repair. In patients with acute and recurrent instability of the shoulder, certain injury patterns are commonly seen involving the glenoid–capsulolabrum complex as well as partial articular surface rotator cuff tears of the supraspinatus, infraspinatus, and/or the subscapularis tendons and articular cartilage injuries of the humeral head and glenoid. Glenohumeral instability repair most commonly involves the glenoid labrum, glenohumeral joint capsule, and/or the glenohumeral ligaments. Repair of these structures has been traditionally performed by open surgical procedures; however, over the past few years, arthroscopic repair has shown nearly equivalent results and is now rapidly becoming the new standard of care in the surgical management of shoulder instability. Both arthroscopic and open anterior capsulolabral repair seek to address anterior shoulder instability by repairing an unstable anterior inferior labrum (Bankart’s lesion), if present, back to the glenoid through the use of sutures or suture anchors followed by a capsular plication where the capsule is folded onto itself and/or stabilized to the labrum to further take up redundancy in the glenohumeral joint capsule. These procedures are detailed in Chapter 91 .
Guiding Principle II: Understanding the Structures That Require Protection During Rehabilitation, How They Are Stressed, and the Rate at Which They Heal
Arthroscopic capsulolabral repair involves a direct repair and retensioning of damaged capsular and possibly labral structures. The repaired tissue needs protection from undue stress for an extended period of time to facilitate appropriate tissue healing. It is well documented that specific portions of the capsule and labrum are selectively tensioned with specific glenohumeral motions. A standard anterior capsulolabral repair, addressing laxity of the anterior–inferior capsule, is most directly stressed by external rotation at all angles of abduction but particularly with the arm abducted to 90 degrees. If the repair is performed arthroscopically, the rotator cuff is not significantly disturbed and therefore does not need specific protection during rehabilitation. However, if an open procedure is performed in which the subscapularis is taken down, the suture line needs extensive protection from active and passive ROM during the first 6 postoperative weeks.
Once the specifics of the capsulolabral repair are known, rehabilitation must only include activities that produce less stress to the healing tissues than the failure strength of the repair. The challenge for the rehabilitation professional is that the clinically detectable measures of tissue healing (e.g., pain, warmth, swelling) are rather crude. To compound the situation, the stresses imparted by many rehabilitation activities remain unknown. An additional challenge is posed because patients generally return to demanding functional activities before the repaired capsulolabral structures return to normal structural strength. Variations in the healing of the capsule, ligaments, and labrum as a result of factors such as health status, tissue quality, and extent of the injury must be carefully considered. Ligament healing times are often derived from animal research with few histologic studies in humans to guide progression of exercise after ligament injury. Ligament healing is traditionally thought to pass through inflammatory, proliferative, and remodeling/maturation phases.
We divided the rehabilitation process into three phases, each of a 6-week duration, because we believe that there are clinical milestones that occur at these times and these divisions partially reflect the three phases of tissue healing. The first 6 weeks postoperatively include the inflammation and the proliferative phases and the beginning of the remodeling phase. Remodeling and final maturation of the tissue continues throughout the remainder of the formal rehabilitation process and may not be complete until 40 to 50 weeks after surgery. Understanding the sequence of the healing process and the effects age and co-morbidities have on the process is paramount for the proper application of these guidelines.
Guiding Principle III: Identification and Skilled Application of Methods Used During Rehabilitation to Manipulate Stress to the Surgical Repair
Perhaps the single most important rehabilitation concept after arthroscopic anterior capsulolabral repair is that the healing capsulolabral structures must receive a gradual, measured, and therefore well-planned increase in stress. Each appropriate increase in stress is a stimulus for further proliferation and differentiation of fibroblasts. In a process analogous to Wolff’s law of bone healing, the result is enhanced structural integrity of the capsulolabral complex as additional collagen fibers are laid down in response to controlled stresses. However, it is equally important to understand that if stress is applied inappropriately to the capsulolabral complex (during rehabilitation or activities of daily living), in terms of either magnitude or timing, the tissues are unable to adequately adapt, and damage either to the healing tissue or stabilizing material (sutures, anchors) is the result. During rehabilitation, three mechanisms allow rehabilitation providers to manipulate stress to the surgical repair to positively affect patient outcome: (1) absolute ROM, (2) submaximal cyclic loading, and (3) dynamic stabilization.
Initially the structural integrity of the repair is based solely on the surgical fixation. As time passes, the labrum begins to “heal” to the glenoid rim in the case of repair of Bankart’s lesion or plicated layers of the capsule begin to bind to one another in the case of a capsular plication or suture capsulorrhaphy. Excessive stretching during ROM activities may overload the structural integrity of these gradually healing tissues. Additionally, much in the same way as micromotion may prevent bony union during fracture healing, submaximal cyclic loading also has the potential to disrupt the tenuous bond between soft tissue layers. Repeated submaximal stress of ligament plication in an animal model has been shown to negatively affect mechanical resistance properties, even as late as postoperative week 12. Although it is unknown what effect the cyclic loading of rehabilitation interventions such as ROM and progressive functional activities have on the capsulolabral repairs, the rehabilitation provider should keep in mind that repeated submaximal tensioning of the repair during the remodeling phases of tissue healing may slowly stretch out the repair. Therefore, even though they are below the failure strength of the capsulolabral construct, repetitive submaximal stresses should be carefully controlled as they pose a potential threat to capsuloligamentous integrity. On the other hand, dynamic stabilization or active stabilization of a joint by the muscles directly surrounding it provides protection to the surgical repair by supporting the joint capsule, increasing joint compression forces, and resisting joint displacement. It is vital to understand that these three mechanisms (absolute ROM, submaximal cyclic loading, and dynamic stabilization) do not exist in isolation but are interrelated in all rehabilitation activities and should be a primary consideration when selecting interventions during rehabilitation of the patient after capsulolabral repair.
Guiding Principle IV: Identifying the Appropriate Length of Immobilization and Rate of Return to Full ROM
Strength of the arthroscopic anterior capsulolabral repair is thought to still be fairly weak during at least the first 12 postoperative weeks, and more general reviews of ligamentous healing indicate that remodeling may continue through 40 to 50 weeks postoperatively. Therefore, controlling the rate at which ROM is regained is vitally important to adequately protect the surgical repair from undue stress during the early and middle postoperative period (about 12 weeks). Gaining ROM too slowly may result in residual stiffness, whereas gaining ROM too quickly may result in recurrent laxity. Unlike open repairs of Bankart’s lesions and open capsular shifts, which use immediate staged ROM because some long-term ROM loss is not unexpected, the more common problem with arthroscopic capsulolabral repairs of the shoulder is regaining ROM too quickly. Therefore, immobilization and staged ROM goals after arthroscopic anterior capsulolabral repair have historically been used during the initial postoperative period to allow healing between adjacent tissue layers.
Strict immobilization (no glenohumeral ROM exercises and constant sling use) after arthroscopic instability repair of the shoulder began during the infancy of these procedures when failure rates were high and surgical procedures were rapidly evolving. Current surgical methods typically use sutures and suture anchors to stabilize the labrum and to plicate the capsule, thus retensioning the capsule and glenohumeral ligaments. Several studies demonstrated that using immediate staged ROM with these surgical techniques yields a very low recurrence rate and a quicker return to function compared with a 3-week period of immobilization. Because of these studies, a range of 0 to 4 weeks of immobilization is recommended during rehabilitation after arthroscopic capsulolabral repair using sutures or suture anchors. We believe that evidence demonstrates that no immobilization is a safe alternative to a short period of immobilization, does not increase the failure rate, and still allows protection of repaired tissues through the staging of ROM goals. We believe that both methods result in little to no long-term ROM loss and that both methods produce excellent functional results.
Controlling the rate of ROM gains is vitally important regardless of whether strict immobilization is used or not because the stability of the surgical repair is thought to be negatively affected by the patient gaining ROM too quickly anytime during the first 2 to 3 months after surgery. Controlling the speed of ROM gains can be accomplished through the use of staged ROM goals. Staged ROM goals can be determined in at least two ways. The surgeon may have a preference based on factors such as the patient’s specific injury and pathology, co-morbidities, amount of natural laxity, surgical history, specific surgical technique (including type of fixation and arm position at the time of capsular plication), and their general philosophy. We offer a staged ROM table ( Table 92-1 ) as a general guideline for instances in which the surgeon has no preference. When using a ROM table, the goal is to have the patient comfortably obtain ROM to the specified angle. In some instances, little to no stretching is needed to achieve these staged ROM goals, and in some instances, regular gentle stretching is needed to achieve the staged ROM goals.