Glenohumeral instability encompasses both dislocation and subluxation events, and instability events commonly affect the general population. Approximately 1% to 2% of the general population will experience a glenohumeral dislocation in their lifetime. The young, active, athletic population is particularly susceptible to shoulder instability events. Over 95% of shoulder instability events occur in the anterior direction.
Over the last few decades, the knowledge regarding the risk factors, diagnosis, nonoperative and surgical management, and rehabilitation principles has continued to improve, permitting clinicians to provide optimal management of shoulder instability patients. A comprehensive history, clinical exam, diagnostic imaging studies, and accurate characterization of each patient’s instability pattern will help enable healthcare providers to properly treat and manage each patient appropriately.
Historically, clinicians used the acronyms TUBS and AMBRI to classify shoulder instability into two broad, etiologic categories:
However, while these acronyms were traditionally helpful to aid providers in the identification and treatment of patients presenting with acute or recurrent instability, these categories do not help the clinician differentiate instability from soft tissue hyperlaxity. As our knowledge regarding the etiology and underlying pathophysiology at clinical presentation evolved over the last few decades, clinicians began to recognize the need to differentiate possible complex shoulder instability patterns that can present in the setting of recurrent and repetitive microtrauma (often low-energy) from acute macrotrauma (often high-energy). Thus, it is more helpful to classify based on
There are few reports in the literature regarding the estimated incidence rate of shoulder dislocations among the general population. The general consensus in the literature cites an incidence rate of traumatic unidirectional dislocations ranging from 1% to 2% in the general population.
One study from the 1980s reported that over a 10-year period the adjusted incidence of initial traumatic shoulder dislocations was 8.2 per 100000 person-years. The incidence rate seen in males was greater than that seen in females. A subsequent study from the 1980s reported that in Denmark the incidence rate of shoulder dislocations was about 17 dislocations per 100000 person-years. A 1995 study from Sweden reported an incidence of 24 dislocations per 100000 person-years. A population-based cohort study of nearly 17000 patients in the United Kingdom investigated over 20 years (1995 to 2015) found:
A 2013 study out of Ontario, Canada similarly found that young male patients had the highest incidence of shoulder dislocation events, in addition to the highest risk of recurrent dislocation events.
A 2010 study reported from United States census data analyzed the epidemiologic trends for emergency department presentations secondary to shoulder dislocations from 2002 through 2006. The authors noted an overall incidence rate of 23.9 per 100000 person-years, with the male incidence rate being about 2.6-fold that of the female incidence rate.
Athletic population considerations
The young athletic population has garnered significant attention in the literature secondary to the multitude of risk factors predisposing these patients to primary and recurrent dislocation events.
A 2007 study by Owens et al. prospectively collected all traumatic shoulder instability events at the United States Military Academy over a 12-month period. The study followed over 4000 students during this period, and the authors found that the probability of a student sustaining at least one shoulder instability event during the academic year to be 2.8%. The study encompassed subluxation and dislocation events. Other pertinent findings included:
A 2014 study reported the prevalence of shoulder dislocation during one season of rugby was about 15%. The authors noted that in rugby players entering the current season with a history of a previous shoulder dislocation managed non-operatively. In this subset of athletes, about 55% sustained a shoulder dislocation during the season. Other collision sports such as football have demonstrated incidence rates up to 0.51 per 1,000 athlete-exposures.
A 2018 epidemiologic study comparing high school and collegiate athletes across nine different sports demonstrated that collegiate athletes are at higher risk of shoulder dislocation compared to their high school counterparts. The overall incidence rate was 2.04 per 100000 athlete-exposures; an exposure defined as one athlete participating in one practice or game/competition.
Multicenter Orthopaedic Outcomes Network (MOON)
The MOON instability cohort published a 2018 study reporting the descriptive epidemiology of patients undergoing shoulder stabilization procedures across a multicenter consortium:
Adolescent and pediatric patient considerations
A recent Level II prognostic cohort study reported results from approximately 2,000 adolescent and pediatric patients ages 10 to 16 years presenting to an emergency department and required closed shoulder reduction. Results showed that the incidence of dislocation was highest among males aged 16 years (164.4 episodes per 100000 person-years), while the incidence was lowest among patients aged 10 to 12 years. Moreover, the re-dislocation rate was highest in 14 to 16-year-old patients (37% to 42% re-dislocation rate) and the lowest re-dislocation rates (0% to 25%) were in patients aged 10 to 13 years old.
The glenohumeral joint is a complex, mobile, multiaxial, ball-and-socket articulation that allows coordinated motion in the frontal, transverse, and sagittal planes. The latter allows for 360 degrees of circumduction. The relatively shallow glenoid fossa articulates with the much larger humeral head to allow for a wide range of physiologic motion. In addition, the joint capsule is relatively lax. Shoulder movements occur secondary to the dynamic and coordinated articulations at four distinct joints:
Static and dynamic stabilizers
The static stabilizers include the glenohumeral articulation, the labrum, the glenohumeral ligaments, rotator cuff interval structures, and the negative intra-articular pressure. The dynamic stabilizers consist of the rotator cuff muscles, the deltoid, and the scapular and periscapular stabilizers.
Shoulder instability cascade
The pathophysiology and pathologic cascade for shoulder instability acute episodes, recurrence, and long-term implications. There is significant variability in the amount of shoulder translation in asymptomatic, normal subjects. However, shoulder instability is a pathologic process that results in an excessive translation of the humeral head on the glenoid that ultimately results in pain, weakness, and shoulder dysfunction.
There have been several anatomic risk factors that have been identified as potential contributors to developing shoulder instability. For example, increasing degrees of glenoid version away from neutral in addition to an inferior inclination of the glenoid vault is associated with anterior shoulder instability.
To accurately diagnose and classify shoulder instability, it is critical to distinguish joint laxity from true instability. The latter characteristically demonstrates the presence of symptoms in association with abnormal laxity. The pathologic soft tissue laxity can be present either from repetitive microtrauma, high-energy acute trauma (e.g., traumatic dislocations), or it can be present congenitally. Shoulder instability implies some degree of disruption to the static and/or dynamic stabilizers of the glenohumeral joint, including the osseous structures, capsule, labrum, and glenohumeral ligaments. In regards to the latter, the anterior and posterior bands of the inferior glenohumeral ligament (IGHL) are the most critical ligamentous structures in the maintenance of shoulder stability.
Unidirectional instability can present following acute trauma or following one or multiple low-energy instability events. The latter may be present in the setting of unidirectional instability with or without hyperlaxity. When there is associated soft tissue hyperlaxity, an accompanying capsulolabral lesion is less likely. In effect, the unidirectional instability is often attributable to the patulous capsular tissue that predisposes the shoulder to recurrent instability events. However, the same unidirectional instability scenario in a patient without soft tissue hyperlaxity most commonly will present with an associated capsulolabral injury.
Following a traumatic, primary shoulder dislocation, there are a significant number of patients that will demonstrate at least a mild degree of either chondral or osteochondral lesions. Bony defects can be on the humeral side, glenoid side, or a combination of both. It has been previously established that bony defects on either side can significantly contribute to the risk of recurrent instability events.
Humeral sided defects
The Hill-Sachs lesion is an impaction injury to the posterosuperolateral humeral head that occurs in association with anterior instability events. Described in 1940 by Hill and Sachs, the authors highlighted the so-called line of condensation that was apparent on the posterosuperolateral humeral head and best viewed on the internal rotation shoulder radiograph. The Hill-Sachs lesion occurs when the humeral head dislocates anterioinferiorly, and the aforementioned area of the humeral head abuts the anterior glenoid rim and upon impact creates a compression fracture on the humeral head. The true incidence of Hill-Sachs lesions remains elusive although studies have cited its association with anterior shoulder instability events to range from 40% to almost 100% of cases, with the highest rates seen in cases of recurrent anterior instability.
The impact of recurrent instability on the Hill-Sachs lesion becomes problematic as the abnormal anterior soft tissue laxity predisposes the Hill-Sachs lesion to repeatedly abut against the harder cortical bone at the anterior glenoid. In addition, Hill-Sachs lesions can be engaging or non-engaging. Engaging lesions have been previously described by Palmer and Widén, and later by Burkhart and De Beer. These occur when the Hill-Sachs lesion’s long axis is parallel to the long axis of the anterior glenoid rim, causing the lesion to engage with the rim during defect engages the rim of the glenoid while the shoulder is in any combination of positions. The authors previously described the athletic position of the shoulder (i.e., 90 degrees of abduction and from 0 to 135 degrees of external rotation). A non-engaging lesion will not engage with the anterior glenoid rim when the shoulder is in an abducted and externally rotated position. The analogous lesion seen in association with posterior shoulder instability is a humeral head defect located at the anterosuperomedial region and is referred to as the reverse Hill-Sachs lesion.
Glenoid sided defects
The prevalence of glenoid bone loss is also not consistently reported in the literature although most authors agree that in the setting of recurrent instability there will inevitably be some degree of glenoid bone loss. Some studies have cited up to 22% of patients will present with some degree of glenoid deficiency after an initial dislocation event, increasing to 25% to 90% of patients presenting with recurrent instability, and in 90% of patients presenting status post failed primary stabilization procedures.
The nature of glenoid defects is best appreciated on three-dimensional CT scans, having the ability to differentiate between a true bony Bankart lesion from the more erosive changes that can be seen representing an attritional bone loss state. The former is considered a true fractured fragment containing a portion of the anterior glenoid rim. The latter often appears rounded off with blunted edges on imaging, indicative of a more chronic, erosive process secondary to recurrent instability or, in the acute setting, a low-energy compression fracture. The description of the location of these defects often references relative to a clock face created by drawing a circle around the glenoid. Saito et al. reported that the most common location of glenoid defects in the setting of anterior instability to be between 2:30 and 4:20.
The pathologic mechanism of glenoid bone defects is likely multifactorial. In general, blunted osseous glenoid defects can present in the setting of either:
Chronic attritional glenoid erosive changes can develop over time following a high-energy, index dislocation event that suffers an accompanying glenoid injury initially. The injury is either managed nonoperatively or ultimately fails surgical fixation to ultimately result in subsequent instability events with progressive attritional glenoid erosion over time.
Glenoid rim fractures and acute avulsion injuries often result secondary to high-energy impact collisions. Moreover, traumatic dislocations yielding associated glenoid injuries can produce large, anterior glenoid rim fracture fragment(s), or smaller glenoid rim avulsion injuries. Burkhart and De Beer advocated that presence of an acute glenoid rim fracture suggests a significant axial load impacted the glenoid rim at the time of dislocation. The authors compared shoulder dislocation events seen in South African rugby players compared to American football players. The former had about a 10% incidence rate of associated glenoid rim fractures, while American football players in this particular study had a 0% association rate of glenoid rim fractures. The authors speculated that the discrepancy was attributable to the fact that during rugby, a greater axial load force of impact is transmitted through the glenoid from the humerus to generate the characteristic anterior glenoid rim fracture. In contrast, the shoulder dislocation mechanism seen during football is more rotational in nature, resulting in a relatively smaller anterior glenoid rim avulsion injury as the inferior glenohumeral ligament pulls the fragment off during the anterior dislocation.
Since the initial description of multidirectional shoulder instability (MDI), our knowledge regarding the pathologic findings and objective criteria for diagnosing MDI remain debated. Part of the clinical ambiguity is attributable to the lack of a precise definition for MDI. Neer and Foster initially described MDI as anterior and posterior instability associated with involuntary inferior subluxation or dislocation. Other authors have defined MDI as instability in at least two to three directions. The estimated prevalence of MDI also remains elusive given the previously mentioned ambiguity.
The same principles applied earlier for unidirectional shoulder instability classifications are also applicable to the MDI setting. Anterior and posterior capsulolabral injuries will often accompany MDI without soft tissue hyperlaxity. MDI patients with soft tissue hyperlaxity will often present with instability in two or more directions and display signs of generalized hyperlaxity on physical exam. Patients more commonly report relatively frequent, recurrent low-energy subluxation events.
Altered shoulder girdle biomechanics
Glenoid bone loss decreases the available articular arc and generates glenoid-humeral mismatch. The former generates a smaller articular arc length and decreased surface area by which the glenoid cavity can resist transmitted axial forces from the proximal humerus. Thus, failing to address glenoid bone loss even at the time of surgical fixation will result in significant shear forces imparted to a repaired capsulolabral interface.
Alterations in the static and dynamic scapular movements present in the setting of glenohumeral instability. Scapular dyskinesia is reportedly present in up to 80% of instability patients. Biomechanical studies analyzing the at-risk scapular posturing leading to pathologic anterior tensile loads and shear forces include excessive:
In addition, scapular dyskinesia predisposing to anterior shoulder instability also includes decreased upward rotation of the scapula during scapulothoracic movements. The end-result of altered scapular posturing yields excessive tensile loads and shear forces experienced by the anterior band of the inferior glenohumeral ligament (aIGHL).
Recurrent instability can develop in the setting of any of the above mentioned underlying pathophysiologic mechanisms. Furthermore, recurrent instability can present following nonoperative and operative management. Several studies have indicated that almost 90% of contact athletes and up to two-thirds of non-contact athletes with significant glenoid bone loss ultimately fail surgical stabilization secondary to associated Bankart lesion or abnormal glenoid morphology affecting overall glenohumeral joint biomechanics.
In 1982, Neer first described a subset of patients with a history of shoulder instability events (or required surgical stabilization procedures) that developed glenohumeral arthritis at long-term follow-up. The condition was officially termed dislocation arthropathy, and in 1983 Samilson and Prieto reported that these arthritic changes could follow even a single dislocation event. Although the role of recurrent dislocations is unclear, the pathophysiology underlying the development of dislocation arthropathy is likely related to acute changes that occur during a primary traumatic instability event, followed by long-term arthritic predisposition secondary to altered glenohumeral joint biomechanics and progressive, attritional, erosive osseous changes that occur secondary to the recurrent instability events.
By definition, dislocation arthropathy describes degenerative changes of the shoulder joint. Hovelius and Rahme conducted a prospective study of 257 primary anterior shoulder dislocations in 255 patients. At 25-year follow-up, 27% had mild glenohumeral arthritis, and 34% had moderate to severe arthrosis. Although the role of recurrent dislocations is unclear, the pathophysiology underlying the development of dislocation arthropathy may be related to acute changes during the primary or recurrent traumatic instability events, the ensuing altered glenohumeral joint biomechanics, and/or attritional changes that occur secondary to the recurrent instability.
Various histologic studies have investigated the proprioceptive characteristics of the soft tissue elements of the glenohumeral joint. Ruffini corpuscles and Pacini corpuscles are distributed throughout the capsuloligamentous complex. The afferent endings are susceptible to injury during instability events, resulting in delayed delivery of proprioceptive signaling that subsequently results in delayed signal transmission and delayed and/or dysfunctional muscle responses, thereby compromising both the static and dynamic soft tissue stabilizing elements supporting the glenohumeral joint. Histopathologic studies comparing biopsied static stabilizing elements during intraoperative arthroscopy were analyzed and compared to macroscopic degree/grade of injury noted during surgery. The authors reported limited variations in cell density, matrix swelling, and collagen fiber disruptions.
Clinicians evaluating patients with either acute or chronic shoulder instability should obtain a comprehensive history. Providers should document any detailed elements regarding the index injury for both first time versus chronic presentation dislocators. In addition, other elements often include the following:
A thorough history also includes sports participation and position(s) (if applicable occupational history and current status of employment, hand dominance, any history of injury/trauma to the shoulder(s) and/or neck, and any relevant surgical history.
C-spine / neck exam
Co-existing cervical radiculopathy should be ruled out in any situation where neck and/or shoulder pathology is in consideration. Observation of neck posturing, muscular symmetry, palpable tenderness, and active/passive ROM should undergo evaluation. Special tests that are helpful in this regard include the Spurling maneuver, myelopathic testing, reflex testing, and a comprehensive neurovascular exam.
Examiners should observe and compare bilateral shoulder girdles for any notable asymmetry, scapular posturing, and muscle bulk comparison or any atrophic changes. The skin should be observed for the presence of any previous surgical incisions, lacerations, scars, erythema, or induration.
Chronic instability patients will almost always exhibit at least a mild degree of asymmetry. The deltoid muscle often demonstrates atrophy in chronic dislocators. The findings can be rather subtle, especially in obese patients.
In the setting of chronic anterior instability, the clinician may be able to appreciate a palpable anterior fullness. Upon observation, the posterior shoulder (when viewed from the side of the patient) will be relatively flat relative to the anterior fullness. Chronic anterior and posterior instability patients may also exhibit corresponding posterior and anterior acromial prominences, respectively.
Scapulothoracic motion and scapular winging should also be evaluated during active and passive motion.
After the observational component of the physical examination, the active and passive ROM is documented. This exam finding may be limited in the setting of initial follow-up in the clinic after an acute instability event, or the setting of any complex instability case, especially in cases of glenoid bone loss.
In the setting of chronic anterior instability, the clinician should attempt to assess the current status of the axillary nerve, although chronic dislocators often exhibit excellent deltoid function as well as internal and external rotator strength. Specific testing of the supraspinatus muscle can be difficult when passive ROM is limited. Any evidence of significant muscular weakness may hint at an underlying associated neurologic deficit.
The clinician should perform a detailed sensory examination in all acute and chronic instability patients. In addition to axillary nerve function, motor function of the elbow, wrist, and hand should undergo an assessment to rule out the possibility of a brachial plexus injury associated with the dislocation. Distal pulses should be assessed at the wrist as well.
Older patients and in the setting of suspected concomitant shoulder pathologies (e.g., rotator cuff injuries or biceps tendon pathology), specialized testing for these pathologies should also be a consideration.
Provocative examination testing/maneuvers:
Shoulder instability considerations
Global tissue laxity should undergo assessment by examining glenohumeral translation and hypermobility at the shoulder joints and other joints in the body if applicable. Hyperlaxity at other joints (e.g., elbow and knee hyperextension) may aid in the clinical diagnosis of underlying MDI-related diagnoses or connective tissue disorders.
Anterior apprehension test:
The anterior apprehension test is performed by lying the patient supine on the examination table. The examiner positions the shoulder to 90 degrees of abduction and 90 degrees of external rotation while applying an anteriorly-directed force to the proximal humerus. The test is positive if it reproduces the symptoms of anterior instability.
Apprehension at lower degrees of abduction may suggest glenoid bone loss. Patients may guard the shoulder during the examination, but in most circumstances, the provider can determine if the apprehensive position is reproducible the patient’s feelings of anterior shoulder instability.
Jobe relocation test:
The Jobe relocation test is utilized with the previous apprehensive testing maneuver. Once the patient reports a subjective feeling of reproduction of the shoulder instability symptoms, the examiner applies a posteriorly directed force while keeping the shoulder in the same apprehensive position. Resolution or improvement of symptoms indicates a positive test result.
The examiner uses one hand to apply an axial load through the elbow to center the humeral head within the glenoid. An anterior and posterior directed force is then applied at 0-, 45-, and 90-degrees of shoulder abduction. Increased translation at increasing degrees of shoulder abduction implies compromise of the IGHL.
Grading of the magnitude of humeral head translation is as follows:
The load-and-shift test is up to 98% specific, but it has poor sensitivity for detection of unidirectional and multidirectional instability.
Other exam considerations
The shoulder also should be examined for associated posterior instability as well as multidirectional instability. In every patient undergoing surgery, examination under anesthesia should take place and the results compared with those of the uninjured contralateral side.
Depending on patient age, the clinician may expect various degrees of associated shoulder pathologies. For example, older patients presenting with acute shoulder instability are susceptible to associated rotator cuff injuries. Pain with weakness against resisted abduction or external rotation may suggest the presence of associated rotator cuff injuries. For example, patients with anterior shoulder instability in end-range positions demonstrate some degree of external rotation weakness. An increased level of passive external rotation with the arm at the side is suggestive of a subscapularis tendon tear, whereas reduced external rotation in 90 degrees of abduction may indicate a medially healed Bankart lesion.
Recommended imaging includes a complete radiographic trauma series, consisting of a true anteroposterior (AP) image of the glenohumeral joint (i.e., the “Grashey” view). The true AP image is taken with the patient rotated between 30 and 45 degrees offset the cassette in the coronal plane. Alternatively, the beam can be rotated while the patient remains neutral in the coronal plane. In addition to AP imaging, an axillary lateral radiograph should be obtained. This view may be difficult to accomplish in the acute traumatic setting. However, the importance of obtaining a complete radiographic series with adequate orthogonal imaging cannot be overemphasized. Unfortunately, it is not uncommon to miss shoulder dislocations, especially posterior dislocations, when an incomplete radiographic evaluation is all that is available.
The axillary lateral view provides essential information about the position of the humeral head relative to the glenoid. Additionally, the presence and degree of degree of anterior (or posterior) glenoid erosion or glenoid dysplasia, as well as any potential humeral head defects can be appreciated on this view as well. Anterior glenoid rim fractures or glenoid avulsion injuries may also be present. The presence of medial neck scalloping or a possible avulsion injury is visible on AP imaging in the presence of an associated humeral avulsion of glenohumeral ligaments (HAGL).
Advanced imaging modalities
Magnetic resonance imaging is the preferred imaging modality to visualize for the presence of associated labral injuries. The addition of intra-articular contrast (i.e., MR arthrography) increases the sensitivity and specificity for the identification of associated injuries. Further, MRI imaging can provide clinicians with an accurate assessment of potential osseous glenohumeral defects or glenohumeral avulsions (off the glenoid or humeral sides).
CT imaging is the preferred imaging modality when attempting to quantify bone loss. Although a plethora of quantification techniques exist, the three-dimensional reconstruction techniques are superior to two-dimensional assessments. The latter relies on the proper sagittal orientation along the long axis of the glenoid to accurately characterize glenoid bone loss.
Three-dimensional en face reconstructions of the glenoid with humeral subtraction have become the gold standard for glenoid assessment given their ability to provide easily reproducible quantification of glenoid morphology.
:The initial management of acute shoulder instability depends on a multitude of factors. The acute management always should consist of manual reduction (if necessary) following confirmation of a dislocation event. The exact timeline for the initial period of immobilization remains debated. The acute management (e.g., sideline team physician management) consists of sling immobilization with avoidance of a return to play until completion of a comprehensive assessment.
Owens et al. previously proposed an algorithm to help guide the management of mid-season traumatic anterior shoulder instability in high-level athletes. The authors suggested a set of considerable clinical and sport-specific factors that could serve to guide the management of instability in athletes.
Relative indications for nonsurgical management of traumatic anterior shoulder instability include:
By contrast, surgical management would be advocated earlier in the management course if the case meets any of the following criteria
A 2014 study by Dickens et al. reported results from a multicenter prospective study of in-season Division I collegiate athletes. The authors reported that despite returning to play at a median of 5 days, 27% of athletes could not complete their season and underwent surgical stabilization.
Physical therapy (PT) and bracing
The optimal approach and technique to address anterior shoulder instability remain controversial.
Open versus Arthroscopic repair techniques
Traditionally, open Bankart repairs offered good to excellent results with minimal risk of redislocation (about 2%) in the setting of minimal osseous and primarily soft tissue only instability cases. Arthroscopic procedures theoretically offer advantages of decreased loss of motion, decreased morbidity, avoidance of subscapularis tenotomy, and the capacity to address concomitant intra-articular pathology, Studies have shown a faster return of preoperative muscle strength.
A 2017 study reported the surgical trends in management from 2008 through 2012. Arthroscopic stabilization procedures are being performed at a rate of greater than 90% to manage anterior shoulder instability, with the annual rates increasing each year during the study period.
The benefits to arthroscopy include the ability to assess and address concomitant associated shoulder injuries. Also, Burkhart and De Beer previously emphasized the importance of utilizing the arthroscopic procedure as a dynamic diagnostic tool to help identify osseous lesions “at risk” of compromising the functional glenohumeral stability following the single performance of an isolated capsulolabral soft tissue repair.
Arthroscopic Bankart Repair
In the setting of primarily soft tissue-based pathology, repair and relocation of the detached capsulolabral complex to its anatomic location are the goals of the surgical technique. Thus, the surgeon aims to restore the static restraining capability of the anterior band of the IGHL. Various suture anchor devices allow for an anatomic repair of the labrum, and techniques will often include capsular plication to address the pathologically lax capsular structures. This concept becomes even more important in the setting of chronic instability cases.
Bone loss considerations
Although the exact percentage of bone loss suggested to trigger a change in surgical fixation technique employed remains debated, more aggressive glenoid augmentation procedures are considered as glenoid bone loss approaches and exceeds 25%. Augmentation procedures include autogenous coracoid transfers (Latarjet technique), tricortical iliac crest, and various allograft tissue augmentation techniques. The distal tibial allograft is a commonly utilized technique in the setting of advanced glenoid bone loss, or the setting of revision surgery.
In the setting of moderate- to large-sized Hill-Sachs lesions, especially engaging lesions, consideration should be given to performing a remplissage procedure. During the arthroscopic procedure, the arm is brought into increasing degrees of shoulder abduction and external rotation to check for a potentially engaging lesion which could lead to postoperative instability event recurrence.
Burkhart and colleagues in 2014 proposed an algorithmic approach. The treatment paradigm broke shoulder instability cases into four subgroups to help guide surgical technique most appropriate to employ:
The differential diagnosis for shoulder instability is much more focused compared to conditions involving nonspecific, chronic shoulder pain, or even rotator cuff-based pathologies or shoulder impingement conditions.
Pertinent elements to consider on the differential include:
In general, patients can receive education from their providers regarding the risk of recurrence following nonoperative and operative management. In general, prognosis depends on a multitude of factors.
In 2007, the Instability Severity Index Score (ISIS) was originally described to guide orthopedic surgeons regarding the open versus arthroscopic management of shoulder instability surgical procedures . A 2019 study validated the ISIS as a predictive tool to assess the risk of recurrent dislocation following arthroscopic Bankart repairs: 
Risk factors associated with recurrence of instability include:
The ISIS is a 10-point scoring system based on these parameters . Patients should be educated to expect, in general, that fewer of the risk factors mentioned above have been shown to result in the following 5-year overall success rates (i.e., no instability recurrence): 
Redislocation following surgical fixation
Following surgical stabilization procedures, the patient is kept immobilized in a sling for the initial 4- to 6-week postoperative period depending on the surgeon's preference and degree/complexity of the shoulder instability pattern. Following arthroscopic procedures, it is worth mentioning that the subscapularis repair (from an open stabilization procedure) is avoided.
During sling use, patients should be encouraged to perform elbow/wrist/finger ROM to avoid stiffness. An ideal time to incorporate these movements is while the patient is showering and/or before bed.
Following the initial period of shoulder immobilization, passive and active ROM exercises are initialized based on surgeon preference. Typically, the extreme provocative positions are avoided (i.e., shoulder abduction and external rotation) until about 8 weeks following surgery. A goal of full active ROM by the 8-week postop mark is reasonable in most clinical cases.
Progressive resistance and gradual strengthening often begin during the 10- to 12-week postoperative period.
Return to sport
Return to sport-specific drills and return to practice and/or competition will vary based on position, sport, level of performance, and the complexity of the injury. In general, return to sport no earlier than 3 months has been advocated in the literature, with a return to high-impact collision sports (e.g., rugby, football) around the 6-month postoperative mark.
Return to work
All patients should understand that the return to work timeline will vary depending on the occupational demands of each individual. A heavy physical workload is a known risk factor for prolonged time lost to return to work. A 2017 study reported a mean time to return to work following arthroscopic Bankart repair of 2 months, with return times as early as 1 to 4 weeks following surgery ranging up to 10 months following surgery.
The mantra for managing acute or chronic shoulder instability events should be: when in doubt, consult an orthopedic or primary care sports medicine specialist for further management. While the majority of shoulder instability injuries eventually require surgical fixation, there are certain situations in which nonoperative management can yield acceptable results. That said, the complexity of the overall assessment and management should include consultation with a surgical specialist with experience in managing a wide range of complex instability patterns to provide the patient with the best chance for an ideal outcome.
Patients and family members (especially when the patient is an adolescent or pediatric patient) should receive education regarding the natural history of shoulder instability events. Patients under the age of 20 years afflicted with at least one shoulder instability event should obtain a referral to a sports medicine specialist for further care and management.
Shoulder instability events often occur in the young athletic population, and therefore the optimal management of these injuries will often include healthcare personnel spanning from athletic trainer’s acute sideline management, primary care (including sports medicine specialists), and orthopedic surgeons. Level of evidence: II-III
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