Background
The shoulder comprises three distinct and complex articulations consisting of the glenohumeral joint, the scapulothoracic joints, and the acromioclavicular joint. Under normal physiologic conditions, there exists an equilibrium between both the static and dynamic stabilizers at all of these articulations allowing the upper extremity to be placed in an infinite number of planes. Disruptions in the normal biomechanics of the shoulder can lead to shoulder stiffness, which, depending on severity of the disease process, can be debilitating. Shoulder stiffness can be classified into primary (idiopathic) shoulder stiffness, which is commonly referred to as frozen shoulder, and acquired shoulder stiffness. Acquired shoulder stiffness can be further subdivided into posttraumatic, postoperative, and several other less common etiologies ( Fig. 19.1 ). This chapter focuses on acquired shoulder stiffness and the various etiologies.
Posttraumatic shoulder stiffness
Introduction
Shoulder stiffness following trauma was first described in 1859 by the French surgeon Joseph-François Malgaigne, who observed restricted range of motion (ROM) in a series of patients who sustained nondisplaced, extracapsular proximal humerus fractures. Since that time, posttraumatic shoulder stiffness (PTSS) has been seen as a distinct subset of acquired shoulder stiffness, although the literature regarding this etiology remains sparse.
Shoulder stiffness following both major and repetitive minor trauma is a relatively common phenomenon. PTSS is the term used to describe painful shoulder stiffness after previous trauma that occurs in temporal relation or is assumed to be causal and otherwise cannot be explained. Analogous to other types of shoulder stiffness such as idiopathic frozen shoulder, PTSS is diagnosed by restricted passive ROM, especially for external rotation, when compared with the contralateral side. The necessary lack of motion for diagnosis is controversial despite multiple efforts to reach a consensus. The difficulty in diagnosing PTSS is usually not in the clinical presentation but in determining a causal relationship between the trauma and shoulder stiffness. This becomes increasingly difficult in the case of a patient who sustains a traumatic injury to the shoulder girdle and undergoes surgical intervention. Although somewhat arbitrary, it is difficult to determine whether the initial trauma is the cause of the restricted motion or whether the surgical intervention precipitates stiffness. In addition, there is often a latency of 4 to 8 weeks between the trauma and the onset of a secondary increase in pain associated with PTSS. Interestingly, studies have shown that the degree of movement restriction does not necessarily correspond to the severity of the injury. In comparison with patients who regain baseline ROM following trauma, patients who develop PTSS have associated increased health care costs, longer absences from work, and often more medicolegal claims.
Pathophysiology
Currently, the exact pathophysiology in the development of PTSS remains largely unknown. In addition, although much is known regarding the pathogenesis of primary frozen shoulder on a molecular-biologic and histologic level, it is not clear whether the development of PTSS differs from this pathway. In this context, the following theories are mostly based on clinical observations of the authors rather than on evidence-based clinical or basic research.
From a clinical perspective, it makes sense to separate the causes of PTSS into intracapsular and extracapsular categories. The intracapsular type includes early inflammatory capsulitis caused by glenohumeral hemarthrosis following intra-articular fractures or soft tissue injuries, chronic capsulitis caused by repetitive microtrauma to the intra-articular structures, thickening of the joint capsule due to prolonged immobilization following trauma, or chronic capsulitis secondary to early posttraumatic osteoarthritis. The entire capsule is not necessarily affected, especially in chronic capsulitis from repetitive microtrauma. Focal segments of the joint capsule can preferentially be affected by chronic inflammatory remodeling. Similar to primary frozen shoulder, the anterior and anteroinferior joint capsule is most frequently affected in PTSS. However, in other entities such as internal impingement, the posterosuperior capsule is preferentially affected, with little to no changes seen in the remaining capsule.
In contrast, extracapsular PTSS does not directly result from intracapsular injuries. Examples include extra-articular fracture malunion, extra-articular scarring and adhesions (e.g., subacromial space), heterotopic ossification, and posttraumatic heterotopic ossification. In a broader sense, spastic paresis of the shoulder following traumatic brain injury (TBI) can be classified as an extra-articular cause of PTSS ( Table 19.1 ).
| Intracapsular PTSS | Extracapsular PTSS |
|---|---|
| Hemarthrosis following intra-articular fractures or soft tissue injuries | Extra-articular fracture malunion |
| Repetitive microtrauma | Extra-articular scarring/adhesions |
| Prolonged immobilization | Posttraumatic heterotopic ossification |
| Posttraumatic osteoarthritis | Spastic paresis after craniocerebral injury |
The pathogenesis of the capsular response due to intra-articular bony or soft tissue injury is not completely understood. Acute hemarthrosis formation and initiation of the inflammatory cascade starts with an overexpression of transforming growth factor-β, tumor necrosis factor-α, platelet-derived growth factor, hepatocyte growth factor, interleukin-1, and interleukin-6. This hyperplasic/hypervascular environment, together with an imbalance of metalloproteinases and their inhibitors and a local increase of substance P, leads to typical histologic changes seen within the joint capsule. These capsular changes include increased density of collagen fibers, increased number of inflammatory cells, neovascularization and neurogenesis, transformation of fibroblasts to myofibroblasts, and chondrogenesis. At present, no studies have directly compared the histologic changes seen in PTSS with postoperative or idiopathic shoulder stiffness.
Epidemiology and risk factors
Although the incidence of idiopathic frozen shoulder is relatively well documented, the incidence of PTSS is relatively unknown. , In one series of 497 patients with diagnosed primary or acquired shoulder stiffness, 80 (16%) were found to be posttraumatic in nature. In another study looking at 22,000 patients with documented shoulder injuries, 5% developed PTSS (unpublished data, Bouaicha et al.). Further supporting the idea that PTSS may result from prolonged immobilization, one study showed that of 64 patients with upper limb fractures who developed PTSS, 10 resulted following clavicle fractures, 5 after fracture of the wrist/carpus, and 1 after an elbow fracture-dislocation.
The severity of an injury does not necessarily correlate with the probability of developing PTSS. Accordingly, it is difficult to predict whether a patient will develop stiffness after a shoulder injury. However, clinical experience shows that the same risk factors for primary shoulder stiffness, such as female sex, age between 40 and 60 years, or endocrine disorders such as diabetes or hypothyroidism, have a high coincidence in patients who develop PTSS. In addition, secondary shoulder stiffness is also seen frequently after TBIs, which as previously described can cause a spastic paresis.
Clinical presentation
The common feature of all forms of primary and secondary shoulder stiffness is the restriction of passive ROM. Although restriction can be seen in all directions, decreased passive external rotation is the most common clinical finding. Patients typically present weeks to months after their initial traumatic injury with increasing pain and difficulty with activities of daily life due to restricted ROM. Stiffness or pain may manifest after a prolonged period of immobilization. Audible or palpable crepitation or a disturbance of the normal shoulder contour may be present, depending on direction of the movement restriction and duration of symptoms. The pain associated with PTSS can be dull or sharp and, in most cases, is projected onto the anterior shoulder region, especially in intracapsular injury patterns. As a result of limited glenohumeral mobility, compensatory mechanisms can lead to scapulothoracic dyskinesia, which is often associated with diffuse periscapular pain due to increased demands on the muscles involved. Some patients present with diffuse distal neuropathic pain and paresthesias, which often cannot be clearly attributed to a particular nerve root or peripheral nerve injury. These patients may have clinical presentations similar to those that present with thoracic outlet syndrome, and indeed this may be in the differential diagnosis. Electrophysiologic and vascular examinations remain nondiagnostic in these cases.
Analogous to the primary frozen shoulder, the described sequence of the shoulder freezing, frozen, and thawing can often be observed in PTSS. In contrast to primary frozen shoulder, PTSS does not follow a typical duration and/or resolution of the disease. However, in our experience, although PTSS can have a prolonged waxing and waning course, most patients have resolution of symptoms within 1 year of injury.
Treatment modalities
The treatment strategies for intracapsular causes of PTSS are analogous to those for the primary frozen shoulder, with an initial prolonged course of conservative treatments ranging from skillful neglect, to gentle mobilizing physical therapy or corticosteroid injections. More invasive measures such as hydrodilation, manipulation under anesthesia, or arthroscopic capsular release are rarely necessary. Elhassan et al. showed that patients who do not improve with conservative measures may benefit from an arthroscopic capsular release.
For the extracapsular causes of PTSS, identifying the cause of the movement restriction is the basis for the treatment strategy. Many causes of extracapsular PTSS, such as fracture malunion or heterotopic ossification, can be identified with plain radiographs. However, in the case of extra-articular scarring or adhesions, advanced imaging may be necessary to aid in diagnosis. Once the etiology is identified and conservative therapies are exhausted, surgical procedures aimed at the specific pathology can be used. This includes corrective osteotomies for extra-articular or lysis of the humeroscapular motion interface.
Postoperative shoulder stiffness
Shoulder stiffness following surgery is a common and often debilitating condition. Clinically, postoperative shoulder stiffness, like idiopathic or PTSS, is characterized by limited active and passive glenohumeral mobility with simultaneous absence of glenohumeral arthritis. Although the clinical picture of postoperative shoulder stiffness is similar regardless of which procedure was performed, it is still important to consider shoulder stiffness in the context of the specific procedure, as prognosis and treatment options depend on upon it. Postoperative shoulder stiffness appears between 3% and 10% of patients 12 months after rotator cuff reconstruction and must be considered as a relevant and major complication after rotator cuff surgery. ,
Shoulder stiffness after rotator cuff repair
Etiology
The extent of postoperative scarring and resulting shoulder stiffness after rotator cuff reconstruction depends on the extent of preexisting primary shoulder stiffness, the surgical method (open or arthroscopic rotator cuff repair), and the postoperative rehabilitation protocol. , In contrast to idiopathic shoulder stiffness, in which inflammatory changes of the joint capsule cause thickening and limit ROM, shoulder stiffness after rotator cuff reconstruction is due to the intra-articular and extra-articular scarring and adhesion formation, which are secondary to the debridement and reconstruction itself. The extra-articular subacromial and subdeltoid bursae create a humeroscapular motion interface between the proximal humerus, which is covered by the rotator cuff tendons, and the overlying structures attached to the scapula. This includes the acromion, deltoid muscle, coracoacromial ligament, coracoid, and the conjoined tendon. The humeroscapular motion interface of these two bursae allows physiologic excursion up to 4 cm. Depending on the extent of the postoperative adhesions in these bursae, the ROM is restricted accordingly. Inflammation of the subcoracoid bursa and shortening of the conjoined tendon are, in addition to the subacromial and subdeltoid bursa, other extra-articular structures which can contribute to postoperative shoulder stiffness after rotator cuff reconstruction. The scars between the coracoid process, conjoined tendon, and the deeper subscapularis tendon result primarily in a limitation of external rotation.
Intra-articularly, both the anterior and posterior parts of the joint capsule can be affected by scarring and contracture. Anterior scarring in the rotator interval region causes restriction of mainly external rotation in shoulder adduction, whereas posterior scarring mainly limits internal rotation.
Incidence
Precise information on the incidence of postoperative shoulder stiffness after rotator cuff reconstruction is difficult because different definitions and follow-up periods exist throughout the current literature. , , , The largest studies found shoulder stiffness after rotator cuff reconstitution had an incidence of 17% after a mean follow-up of 4 months. , , , However, Chung et al. showed that, over time, postoperative shoulder stiffness tends to improve. They showed that, although 19% of patients were considered to have a stiff shoulder at 3 months postoperatively, only 7% remained stiff at 12 months follow-up. Similarly, Denard et al. described in his systematic review a similar transient shoulder stiffness after rotator cuff reconstruction, with 10% having a stiff shoulder within a year postoperatively; however, only 3% of patients reported permanent stiffness. Transient shoulder stiffness was defined by Denard et al. in their review as shoulder stiffness that responded to nonoperative treatment and resistant stiffness was described as shoulder stiffness that did not respond to nonoperative management and required arthroscopic capsular release. Resistant shoulder stiffness was seen in 0% to 5% in patients with sling immobilization protocols (sling for 6 weeks after surgery) and in 0.2% to 4.2% , of patients with early mobilization protocols. ,
Risk factors
Huberty et al. investigated 489 arthroscopic rotator cuff reconstructions to determine the risk factors of developing postoperative shoulder stiffness after arthroscopic rotator cuff reconstruction. They found that coexisting calcific tendonitis, prior primary adhesive capsulitis, partial articular supraspinatus tendon avulsion type rotator cuff tear, concomitant labral repair, workmen’s compensation insurance, and age at surgery younger than 50 years were all independent risk factors for developing stiffness after arthroscopic rotator cuff repair. Interestingly, repairs of larger rotator cuff tears were less likely to be associated with stiffness. However, these results are disputed by Chung et al., who found that in their cohort of 288 patients both increased age and larger rotator cuff tears were risk factors for the development of postoperative shoulder stiffness after rotator cuff repair. Preoperative shoulder stiffness, which is present in approximately 25% of patients with rotator cuff tears and duration of stiffness symptoms for more than 6 months before arthroscopic rotator cuff repair have also been shown to be risk factors for postoperative shoulder stiffness after rotator cuff repair. , Open rotator cuff repair has been shown to have increased rates of postoperative shoulder stiffness, more extracapsular adhesions, and higher levels of inflammation compared with arthroscopic rotator cuff repair. , ,
Prevention
Assessment of risk factors for postoperative shoulder stiffness can help to adjust individual rehabilitation protocols according to the risk profile. Koo et al. demonstrated that in patients with an increased stiffness risk profile, early mobilization reduces the probability of developing postoperative shoulder stiffness. This was routinely implemented in the prearthroscopic rotator cuff repair era, in which early mobilization with stretching exercises were initiated to prevent adhesions. , The introduction of arthroscopic shoulder surgery reduced the extent of scarring and subsequent shoulder stiffness. As a result, the mobilization protocols after rotator cuff reconstructions became more passive and delayed. Numerous studies have shown that the immobilization of the operated arm for 4 to 8 weeks leads to increased shoulder stiffness in the early course, but in the long term no difference in ROM when compared with early mobilized patients. , , Several levels I and II studies have shown that immobilization of the arm for 6 weeks after rotator cuff reconstruction does not negatively affect long-term shoulder mobility and that the rerupture rate is significantly lower than with early mobilization. , Koh et al. were able to show in a prospective randomized study that the retear rate 1 year after rotator cuff reconstruction of patients who underwent 4 weeks immobilization did not differ from those that underwent 8 weeks of immobilization. However, the incidence of shoulder stiffness was significantly higher in patients who underwent 8 weeks immobilization than in patients who underwent 4 weeks of immobilization. Postoperative stiffness can be reduced by performing an extensive rotator interval release or a circumferential capsular release during arthroscopic reconstruction of the rotator cuff, especially when preoperative shoulder stiffness is present. However, the increased glenohumeral mobility after simultaneous rotator interval and capsular release is not clinically relevant 1 year postoperatively compared with those that did not undergo extensive release. ,
The short-term postoperative shoulder stiffness observed after arthroscopic rotator cuff reconstruction is to be expected, and it is important that patients are informed during preoperative evaluation. In a single-center study which included 1533 patients who underwent an arthroscopic rotator cuff repair by the same surgeon, 35% of patients developed temporarily shoulder stiffness which was defined as decreased external rotation (<20 degrees) in shoulder adduction after 6 weeks. Importantly, the same 35% of patients with decreased external rotation showed a significant lower retear rate (7% vs. 15%) compared with the 65% of the patients with more than 20 degrees of external rotation. Similar observations were made in another study in which patients with less external rotation and glenohumeral mobility after 3 months had a lower incidence of rerupture compared with patients without glenohumeral stiffness.
Treatment
Postoperative shoulder stiffness is less responsive to conservative treatments options than idiopathic or PTSS. Despite this, most patients who experience postoperative stiffness after rotator cuff repair often recover ROM within a year postoperatively and as stated earlier have lower rerupture rates. It is important to inform patients with postoperative shoulder stiffness after rotator cuff repair about the favorable natural course, because this may help to provide necessary motivation for the protracted and strenuous physiotherapy, which in most cases is effective. In the rare cases of chronic stiffness, which is refractory to a conservative approach, operative intervention is a reasonable approach. MUA is a therapy option for patients who do not achieve any improvement in mobility despite conservative treatment. However, in three level I studies with a total of 271 patients, no superiority of the MUA could be seen compared with the control group, which were treated with conservative therapy measures. , , Because of the limited efficacy and reoperation rate of approximately 15% and also because of the relevant possible complications such as proximal humerus fractures, glenoid rim fractures, plexus lesions, or shoulder dislocations which occur approximately in 1%, , , at our institution we prefer to perform the manipulation under arthroscopic control after the arthroscopic release has been performed. ,
In the series by Huberty et al., 5% of the patients with postoperative shoulder stiffness underwent arthroscopic capsular release. Patients treated at our institution for persistent postoperative shoulder stiffness underwent physiotherapy for an average of 7 months before the decision was made to perform an arthroscopic capsular release. Arthroscopic capsular release with lysis of adhesions in the humeroscapular motion interface, as described later, can significantly improve shoulder function and patient satisfaction. At our institution, we have found a significant improvement in subjective shoulder value (32% preoperative vs. 69% postoperative) and Constant and Murley score (36 points preoperative vs. 81 points postoperative) after arthroscopic capsular release with a mean follow-up of 43 months. In our patient population, five patients (10%) required a second capsular release due to recurrent stiffness, with three of the five patients demonstrating a significant improvement.
Postoperative shoulder stiffness following surgical repair for shoulder instability
The surgical treatment of anteroinferior shoulder instability often results in a reduction of glenohumeral external rotation. Although there are many different surgical treatment options for shoulder instability, to some extent all involve reinforcing and tightening of the anterior capsule and/or the glenohumeral ligaments. , , , This anterior reinforcement inherently leads to a partial loss of the glenohumeral external rotation ability, which can best be assessed by comparing with the contralateral arm. Not surprising, partial loss of external rotation is one of the most frequently reported postoperative complications following anterior shoulder stabilization. The range of the impairment differs across the literature; however, most studies describe a decrease in external rotation of 5 degrees or less when compared with the contralateral side. , Rahme et al. reported an external rotation loss of 25% compared with the nonoperated opposite side in their population of patients who underwent open Bankart repair. The loss of external rotation may be less pronounced after arthroscopic stabilization procedures than after analogous open procedures as well as after revision stabilization procedures. The extent of external rotation loss is difficult to predict. This is likely because, in addition to the purely mechanical reinforcement of the anterior capsular and ligamentous structures, physiologic scarring and contracture are individual specific. Shibano et al. showed in a computer simulation the extent of the external rotation loss is dependent on the aggressiveness of the imbrication of the anteroinferior capsule. They found that 3-, 6-, and 9-mm imbrications of the anteroinferior glenohumeral ligament (AIGHL) led to 10, 22, and 36 degrees loss of external rotation, respectively. In addition to reinforcement thickness, superior deviation from the AIGHL insertion significantly decreased maximum external rotation.
During open stabilization operations, detachment of the subscapularis leads to more postoperative shoulder stiffness. Accordingly, it is recommended to perform a splitting of the subscapularis tendon to expose the anterior glenoid as opposed to a complete subscapularis detachment. However, detachment is occasionally used during revision procedures, when excessive scarring exists. The detached subscapularis tendon must be reattached to its insertion and immobilized postoperatively, which likely also contributes to postoperative stiffness.
Both the anterior glenohumeral joint capsule and the rotator interval open during external rotation and contract during internal rotation. Performing the imbrication of the anterior capsule with the arm held in an internally rotated position leads to more loss of postoperative external rotation than when the imbrication is performed while the arm is held in neutral position during arthroscopic Bankart repair. The insufficiency of the anterosuperior glenohumeral joint capsule is seen in inferior and/or multidirectional instability. , By imbricating the interval described for the treatment of multidirectional shoulder instability, partial loss of external rotation may also occur. The tightening of this interval leads to less loss of external rotation compared with the tightening of the anteroinferior capsule structures. Patients who undergo posterior capsular shift procedures may develop internal rotation deficits. In these patients, the release of the posterior capsule can result in significant improvement in shoulder ROM.
Prolonged immobilization is a risk factor for the development of shoulder stiffness after stabilization surgery. Nevertheless, the postoperative treatment after open or arthroscopic stabilization surgery has the primary goal of not jeopardizing the glenohumeral stabilization. Gaining glenohumeral mobility and strength are secondary goals. Accordingly, we prefer to immobilize the operated shoulder for 4 weeks. After 4 weeks, gentle pendulum exercises can begin. After 6 weeks, the sling is removed and active ROM can begin for activities of daily living. The formal physical therapy program varies on patient stiffness. We typically allow therapist-guided gentle stretching after 8 weeks, and after approximately 12 weeks, strengthening can begin. After 16 weeks, stiffness can be more aggressively treated; however, forced mobilization should always be avoided.
Independent of the stabilization procedure performed, improvement in external rotation can be expected up to 4 months postoperatively, and it is important that patients are frequently reminded of this during their rehabilitation. Within the immediate 6-month postoperative period following shoulder stabilization surgery, the diagnosis of postoperative shoulder stiffness is difficult to make because, to a certain extent, the partial loss of external rotation is a consequence of the surgery itself. Nevertheless, if 9 months after stabilization surgery the glenohumeral external rotation in shoulder adduction is less than 20 degrees, this meets our diagnostic criteria and is an indication for arthroscopic release and manipulation under anesthesia at our institution. This is important because a persistent external rotation deficit represents a significant risk factor for the development of early glenohumeral arthritis.
Arthroscopic capsular release for shoulder stiffness after rotator cuff repair/shoulder stabilization surgery
If conservative treatments are unsuccessful in the treatment of postoperative stiffness, arthroscopic capsular release is indicated. The surgical technique for the treatment of shoulder stiffness after rotator cuff reconstruction and shoulder stabilization surgery is the same. The arthroscopic capsular release for the treatment of stiffness after total anatomic shoulder replacement differs significantly and is therefore described later in this chapter.
For patients in whom a concerted conservative approach has failed and who experience recalcitrant shoulder stiffness, arthroscopic capsular release is offered. The main objective is to perform a systematic release, as indicated, of the rotator interval, the superior glenohumeral ligament, the coracohumeral ligament, the anterior capsule, the middle glenohumeral ligament, the inferior glenohumeral ligament (anterior and posterior bands), the inferior capsule, and the posterior capsule.
There are several benefits to an arthroscopic release, many of which are simply the benefits of arthroscopic surgery over similar open procedures. One particular advantage of the arthroscopic approach is the enhanced visualization that this approach affords the surgeon. The pathologic capsule can be visualized directly and can be released accordingly. Comorbid conditions affecting the shoulder can be addressed in a relatively atraumatic fashion. Specifically, biceps tendon disease may be addressed simultaneously with a tenotomy or tenodesis with little to no effect on the capsular release or subsequent physical therapy. Concomitant synovitis, which appears to be ubiquitous, may be addressed throughout the joint. The evaluation of the subacromial space and the need for soft tissue or bony decompression is easily achieved. Finally, aggressive physical therapy is appropriate to start the same day as surgery.
Technique
We record a detailed assessment of the passive ROM for forward flexion, abduction, external rotation (in both adduction and abduction), and internal rotation prior to starting the procedure. The procedure is performed under general anesthesia in combination with an interscalene pain catheter for the postoperative mobilization therapy. The patient is placed in a beach chair position with a pneumatic arm holder (Spyder Arm Holder, Tenet Medical) to aid in positioning the extremity. A standard posterior portal is placed approximately 1 cm medial to the edge of the posterolateral acromion and 2 cm inferior to the acromion. Routine arthroscopic equipment is used, and a radiofrequency device for tissue ablation and coagulation is required. We prefer not to manipulate the joint before arthroscopy because this may create a substantial hemarthrosis.
A standard anterior superior portal is created with an outside-in technique just lateral to the coracoid, using an 18-gauge spinal needle to localize the incision. A standard 5.5 mm cannula is inserted, often over a metal trocar, because the tissue in the rotator interval as well as the anterior capsule may be hypertrophic. We attempt a diagnostic arthroscopy, but if the glenohumeral joint is too tight to safely visualize structures without risking chondral damage, comprehensive visualization is completed after the release. Synovitis is addressed, and the biceps is thoroughly evaluated. The biceps is aggressively treated with tenotomy or tenodesis if there are signs of significant tendinopathy, partial tearing, tenosynovitis, or subluxation or if the excursion of the biceps in the intertubercular groove is restricted. A systematic capsular release follows.
We start our capsular release within the glenohumeral joint, even though other authors have described good results with debridement of the interval from an extra-articular arthroscopic approach. Starting above the superior glenohumeral ligament, a hook-tipped radiofrequency device is used to divide the superior glenohumeral ligament and the anterior capsule to the superior border of the intra-articular subscapularis. During this release, the rotator interval, which is generally contracted, is released and the humeral head translates inferiorly and laterally, allowing the arthroscope to be advanced and markedly facilitating visualization. The middle glenohumeral ligament is released as it crosses posterior to the subscapularis. The anterior capsule is released inferiorly past the anterior band of the inferior glenohumeral ligament. From this position, the axillary nerve is in close proximity and attention is directed to the posterior capsule.
For patients with restricted internal rotation, a posterior capsular release follows. A switching stick is placed to maintain the position of the posterior portal, and the arthroscope is placed in the anterior portal. Once anterior visualization is confirmed, a 5.5 mm cannula is placed over the switching stick and advanced intra-articularly. The hook-tipped radiofrequency device is placed through the posterior cannula, and the cannula is gently moved to lie just outside of the joint ( Fig. 19.2 ). This allows the radiofrequency device to release the capsule just adjacent to the glenoid. In this region, the capsule overlies the muscular component of the posterior rotator cuff, and this allows confirmation of a complete posterior capsular release ( Fig. 19.3 ). The release extends inferiorly through the posterior band of the inferior glenohumeral ligament. The radiofrequency device is then used to carefully work inferiorly, keeping in mind that the axillary nerve is in close proximity to the capsule. The inferior capsule is carefully released, layer by layer, until the posterior and anterior capsulotomies are connected ( ).
