Primary, Idiopathic Frozen Shoulder

Shoulder stiffness is a general term that encompasses a spectrum of pathology. It was first described as a clinical entity in the late nineteenth century by both Duplay in France and Putnam in the United States. The original term for the condition was scapulohumeral periarthritis, which encompassed a number of painful afflictions of the shoulder resulting in stiffness. As knowledge has developed about the specific conditions that can cause a stiff shoulder, this term has fallen out of favor.

In 1934 Codman described a clinical pattern of muscle spasms and glenohumeral stiffness, which he termed the frozen shoulder. He stated that this condition was “difficult to define, difficult to treat, and difficult to explain from the point of view of pathology.” In many respects this is still true today.

A decade after Codman, Neviaser described a similar condition, a “chronic inflammatory process involving the capsule of the shoulder causing a thickening and contracture of this structure which secondarily becomes adherent to the humeral head.” He called it adhesive capsulitis , a term he believed better represented the underlying pathology. The term adhesive capsulitis, however, has sometimes been used indiscriminately to describe both the idiopathic frozen shoulder and shoulder stiffness related to other causes. Because these are now considered separate entities, it is probably no longer appropriate to use the same term for both.

At a symposium sponsored by the American Academy of Orthopaedic Surgeons in 1992, a workshop committee defined frozen shoulder as “a condition of uncertain etiology characterized by significant restriction of both active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder.”

In an attempt to obtain a consensus definition and classification of frozen shoulder/adhesive capsulitis from 190 shoulder experts from around the world, Zuckerman proposed the definition of frozen shoulder to be “a condition characterized by functional restriction of both active and passive shoulder motion for which radiographs of the glenohumeral joint are essentially unremarkable except for the possible presence of osteopenia or calcific tendonitis.” He also classified the condition as primary or secondary based on whether an etiology or associated condition could be identified. He subclassified secondary frozen shoulder as intrinsic (due to rotator cuff or biceps disorders), extrinsic (due to an abnormality remote to the shoulder), or systemic (occurring with associated conditions, such as diabetes mellitus, hyperthyroidism, hypothyroidism, or hypoadrenalism). However, only 66% of the shoulder surgeons agreed with this subclassification of secondary frozen shoulder. We find it optimal to differentiate primary, idiopathic frozen shoulder from secondary frozen shoulder due to surgery, trauma, or other causes (see Fig. 19-1 ). We do not consider shoulder stiffness associated with a systemic disease, such as diabetes, to be a secondary frozen shoulder.

Secondary Frozen Shoulder

The earliest description of shoulder stiffness following trauma was recorded by Malgaigne in 1859. He wrote with regard to minor nondisplaced, extracapsular fractures about the shoulder :

There remains long afterward a stiffness, and a difficulty in moving the shoulder; and however great care may be taken, the motion of elevation of the arm will always remain limited; at least I have in no case seen it perfectly restored, even after the lapse of 11 to 15 months.

There is less controversy and confusion surrounding the nomenclature of this clinical entity. Other commonly used terms for the same condition include posttraumatic stiff shoulder and secondary stiffness . It is unclear whether acquired stiffness can recover without intervention; this is difficult to study because of the heterogeneity of this patient population.

Some degree of shoulder stiffness is typical after bone or soft tissue injuries around the shoulder. Restriction in shoulder motion has been reported after simple contusions, subluxations, dislocations, acromioclavicular joint injuries, clavicle and scapula fractures, and particularly after proximal humerus fractures in the elderly.

Especially after repetitive, low-level trauma, localized contractures can develop and can cause motion loss in specific patterns. Isolated posterior capsular contracture is the most commonly described. Neer discussed the impingement syndrome and encouraged therapeutic stretching in forward elevation, internal rotation, and cross-body adduction. Thomas and colleagues and Ticker and colleagues made similar recommendations. In a review of 30 patients from a prospective study of refractory shoulder stiffness, 11 experienced isolated restriction in motion that was attributed to posterior capsular contracture. In each of these patients an associated pathologic process was identified, with a partial-thickness rotator cuff tear being the pathology in seven cases.

Surgical procedures are widely recognized to be a cause of shoulder stiffness. Anterior or posterior capsulorrhaphy, inferior capsular shift, and rotator cuff surgery can all result in limitation of motion, often by design. Tauro found a relatively high incidence of stiffness in patients who underwent surgery for a rotator cuff tear. Patients with more pronounced stiffness often experienced difficulty in regaining normal motion after surgery.

Stages

Frozen shoulder is classically characterized by three stages: freezing, frozen, and thawing ( Fig. 19-6 ).

The traditional stages of primary, idiopathic frozen shoulder with symptom progression and resolution.

Differentiating Primary From Secondary Frozen Shoulder

Secondary frozen shoulder does not follow a predictable course like idiopathic frozen shoulder. There are, however, predictable patterns of motion loss after certain injuries. A rotator cuff strain typically causes restricted forward elevation, internal rotation, and cross-body adduction. This is thought to be related to contracture of the posterior capsule. Articular-sided partial rotator cuff tears are also associated with posterior capsular contractures. Nonanatomic instability repairs result in diminished external rotation. Immobilization after proximal humerus fractures tends to cause a global loss of motion as adhesions form in the subacromial-subdeltoid plane.

Radiographs

Radiographs are routinely performed for any patient with a stiff shoulder. Specific conditions to be ruled out include fracture, malunion, arthrosis, osteonecrosis, and chronic dislocation. The specific views that are obtained vary depending on the clinical scenario, but a minimum of two orthogonal views is mandatory, including anteroposterior and axillary lateral views. Additional films, such as cervical spine radiographs, may be warranted depending on the clinical suspicion. Radiographs are essential as it can often be difficult to differentiate primary, idiopathic frozen shoulder from glenohumeral arthritis based on history and examination alone.

Routine shoulder radiographs in patients with shoulder stiffness and no history of trauma or surgery are typically normal. Osteopenia of the humeral head may be seen and is probably related to disuse of the extremity. In approximately 50% of 74 cases of frozen shoulder, Lundberg and Nilsson reported bone loss within a short period. They considered this to be the result of an inflammatory process and not due to disuse alone.

Arthrography

In 1957 Kernwein and colleagues performed arthrographic studies in 12 patients with frozen shoulder. At open biopsy, they found that the capsule and coracohumeral ligament were very contracted, thickened, and inelastic. They also noted the presence of subacute inflammation. Later, Neviaser described the arthrographic findings of adhesive capsulitis, which included decreased joint capacity, obliteration of the reflected axillary fold, and variable filling of the bicipital tendon sheath. No correlation between arthrographic findings and treatment outcome has been found. In routine practice today, arthrography is rarely used.

Nuclear Imaging

A bone scan is rarely indicated in the evaluation of a frozen shoulder because these have not proved to be useful in diagnosis, management, or prognosis. Positive bone scans have been reported in as many as 96% of frozen shoulder patients. However, no association has been demonstrated between bone scan activity and the severity of disease, duration of symptoms, arthrographic findings, or ultimate outcome. A bone scan should be ordered only if there is suspicion of a neoplastic process.

Magnetic Resonance Imaging

As techniques and access have improved, magnetic resonance imaging (MRI) has become widely used for evaluating shoulder disorders, including stiffness. Emig and colleagues reported on the MRI characteristics of 10 patients with a frozen shoulder compared with patients without a frozen shoulder. They found the joint capsule and synovium in the frozen shoulder patients to have a combined thickness greater than 4 mm, but they did not observe any significant differences in the volume of intra-articular fluid seen on the MRI scan or in the thickness of the rotator cuff and rotator interval capsule. In a similar study Sofka and colleagues evaluated 46 shoulders with the clinical diagnosis of idiopathic frozen shoulder and attempted to correlate the clinical stage with the MRI characteristics. They found a mean thickness of the axillary pouch of 7.5 mm; this was significantly greater than the axillary pouch measurements in other stages, with means of less than 5.5 mm. Normal capsular and synovial thickness has been found to be less than 3 mm. Abnormalities within the rotator interval are also common. Mengiardi, Gerber, and colleagues described the “subcoracoid triangle sign” as obliteration of the normal-appearing fat between the coracoid process and the coracohumeral ligament on the sagittal oblique images.

The use of IV gadolinium can improve the diagnostic capability of MRI in patients with frozen shoulders. Connell and colleagues noted soft tissue density showing variable enhancement in the rotator interval and partially encasing the biceps anchor on MRI after gadolinium administration. They also noted thickening and gadolinium enhancement of the axillary pouch. Carrillon and colleagues performed IV gadolinium administration followed by MRI and demonstrated enhancement of the synovial lining in patients with frozen shoulder. Tamai and Yamato found enhancement of the joint capsule, which was not seen in patients with subacromial impingement. However, a study that compared findings on MR arthrography in patients with and without frozen shoulder did not identify any specific diagnostic findings for frozen shoulder.

Despite interest shown in it, MRI has not proved to be essential in the diagnosis or management of patients with stiff shoulders, and its routine use in this setting is not supported. Specific indications include concern for underlying rotator cuff integrity and the possibility of a soft tissue or bone neoplasm.

Ultrasound

Several investigators have reported on the use of ultrasound in the evaluation of frozen shoulder. Ryu and colleagues noted that the main sonographic feature of frozen shoulder was a constant limitation of the sliding movement of the supraspinatus tendon against the scapula. They reported sensitivity of 91%, specificity of 100%, and accuracy of 92% when comparing ultrasound with arthrography as the gold standard for diagnosis. As with MRI, ultrasound is not a required diagnostic study and is usually indicated only for evaluating the rotator cuff in patients whose physical examination suggests the possibility of a rotator cuff tear coexisting with shoulder stiffness. With the use of ultrasound, Homsi and colleagues found that coracohumeral ligament thickness was greater in idiopathic frozen shoulder patients than in controls.

Arthroscopy

Before performing arthroscopy, the diagnosis of stiffness should already have been made and perhaps confirmed by examination under anesthesia. Arthroscopy allows evaluation and possible treatment of additional pathology, such as rotator cuff tears, impingement, biceps disease, and articular cartilage lesions.

Neviaser described four arthroscopic stages of adhesive capsulitis and proposed that these stages could be used to guide treatment planning :

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  A mild erythematous synovitis

  
  
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  Acute synovitis with adhesions in the dependent folds of the synovial lining

  
  
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  Maturation of adhesions with less reactive synovitis

  
  
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  Chronic adhesions without synovitis

Arthroscopic treatment of shoulder stiffness is discussed in detail later in this chapter.

Medication

Various types of analgesics and nonsteroidal antiinflammatory drugs (NSAIDs) have been used as supportive measures to manage the pain and inflammatory component of the stiff shoulder. Their effectiveness in alleviating the pain component has been well established. Some authors have reported greater improvement in pain in patients who were managed with nonsalicylate analgesics than in those administered NSAIDs. Others have reported that oral steroids produce significantly better improvement in ROM, function, and pain relief in patients with frozen shoulder, but these benefits were not maintained beyond 6 weeks. Greater improvement can be expected in patients who combine the intake of such medications with a regular exercise program. Some physicians prescribe short-term, low-dose oral steroids for frozen shoulder, as these can act as a powerful antiinflammatory. Although risks associated with prescribing these medications are small, physicians should still discuss them with patients. We do not routinely prescribe oral steroids for patients as intra-articular steroid injections have been shown to be superior.

Physical Therapy

Physical therapy is a mainstay of initial treatment for shoulder stiffness that has been present for less than 3 to 6 months or in patients who have had no previous treatment. Patients are usually started with active-assisted ROM and gentle passive stretching exercises. Most exercises are easier in the sitting or supine position. Repetition is probably more important than doing one long session. We recommend short sessions of 5 to 10 minutes repeated several times per day, with the goal of trying to push the affected shoulder just slightly past the point of pain during each session. Sometimes it is helpful to have a daily progression chart that the patient can follow. Generally, improvement is seen in small increments. As a result, patients sometimes do not acknowledge their improvement and can become discouraged and frustrated. Patients are encouraged to take NSAIDs and apply heat to the affected shoulder before exercise and to apply ice after exercise. This regimen can help reduce discomfort and improve compliance with the exercises.

Other modalities, such as microwaves, short waves, and heat lamps are sometimes considered as additional measures in the rehabilitation process, although they have not proved to be particularly beneficial in any specific phase of shoulder stiffness. Similarly, adding ultrasound to the physical therapy exercises has not shown any additional benefit to therapy alone. Other modalities, such as electrophysiotherapy, massage, or more atypical modalities, such as hyperbaric oxygen and magnetotherapy have been used, but no additional benefit from these could be proved, and none of these treatments fits into a standard shoulder rehabilitation algorithm.

Adding stimuli to distract the mind of the patient from painful sensations has been shown to be helpful during physical therapy exercises. In one study, using audio analgesia as an adjunct to mobilization exercises in patients with chronic frozen shoulder resulted in significant improvement in the recovery of motion and a reduction in the number of treatments necessary for recovery. Using the same rationale, transcutaneous nerve stimulation has been used in patients with frozen shoulder undergoing physical therapy. Rizk and colleagues used transcutaneous nerve stimulation on a group of 28 patients to control their pain during the application of progressive abduction traction. Jurgel and colleagues reported on 10 patients with frozen shoulder who were treated with 4 weeks of rehabilitation that combined exercises with massage and electrical therapy and were able to demonstrate that this protocol improved shoulder ROM in all directions except rotation. They compared this group to a group of 28 patients treated with heat and therapeutic exercises and observed that the increase in ROM was significantly greater in the former group. This may be explained by the strong attachments between collagen fibers, which show high resistance to suddenly applied tension but which also tends to creep when prolonged tension is applied.

Exercises should be performed gently. Forceful stretching maneuvers are contraindicated, especially in the early phases of frozen shoulder. All forms of light resistance strengthening should be postponed until the patient has recovered ROM.

For patients to see improvement from therapy, they must assume primary responsibility for their condition. They should understand and participate actively in the prescribed exercises and be prepared to tolerate some amount of discomfort. Although it can take several months, a closely supervised physical therapy program will lead to improvement in pain and ROM in up to 90% of patients with chronic frozen shoulder. In addition, physical therapy has been shown to improve health-related quality of life.

Nicholson reported on the therapeutic advantage of performing passive stretching in abduction in addition to active ROM exercises. Watson-Jones recommended 3 minutes of active stretching each hour and demonstrated that of 226 frozen shoulders treated with this stretching exercise program alone, only 5% failed to regain satisfactory ROM within 6 months. In another study, 90% of 75 patients who completed a nonoperative program for frozen shoulder achieved satisfactory results, with only 7 patients requiring more aggressive intervention. Russell and colleagues found that a hospital-based group physical therapy program was more effective for restoring ROM and functional scores than individual therapy or a home-based program.

Dudkiewicz and colleagues reported long-term follow-up (mean, 9.2 years; range, 5.5 to 16 years) on 54 frozen shoulder patients who were managed conservatively with physical therapy and NSAIDs. Good long-term outcomes were reported with significantly improved motion in all the measured directions.

Occasionally, physical therapy does not help to improve symptoms in patients with frozen shoulder and at times can even exacerbate them. In one report only 60% of patients who received physical therapy, along with other modalities, achieved the ability to sleep pain-free after 5 months of treatment. Hazelman reported on a group of patients who received physical therapy alone; one third of them experienced an increase in pain, and only half of this group experienced significant improvement with exercises. Diercks and Steven conducted a prospective study on 77 patients with frozen shoulder to compare the effect of intensive physical therapy and manual stretching versus home exercises within the pain limits (“supervised neglect”). At 24 months’ follow-up, 89% of patients treated with supervised neglect had normal or near-normal painless shoulder function with a Constant score greater than 80. However, only 63% of patients in the group that received intensive physical therapy reached a Constant score of 80 or higher.

Lin and colleagues demonstrated the existence of trapezius muscle imbalance with overactivity of the upper compared with the lower trapezius muscle in patients with frozen shoulder. They concluded that this imbalance in the trapezius muscle might contribute to scapular substitution in compensation for impaired glenohumeral motion and thus rehabilitation of the trapezius should be included in the therapy protocol for patients with frozen shoulder.

Injections

Several different types of injections have been described for treating shoulder stiffness. The simplest types include intra-articular and subacromial injections. Most of the reports on intra-articular injections involve patients with frozen shoulder and not those with acquired stiffness. Intra-articular injections can be administered along with distention arthrography (brisement), combining chemical and mechanical modalities of treatment. Other types of injections include periarticular (trigger point) injections and nerve blockade injections (of the suprascapular and upper and lower subscapular nerves).

Other Modalities

Manipulation Under Anesthesia

Historically, closed MUA has often been recommended as the next step after the failure of nonoperative treatment in patients with stiff shoulder. However, cases of acquired stiffness in which extra-articular adhesions have developed, as well as changes to the articular anatomy, might not respond well to manipulation. Manipulation might be attempted in the acute phase of motion loss when therapy has failed to result in regained motion.

Patients with worsening symptoms after at least 3 months of an appropriate nonoperative exercise program are candidates for MUA. Most reports of MUA have been for patients with frozen shoulder, and the results of this intervention are varied. In one study a greater degree of improvement was achieved in patients who were symptomatic for more than 6 months before manipulation compared with those with a shorter duration of symptoms. This is probably related to the timing of the intervention in relation to the inflammatory phase of frozen shoulder. This phase is usually painful, and as pointed out by Neviaser and Neviaser, any operative intervention in this stage is likely to exacerbate the patient’s symptoms and motion loss because of increasing capsular injury. Manipulation should be postponed until pain is experienced only at the extremes of motion, which indicates resolution of the inflammatory phase.

In reports by Neviaser and DePalma the immediate effects of manipulation on structures about the shoulder were observed with arthroscopic and open surgery. Tears were seen in the subscapularis muscle and tendon, the anterior and inferior capsule, the supraspinatus tendon, and the long head of the biceps tendon. In addition, because many patients with frozen shoulders have osteopenia of the proximal humerus, fractures may occur with manipulation. Harryman reported on a referred patient with a complete brachial plexus palsy after MUA that resulted in anteroinferior dislocation. The reported cumulative risk of an adverse event after MUA is less than 1%.

Although complications can arise, other authors have contended that manipulation is a safe and reliable treatment if performed appropriately. Atoun and colleagues manipulated 32 shoulders and showed that manipulation was not associated with rotator cuff tears, fractures, dislocations, or nerve palsies in their cohort.

As with patients with severe osteopenia, MUA is not recommended for patients with long-term diabetes mellitus (lasting longer than 20 years) because these patients are extremely resistant to this method of treatment. In two studies with short follow-up of approximately 6 months, recurrent stiffness was reported to be between 5% and 20%. However, in a study with a longer follow-up of patients with long-term, insulin-dependent diabetes, Janda and Hawkins reported an unacceptably high rate of recurrent stiffness after MUA.

Manipulation can be performed under either regional or general anesthesia, although anesthesia with local injection combined with hydrostatic distention has also been reported. It is essential during the manipulation that complete muscle paralysis be achieved. A regional block is advantageous because the patient can witness the improved ROM immediately after surgery. The immediate postoperative pain is also eliminated, which allows immediate participation in ROM exercises. The block can be administered as a single injection or with placement of an indwelling interscalene catheter. A single block of 0.5% bupivacaine provides anesthesia for approximately 12 hours and can be repeated on postoperative days 1 and 2 for continued analgesic effect. If an interscalene block is used, the patient can be maintained on a continuous drip of bupivacaine that provides continuous pain relief during the patient’s hospital stay and substantially improves the patient’s ability to comply with the intensive physical therapy exercises postoperatively. The addition of systemic steroids has not been shown to have any lasting benefit.

Codman and Neviaser both described attaching the arm to the bed in a position of abduction and external rotation in order to maintain the motion obtained by the manipulation. This maneuver can require significant narcotic analgesia and primarily stretches the anteroinferior portion of the capsule, with the remaining sections of capsule left in a position that can lead to recurrence of the contracture. Other authors have recommended traction to stretch residual contractures and improve motion.

To perform the manipulation, the patient is placed supine on the operating room table. Complete muscular paralysis facilitates the procedure and minimizes the risk of fracture. The axillary border of the scapula is stabilized, allowing isolated glenohumeral movement. A constant controlled force is applied to the proximal end of the humerus while the scapula is kept stable; any sudden force increases the risk of fracture or injury to shoulder soft tissues. Gradual traction and flexion are carried out first until an audible and palpable release is heard and felt, indicating rupture of the inferior capsule. The arm is then manipulated into adduction across the patient’s chest to stretch or rupture the posterior capsule and restore internal rotation. We perform these manipulations first in order to minimize the theoretical risk of fracture due to the increased torque produced with the rotational movements that follow. The arm is then moved to the side of the body and is held at the supracondylar level while the forearm is rotated very gently into external rotation, taking care not to exert an excessive force that would risk elbow ligament injury. Abduction in the scapular plane is performed with additional internal and external rotation to further release the anterior and posterior capsule. Some steps may be gently repeated until ROM similar to that of the contralateral shoulder is achieved.

Charnley warned against beginning the manipulation with an abduction force because he believed that external rotation had to be achieved first to prevent dislocation. Nevertheless, many authors recommend starting with an initial abduction force. A good prognostic sign is the production of crepitus followed by immediate full ROM. If crepitus does not occur, increased force should not be applied. Repeat manipulation may be indicated if the recovered motion is not symmetrical to the opposite side or if motion loss recurs within a short period postoperatively. Some authors have reported good results with translational rather than rotational manipulative forces and recommend their application to lessen the chance of fracture.

Although its use has not been proved to enhance the outcome in patients with stiff shoulders, many authors recommended corticosteroid injections after MUA to reduce pain, diminish local inflammation, and decrease the chances of early healing of the disrupted capsule. In a study of more than 100 patients who underwent MUA, codeine was the only medication required to control pain in the immediate postmanipulation period. In a study by Weiser in which MUA was performed under a local anesthetic, there was full recovery in 60% of patients with three to five treatment sessions. In another study by Thomas and colleagues, 30 patients with frozen shoulders were randomly allocated to one of two groups, one with manipulation and intra-articular steroid injection and the other with intra-articular steroids alone. Of the patients managed with MUA and steroid injection, 80% had decreased pain at follow-up; 40% achieved good ROM, whereas only 47% of patients who received steroid alone had decreased pain, and only 13% achieved good ROM.

The reported outcomes of MUA with or without steroid injection have been highly variable. Good results have been reported in most reviews, except with the long-term diabetic population that is resistant to this treatment and is at a high risk of developing recurrences. Haines and Hargadon reported on 78 patients with a mean preoperative duration of symptoms of 2 to 6 months who underwent MUA and steroid injection. At a mean follow-up of 12 weeks, 83% of the patients regained 80% of their glenohumeral motion. Hill and Bogumill reported on 14 frozen shoulder patients with a mean preoperative duration of symptoms of 5.4 months, who underwent MUA and steroid injection. At a mean follow-up of 22 weeks, 75% of the patients were pain-free. Kivimaki and Pohjolainen reported on 24 patients who underwent either MUA alone or MUA with steroid injection and found same results in both groups at 4 months’ follow-up.

Weber and colleagues reported on 43 patients with frozen shoulder and a mean preoperative duration of symptoms of 6 months who underwent MUA along with inpatient physiotherapy. At a mean follow-up of 4.7 years, 73% of the patients had gained full recovery of function. Harmon reported on MUA in three separate follow-up studies 2 to 3 years after manipulation, in which 64% to 94% of patients achieved painless motion. Dodenhoff and colleagues reported on 37 patients with a mean preoperative duration of symptoms of 8 months who underwent MUA. They found that 94% patients were satisfied with their result, but 12.8% retained significant persistent disability.

Othman and Taylor reported on 74 patients who underwent MUA and found that significant improvement in range and comfort occurred as early as 3 weeks postoperatively. Sharma and colleagues reported on 32 patients who underwent either MUA or distention with local anesthesia and found significantly better results in the distention group. In a study by Reichmister and Friedman 97% good results were reported in patients who underwent MUA, but 8% of their patients required a second manipulation. Melzer and colleagues reported on 110 patients, comparing those who underwent physiotherapy with medication, as needed, with those who underwent MUA; they concluded that physiotherapy was better than MUA. In a study by Farrell and colleagues MUA was performed on 25 patients with frozen shoulder. The authors reported significant improvement in pain and function, which was maintained for 15 years postoperatively.

Ekelund and Rydell reported on 22 patients who underwent distention arthrography with local anesthetic and steroid followed by MUA and found that 91% of patients had no or slight pain and 83% had almost normal ROM. Similar studies have been performed with local intra-articular anesthesia and manipulation, with the authors claiming successful pain relief and recovery of motion in almost two thirds of patients, with a greater percentage of patients relieved of discomfort alone. Lundberg noted that MUA did not affect the natural history or the time course of the disease.

Manipulation and Arthroscopy

MUA usually produces capsular rupture, leading to improved motion, but does not affect intra-articular synovitis. Synovitis may be a major precipitating factor in the development of shoulder stiffness and a contributing factor leading to the recurrence of contracture. In a study by Pollock and colleagues 83% of patients with frozen shoulder who were treated with MUA and arthroscopic debridement achieved a successful result, although patients who were recalcitrant to treatment underwent additional release of the coracohumeral ligament. In a study by Andersen and colleagues 79% of patients who had MUA followed by arthroscopic debridement were pain-free, and 75% had normal ROM at 12 months of follow-up. In a recent study Rill and colleagues demonstrated that frozen shoulder patients with pain and stiffness refractory to conservative means did well following manipulation and arthroscopic release.

Open Surgical Release

Patients who have acquired stiffness resulting from contracture of the extra-articular soft tissues, such as after a Putti-Platt procedure, are unlikely to benefit from MUA. They might not be good candidates for arthroscopic release because the contracture involves both the subscapularis tendon and the capsule. Open surgical excision of the scar and release of extra-articular adhesions, with or without Z-plasty of the capsule and subscapularis tendon, may be the treatment of choice in this population.

Historically, Codman described open lysis of adhesions in the subacromial and subdeltoid bursae. In patients who experience recurrent stiffness after MUA, Neviaser found it necessary to perform an arthrotomy through an anterior axillary approach, releasing periarticular adhesions and the contracted articular capsule from the humeral head. Leffert recommended targeting the structures responsible for restricted motion with a surgical release when patients failed to improve after 6 months of a nonoperative treatment regimen. Lippman suggested the open release of adhesions around the long head of the biceps tendon to liberate the shoulder from stiffness. Simmonds proposed complete excision of the long head of the biceps tendon in cases of severe frozen shoulder. He noted no intra-articular adhesions between the surface of the joint and the articular capsule when he performed these procedures; however, the operative management that he described did not lead to improvements in ROM. Matsen and Kirby recommended open surgical release of the capsule in patients with shoulder stiffness if they failed to improve after 6 months of home exercise therapy. They found this approach to be safer than MUA for patients with osteoporosis and recalcitrant stiffness.

Harmon performed soft tissue release of contracted tissues about the joint in eight patients who failed to improve after gentle manipulation and found the outcome to be similar to that in patients who underwent closed manipulation alone, except two patients who had intractable stiffness. He also treated 30 cases of stiffness with acromioclavicular joint and acromial excision and was able to restore active abduction to around 160 degrees by the third postoperative month.

Kernwein and colleagues performed open release of the capsule and coracohumeral ligament in 4 of 12 patients with frozen shoulder. Tissues were found to be markedly thickened and inelastic. In a study by Ozaki and colleagues the authors reported their findings during the surgical release of 17 patients who had recalcitrant shoulder stiffness. They found that the contracted coracohumeral ligament in the rotator interval was the major tether restricting glenohumeral motion, and they noted that the long head of the biceps tendon was inflamed and stenosed beneath this contracted structure. Nobuhara and colleagues, who performed rotator interval capsular release on 21 shoulders and obtained remarkable improvement in ROM, also appreciated the role of the rotator interval in stiff shoulders.

In one study 25 of 75 patients who failed therapy and MUA underwent open surgical release. At surgery, the coracohumeral ligament was found to be fibrotic and contracted and was excised. Of these 25 patients, 20 achieved good or excellent results; outcomes were worse in patients with long-term diabetes.

As an alternative to the open release of contracted tissues, Baumann described denervation of the ventral aspect of the shoulder capsule, reporting that this method caused a progressive decrease in or total elimination of shoulder pain in 85% of 20 shoulders treated in this fashion. However, this is the only report about this particular technique.

Another population who develops internal rotation contracture is that of patients who had a stroke; as a result, their internal rotator muscles, including the pectoralis major and the subscapularis muscles, spasm and eventually shorten and contract. Braun and colleagues incised the pectoralis major muscle, excised the subscapularis tendon, and preserved the anterior capsule in 13 patients who had this problem. Ten of these 13 patients regained complete pain relief, 20 degrees of external rotation, and 90 degrees of abduction.

When we perform an open surgical release, our preference is to place the patient in the beach chair position. An interscalene nerve block is performed usually along with general anesthesia. Patients are admitted postoperatively for 48 hours and undergo supervised physical therapy exercises.

We favor the deltopectoral approach unless a prior incision dictates another approach. Layered dissection is performed to excise scar in all tissue planes. The shoulder is placed in abduction and slight flexion to relax the deltoid. Adhesions in the subdeltoid plane are released, taking special care not to injure the axillary nerve, which can be palpated in the substance of the deltoid 3 to 5 centimeters distal to the lateral aspect of the acromion. Once all adhesions have been removed from the subdeltoid region, the humerus may rotate freely beneath the deltoid and the dissection is extended medially to release the adhesions from the subacromial space.

Next, the interval between the conjoined tendon and subscapularis muscle is addressed. The axillary nerve is identified and protected throughout the procedure to allow thorough releases to be performed safely. Adhesions are released by a combination of blunt and sharp dissection. The subscapularis tendon is identified and the rotator interval is released from the humerus to the coracoid.

The shoulder is examined at this point to evaluate the effectiveness of the release. In patients with severe internal contractures the subscapularis tendon as well as the anterior capsule is usually shortened and scarred. In such a case, the subscapularis tendon and capsule can be released in the coronal plane using Z-plasty. With this method, the superficial half of the tendon remains attached to the muscle, and the deep half remains attached to the lesser tuberosity. Stay sutures may be placed in the superficial tendon and are used to pull on the muscle, aiding the dissection and the excision of scars tethering the subscapularis muscle to the surrounding tissues. This often requires identification of the axillary nerve and placement of a vessel loop around it to protect it. However, we rarely now perform this procedure to lengthen the tendon. Instead, a complete release of the subscapularis from the anterior glenoid neck and subcoracoid space as well as anteriorly, after identifying the axillary nerve, can achieve sufficient excursion of the tendon to restore physiologic external rotation.

The posterior and inferior capsules are released further if abduction and internal rotation are still limited. A humeral head retractor is placed to retract the head posteriorly to expose the posterior capsule, which is then released from inferior to superior. The shoulder is then placed in maximal external rotation with the arm at the side of the body, and the subscapularis is repaired in a lengthened position using large nonabsorbable braided sutures.

Once the repair is completed, the shoulder is reexamined and the safe zone of early passive ROM is determined. This information is relayed to the physical therapist who will be performing the passive ROM exercises on the patient. In postoperative rehabilitation early, passive rather than active ROM is started until soft tissue healing is substantial at around 4 weeks.

Disadvantages of open surgical release include postoperative pain and the need to protect a repaired or lengthened subscapularis tendon, which explains the less predictable results reported using this technique in patients with acquired stiffness. Many of these patients have a concomitant injury to the joint or more extensive soft tissue damage that can limit motion recovery. Successful outcomes are determined by the quality of the surrounding tissue envelope and the status of the articular surfaces.

Arthroscopic Capsular Release