Adhesive Capsulitis (Frozen Shoulder)

Codman originally coined the term frozen shoulder to describe a condition with the following signs and symptoms[11] :

• Slow-onset shoulder pain
• Localized discomfort near the deltoid insertion
• Inability to sleep on the affected side
• Restricted glenohumeral elevation and external rotation
• A normal radiologic appearance

The inclusion criteria for FSS include painful restriction of active and passive glenohumeral and/or periscapular motion.

Despite these criteria, diagnosing FSS can be controversial because there is little consensus on the specific shoulder motion restrictions or duration of symptoms needed to qualify a patient as having a frozen shoulder. Although various authors have classified patients with FSS as those with limited abduction from 45-135º, FSS is still primarily a clinical diagnosis based on clinical motion loss and symptoms.

Frozen shoulder syndrome (FSS) usually affects patients aged 40-60 years. The incidence of FSS is not precisely known; however, it is estimated that 2% to 5% of the general population[12] develops the disease over their lifetime. Men tend to be affected less frequently than women, and there is no predilection for race. In general, bilateral shoulder involvement is rarely simultaneous and instead occurs sequentially.

Diabetes mellitus is an independent risk factor for FSS. A meta-analysis by Zreik concluded that diabetic patients are 5 times more likely to develop adhesive capsulitis compared with non-diabetic controls. They reported a 13.4% overall mean prevalence of adhesive capsulitis in patients with diabetes, and a 30% mean prevalence of diabetes in a population with adhesive capsulitis. Zreik found no significant difference in the prevalence of the disorder with type 1 versus type 2 diabetes, or between patients on insulin therapy and those on oral hypoglycemic agents.[13]  

Duplay was one of the first physicians to present the concept of periarticular tissue pathology rather than periarticular arthritis as the cause of frozen shoulder.[14] Despite a lack of evidence linking frozen shoulder to a specific etiology, various triggers that may predispose patients to this problem appear to exist. A few reported etiologic agents include the following:

• Trauma
• Surgery (including but not limited to shoulder surgery)
• Inflammatory disease
• Diabetes
• Regional conditions
• Various shoulder maladies

In addition, an autoimmune theory has been postulated, with elevated levels of C-reactive protein and an increased incidence of HLA-B27 histocompatibility antigen reported in patients with frozen shoulder versus controls.[15, 16] DePalma proposed that muscular inactivity was a major etiologic factor,[17] while Bridgman identified an increased incidence of FSS in patients with diabetes mellitus.[18] Finally, frozen shoulder also has been associated with the following disorders:

• Cervical spine disease
• Parkinson disease ^[19]
• Hyperthyroidism ^[20]
• Hypothyroidism 
• Ischemic heart disease

Most patients with FSS have undergone a period of shoulder immobilization. Reasons for immobilization can be diverse; however, the common finding in all of these patients is a period of restricted shoulder motion. In a study of neurosurgery patients who immobilized their shoulders for varying periods, Bruckner noted an incidence of frozen shoulder that was 5-9 times greater than that found in the general population.[21]

Prior to examining the patient, a thorough clinical history should be elicited. Specifically, information should be gathered regarding the following:

• Onset of symptoms
• Any antecedent trauma or surgery
• Affected side(s)
• Duration of symptoms

The patient should also be queried about any existing medical conditions, particularly diabetes mellitus, thyroid disease, Parkinson disease, stroke, and heart disease. Given the strong association of adhesive capsulitis with diabetes, it is imperative to screen any new patient presenting with possible frozen shoulder syndrome for diabetes or prediabetes.[22] Adhesive capsulitis has also been reported in patients with hyperthyroidism, hypothyroidism, and ischemic heart disease. Questions should be directed toward any upper extremity neurologic complaints, including cervical radiculopathy. Any history of cervical pain or radiculopathy should be thoroughly evaluated during the clinical examination to exclude a diagnosis of cervical spondylosis or cervical disc disease.

Any previous treatments that the patient has received for their condition should be documented, as should the individual's current medication list.

Refractory shoulder periscapular pain and limited glenohumeral motion that persists despite attempted conservative treatment are indications for surgery. Conservative treatment can include the following:

• A course of prednisone[23]

• A course of a nonsteroidal anti-inflammatory drug when not on prednisone

• A subacromial or glenohumeral intra-articular injection at least once but not more than twice within a 3-month period

• Physical therapy for range of motion of the shoulder[24, 25, 26]

• A physician-directed home therapy program has been shown to have efficacy in helping restore range of motion[27]  

Critical to the understanding of frozen shoulder syndrome is the concept that shoulder function involves not only the glenohumeral joint but also scapulothoracic articulation. Clinicians must understand the essential role that the scapula plays in facilitating glenohumeral motion. Scapulothoracic and glenohumeral motion occur simultaneously following initial arm abduction. In healthy individuals, approximately one third of arm elevation in abduction is attributed to scapulothoracic motion, while two thirds is provided by glenohumeral motion.

The glenohumeral joint is enclosed by the joint capsule and is surrounded by two sleeves of muscles. The capsule normally is a loose structure with a surface area nearly twice as large as that of the humeral head. The rotator cuff tendons adjacent to the joint capsule thicken the capsule anteriorly, posteriorly, and superiorly, while the glenohumeral ligaments represent further areas of joint capsule thickening.

Histologically, the capsule consists of bundles of type I collagen. Synovial cells line the inner surface of the capsule and enclose the long head of the biceps tendon.

Contraindications to surgical intervention for recalcitrant frozen shoulder include the following:

• Concomitant neurologic complaints or abnormalities originating from the cervical spine

• An inadequate trial of conservative therapy (< 3 mo)

• Ongoing infection of any type[28]

• Isolated capsular release in the face of adhesive capsulitis and concomitant glenohumeral arthritis (in this situation, capsular release or lengthening should be performed in conjunction with total shoulder arthroplasty)

• An ongoing oncologic process involving the affected shoulder

Immune, inflammatory and fibrotic changes appear to be involved in the pathophysiology of FSS.[29] The current hypothesis posits inflammation in the joint capsule[30]  followed by development of adhesions and fibrosis of the synovial lining.[31] Thickening and contraction of the glenohumeral joint capsule and formation of collagenous tissue surrounding the joint reduces joint volume. 

Biomarkers in synovial fluid suggest chronic inflammation is present.[32] The following markers have been identified in FSS[33, 34] :

• Intercellular adhesion molecule–1 (ICAM-1; CD54)
• Transforming growth factor–beta (TGF-β)
• Tumor necrosis factor–alpha (TNF-α)
• Interleukin-1 (IL-1) alpha and beta
• IL-6
• Platelet-derived growth factor (PDGF)

Matrix metalloproteinases are involved in the construction of extracellular matrix and in the various cytokines that control collagen deposition. Drugs that inhibit matrix metalloproteinase can induce conditions very similar to FSS and Dupuytren disease.[12]

Following the synovial inflammatory process, a high number of fibroblasts and myofibroblasts suggest a fibrotic process in the capsule. The condition is thought to result from progressive fibrosis and eventual contracture of the capsule of the glenohumeral joint, which causes pain and stiffness.[34, 35]

Microvascular diseases such as diabetes mellitus may cause abnormal collagen repair, which predisposes patients to FSS.[36] Increased glycosylation of collagen protein and increased formation of abnormal glycation end products and their subsequent accumulation have a detrimental effect on cellular and extracellular processes that might facilitate adhesion and fibrosis.[37] Neovascularization with vascular endothelial growth factor (VEGF) staining has also been identified in diabetic tissue samples.[12]

FSS has a favorable natural history. It is generally a self-limiting condition that can be treated with physical therapy and typically resolves in 1-3 years.[38]  Time to recovery does not differ between primary and secondary FSS. No difference in pain and disability of FSS in patients with and without diabetes has been reported.[39]  Patients with FSS do not have a lower shoulder activity level than sex- and age-matched controls.[40]  

However, several studies have demonstrated long-term pain and shoulder stiffness following conservative treatment. Long-term disability has been reported in 15%,[8]  permanent functional loss in 7-15%, and persistent symptoms in 40%.[41]

Patients in the initial (freezing) stage of frozen shoulder syndrome (FSS) will describe the following:

• Insidious onset of vague, dull pain at the deltoid insertion
• Pain with shoulder movement
• Nagging pain at night, with sleep deprivation and the inability to sleep on the affected side
• Marked limitation of active and passive shoulder rotation, particularly external rotation

The pain of FSS can be described as dull or aching.  The pain leads to significant disability, affecting the activities of daily living, work, and leisure.[31]

During the second (frozen) stage, patients will complain of stiffness and severe loss of shoulder motion. The pain will be less pronounced. Patients will endorse the inability to reach over their head, to their side, and across their chest with the affected arm, or to scratch their back or put on a coat. The contralateral shoulder often becomes symptomatic years after FSS develops in the first shoulder.[12]

The patient's posture should be observed while he or she is wearing a gown and sitting on a stool. The examiner should note whether the patient is listing to one side because of pain, or holding the neck to one side because of spasm or pain. Such initial observations help determine whether a cervical condition may be contributing to the patient's symptomatology.

On examination, the patient will have tenderness at the deltoid insertion and over the anterior capsule and posterior capsule with deep palpation. Compensatory scapulothroacic motion can create pain around the medial scapula. Forward flexion, abduction, and internal and external rotation of the shoulder should be assessed. Active and passive range of motion at the glenohumeral joint will be reduced, compared with the unaffected shoulder. Limitation of external rotation and abduction will be the most prominent findings.

Frozen shoulder syndrome (FSS) is a clinical diagnosis. Laboratory and imaging studies can be used to rule out other conditions and to confirm the likelihood of the correct diagnosis. Accurate diagnosis is essential because the treatment for FSS differs from the treatment for other shoulder entities. 

Laboratory studies rarely are required for the evaluation of adhesive capsulitis. However, if a predisposing medical condition that may be contributing to adhesive capsulitis is suggested, the following tests may be ordered:

• Complete blood cell count (CBC)
• Erythrocyte sedimentation rate (ESR)
• C-reactive protein (CRP)
• Blood glucose
• Hemoglobin A1c 
• Thyroid-stimulating hormone (TSH)
• Free thyroxine index (FTI)
• Free thyroxine (FT4)

Although an orthopedic surgeon may order these tests, results should be forwarded to the patient's primary care physician for further evaluation.

Imaging studies are not indicated in the diagnosis of FSS. No imaging modality has been definitively shown to provide greater diagnostic value, due to the heterogeneity of techniques used, and the presence of potential confounding factors limits definitive conclusions from imaging study findings. However, more recent studies are moving toward defining the criteria for imaging studies to aid in the staging of FSS. Common findings in FSS are thickening of the coracohumeral and inferior glenohumeral ligaments. Zappia et al notes that imaging may be used to exclude articular or rotator cuff pathology, that thickening of the coracohumeral and inferior glenohumeral ligaments are common findings in FSS, and that rotator interval fat pad obliteration has 100% specificity for adhesive capsulitis.[42]

Radiography

Routine radiographs do not have a role in the diagnosis of FSS. However, plain films of the shoulder should be obtained in all cases to rule out any other pathologic process. These radiographs should include the following[43] :

• Anteroposterior (AP) view of the glenohumeral joint in neutral rotation
• Supraspinatus outlet view
• Axillary lateral view (if possible)

Ultrasonography

Ultrasound (regular and Doppler) for the diagnosis of FSS remains controversial. Overall, these studies have shown utility for measurement of acohumeral ligament thickness and presence of a hypoechoid region with increased vascularity in the rotator interval, with fibrovascular inflammatory tissue. 

Arthrography

Arthrography, which involves intra-articular injection of diluted iodinated contrast medium, can aid in both the diagnosis and treatment of FSS. The following findings are suggestive of FSS[42] :

• Reduced capsular distention, with irregular internal profile and internal septa (medial leakage of contrast)
• Lack of distention of subscapular bursa
• Atypical contrast leakage in the biceps sheath

Milena et al report that the findings on computed tomography (CT) arthrography are comparable to those on magnetic resonance imaging (MRI). Diagnostic signs are decreased width of the axillary recess and thickening of the lateral wall.[44]

Positron emission tomography/computed tomography

Duchstein et al suggest that 18-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) may have a role in diagnostically challenging cases, such as distinguishing the first phase of frozen shoulder from subacromial impingement. Their study in 20 patients, found that, in general, patients with frozen shoulder showed increased FDG uptake in the affected shoulder regions, whereas those with subacromial impingement showed no uptake. Combining visual assessment with semi-quantified analysis resulted in sensitivity of 100% and specificity of 93% for the distinction between the two disorders.[45]

Magnetic resonance imaging

MRI is not initially indicated in cases of FSS. However, if the patient does not improve after a period of time (6 weeks to 3 months), then MRI is appropriate to rule out a possible rotator cuff tear or intra-articular pathology.[46, 47]  Chi et al concluded that non-contrast MRI (ie, without direct MRI arthrography), in conjunction with clinical criteria, can support accurate diagnosis of FSS.[48] However, a study by Erber et al found that the addition of contrast-enhanced sequences can significantly increase the sensitivity of MRI for this diagnosis.[49]

A 2018 systematic review and meta-analysis identified six features on non-arthrogram MRI that may be used to diagnose FSS, as follows[50] :

• Coracohumeral ligament thickening (diagnostic odds ratio [DOR] 13)
• Fat obliteration of the rotator interval (DOR 8)
• Rotator interval enhancement (DOR 44; sensitivity and specificity > 80%)
• Axillary joint capsule enhancement (DOR 52; sensitivity and specificity > 80%)
• Inferior glenohumeral ligament hyperintensity (DOR 31)
• Inferior glenohumeral ligament thickening (DOR 28)

Zappia et al hypothesize that the high pericapsular signal intensity corresponds to hypervascular synovitis during the frozen phase of FSS.[42]  Park et al have correlated MRI findings with the clinical stage of FSS; see Table 2, below.[51]

Table 2 MRI findings according to clinical stage of FSS (Open Table in a new window)

Common arthroscopic findings in patients with adhesive capsulitis are the following:

• Proliferative synovitis
• Capsular and intra-articular subscapularis tendon thickening
• Fibrosis
• Chronic inflammatory cells

Significant synovitis is noted mostly in the anterior capsule, but is not limited to that area. In addition, most patients demonstrate significant subacromial fibrosis. One study found that approximately 40% of patients had significant subacromial fibrosis, regardless of preoperative etiology.

The goals of treatment for frozen shoulder syndrome (FSS) are to relieve pain and restore movement and shoulder function. FSS is self-limiting; long-term outcomes are essentially the same, regardless of the treatment used.[41, 22]

Physiotherapy and home exercise are first-line treatments for all stages of FSS.[12, 52]  These are often combined with anti-inflammatory medications and glenohumeral joint corticosteroid injection.[53]

Most patients with adhesive capsulitis are treated nonoperatively; more than 90% respond to conservative interventions to control pain and restore motion. Invasive options for refractory cases include extracorporeal shockwave therapy, manipulation under anesthesia, hydrodilatation (hydrodistention), and selective arthroscopic capsular release.

Idiopathic adhesive capsulitis affecting the glenohumeral joint is believed to be self-limiting and is often treated effectively with physical therapy and anti-inflammatory medications. However, studies on the natural history of the condition have noted long-term pain in many patients who receive nonoperative treatment, with as many as 10% of patients never fully recovering normal shoulder activities.[31, 54]

Nonsteroidal anti-inflammatory drugs

Various authors have reported an inflammatory component to frozen shoulder syndrome, especially early in the course of the disease. Therefore, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful in patients with recent-onset symptoms. With diminished inflammation and pain, the patient is better able to tolerate physical therapy. Before prescribing any medication, however, the clinician should query the patient about any contraindications to NSAIDs.

NSAIDs have not demonstrated great efficacy in individuals who present with prolonged symptoms. They have not been shown to improve pain or function compared with placebo.[12]

Oral glucocorticoids

Oral corticosteroids can be prescribed in lieu of NSAIDs, as they provide a stronger anti-inflammatory effect, however they should not be given routinely due to their potential adverse effects. The use of low-dose oral corticosteroids is recommended only in cases of severe refractory frozen shoulder that has either been present for an extended period (ie, longer than 2 months) or is causing significant pain.[13, 55, 56] Although oral corticosteroids provide significant short-term benefits, the effect may not be maintained beyond 6 weeks.[57]

Due to the potential adverse effects of corticosteroids, the patient should be thoroughly questioned regarding past medical history, including diabetes mellitus. Diabetes mellitus is not an absolute contraindication to the use of oral corticosteroids, but given the potential hyperglycemic effects of corticosteroids, these agents should be used judiciously and the patient's blood glucose should be closely monitored.  

Oral steroids are typically given in a 3-week tapered course of prednisone, although treatment may range from 2-6 weeks.[57] See Table 3, below.

Table 3. Prednisone Dosing in Patients With Refractory Frozen Shoulder Syndrome (Open Table in a new window)

Corticosteroid injections

A local corticosteroid injection can be used in conjunction with oral NSAIDs or oral corticosteroids.[58, 59]  Studies have shown 20 mg triamcinolone as an optimal dose.[22] The corticosteroid may be combined with a local anesthetic (eg, lidocaine). Intra-articular or subacromial injections have equal efficacy.[60] Corticosteroid injections provide rapid relief that typically lasts for 6 weeks. Long-term outcomes are similar to those with placebo.[34]

A randomized trial that compared ultrasound (US)-guided injection with blind injection found that by the second week postinjection, improvement in pain intensity, range of motion, and shoulder function score was significantly greater in the US-guided injection group than in the blind injection group. Beyond the third week, however, there were no further significant differences in the improvement between the 2 groups.[61]

Adverse effects must be considered. Triamcinolonone injections can result in Cushing syndrome in patients on protease inhibitors (ritonavir/norvir). Administer injections with caution in patients who have diabetes.[62]

Extracorporeal shockwave therapy (ESWT) shows promise as a therapy for adhesive capsulitis.[63] ESWT compared favorably with oral steroids as a short-term treatment for primary adhesive capsulitis in a prospective, randomized, controlled, single-blind clinical trial by Chen et al in 40 patients. From the fourth week of treatment, the ESWT group showed significant improvement superior to that in the steroid group; at the sixth week, improvement in activities of daily living (ADL) achieved significance and was better than that in the steroid group.[64]

Results of an observational study by Santoboni and colleagues suggest that ESWT may offer a safer alternative to steroid injections or surgery for treatment of adhesive capsulitis in patients with diabetes. In their study, which included 50 consecutive patients with an overall mean pain duration of 15.7 months, significant functional improvements compared with baseline were evident at 2 months, with further amelioration at 4 and 6 months.[65]

All patients received ESWT once a week for 3 weeks, with 2400 shots in an anterior-to-posterior direction on the anterior shoulder joint using a low/moderate-energy flux density (0.06–0.14 mJ/mm2, depending on individual pain tolerance). No relevant adverse effects were reported.[65]

A subgroup of patients with frozen shoulder syndrome fail to improve despite treatment with aggressive nonsurgical therapy and medication. These patients frequently are referred to as having a refractory or recalcitrant frozen shoulder. Specifically, these patients demonstrate minimal improvement in shoulder pain and motion over a 3-month period, despite the use of aggressive nonoperative measures, including medications and physical therapy. In these refractory cases, more invasive techniques (eg, manipulation under anesthesia, hydrodilatation, surgical release) may be needed.

Manipulation under anesthesia

Manipulation of frozen shoulders under general anesthesia is intended to rupture the contracted capsule, and in some studies it has been shown to accelerate healing.[66] This technique has been combined with other modalities, including local corticosteroid injection, hydrodistention,[67] and limited capsular release.[68] Significant complications have been reported, however, ranging from humeral shaft fractures to rotator cuff tears and transient brachial plexus injuries.[66]

Hydrodilatation

Hydrodilatation (also termed hydrodistention and distention arthrography) involves the ultrasound-guided injection of a large volume of saline—typically along with a corticosteroid, local anesthetic, and contrast medium—into the joint space.[66] The therapeutic effect of hydrodilatation was initially attributed to rupture of the capsule, but capsular distention may in fact be the mechanism.[66]

Studies of hydrodilatation have yielded conflicting results, especially with regard to patients with diabetes mellitus. For example, a systematic review and meta-analysis concluded that hydrodilatation has only a small, clinically insignificant effect on adhesive capsulitis.[69] On the other hand, the largest single study, in 109 shoulders, concluded that hydrodilatation is effective, although patients with severe cases and those with diabetes tended to respond less well in the long term.[70] A study of 90 patients who underwent hydrodilatation after failure of initial treatment that included physiotherapy and at least one corticosteroid injection reported clinically important improvements in pain and function that remained clearly substantial at 24 weeks.[71]

Arthroscopic capsular release

Ogilvie-Harris et al and Warner et al have demonstrated the efficacy of arthroscopic capsular release for the refractory frozen shoulder.[72, 73, 74] Based on these reports and work by others, a selective arthroscopic capsular release is recommended for patients with refractory frozen shoulder.[75]

Once the patient is under anesthesia, a detailed preoperative assessment of the affected and unaffected shoulder's passive ROM is performed. Typically the affected shoulder exhibits global loss of motion, with the contracture affecting the entire capsule.

Standard arthroscopic shoulder portals are established. Based on the preoperative examination, the glenohumeral joint capsule is released with electrocautery, as seen in the image below. Typically a circumferential capsular release is performed. Ahn et al developed an ultrasound-guided interventional release of the rotator interval using a round needle designed specifically for this procedure. All 13 patients experienced significant improvement.[76] Care is taken to avoid any release of the intra-articular subscapularis tendon. Before the patient is taken from the operating room, the shoulder ROM is documented and compared with the presurgical ROM.

True anteroposterior view of the glenohumeral joint (left); axillary lateral view (middle); supraspinatus outlet view (right)

With 24-48 hours of postoperative pain relief provided by a preoperative interscalene block, ROM exercises should be initiated on the day of surgery. An interscalene catheter can be placed when performing the interscalene block to allow for an extended period of pain relief. A 2-week course of oral corticosteroids also should be initiated on the day of surgery.

A review by Miyazaki et al of surgical treatment in 56 shoulders with FSS concluded that that inferior capsulotomy yields the best results. In addition, these authors reported lower reoperation rates in patients who receive interscalene catheter anesthetic infusion for postoperative rehabilitation.[77]

Further inpatient care is indicated only in refractory patients. Patients receiving arthroscopic or open capsular release frequently remain in the hospital for several days to permit interscalene anesthesia and aggressive, monitored physical therapy. However, patients rarely have to return to the hospital following the initial surgery.

A small number of patients with adhesive capsulitis relapse, despite surgical intervention and physical therapy. Admitting these patients for interscalene anesthesia and aggressive physical therapy may be appropriate.

Most patients with adhesive capsulitis use either an anti-inflammatory medication or a short course of an oral corticosteroid. Occasionally, patients may require medication for pain. A chronic-pain medication such as gabapentin or amitriptyline is preferred for these symptoms.

Patients with adhesive capsulitis—those who have been treated with conservative therapy and those who have had surgical intervention—should be closely monitored as outpatients. Usually, supervised or home physical therapy is a component of treatment. In addition, the patient may be taking oral corticosteroids, and so require monitoring for adverse effects. The patient should be assessed every several weeks to document progress.

The patient should be seen at 2-week intervals for the first month after surgery. Thereafter, follow-up intervals can be increased from 6 weeks to 3 months, as needed.

The predominant complication arising from adhesive capsulitis is residual shoulder stiffness or pain. Several reports have indicated that most patients may continue to have pain and/or stiffness for up to 3 years following conservative treatment. In addition, humeral fracture, biceps tendon rupture, and subscapularis tendon rupture have been reported after shoulder manipulation.

FSS has a favorable natural history. It is generally a self-limiting condition that can be treated with physical therapy and typically resolves in 1-3 years.[38] Time to recovery does not differ between primary and secondary FSS. No difference in pain and disability of FSS in patients with and without diabetes has been reported.[39] Patients with FSS do not have a lower shoulder activity level than sex- and age-matched controls.[40]

However, several studies have demonstrated long-term pain and shoulder stiffness following conservative treatment. Long-term disability has been reported in 15%,[8] permanent functional loss in 7-15%, and persistent symptoms in 40%.[41]

Several studies have noted improved symptoms following arthroscopic capsular release, as follows:

• Warner and colleagues reported an improvement in the Constant and Murley score of 48 points with a mean follow-up of 39 months. ^[78]
• Pearsall and colleagues found that 83% of patients reported their shoulder to be normal or near normal at an average of 22 months following capsular release. ^[79]
• Ogilvie-Harris noted that 15 of 18 patients treated with arthroscopic capsular release had an excellent result at 2-5 years following surgery.
• A review of the literature indicates that in patients with refractory adhesive capsulitis, a near-excellent to excellent result in 75-90% of cases can be expected in patients treated with arthroscopic capsular release and an aggressive postoperative physical therapy regimen.

Possible alternative treatments for frozen shoulder syndrome (FSS) include the following:

• Other interventions that can be combined with physiotherapy include suprascapular nerve blocks, which may increase patients' pain tolerability for effective mobilization,[80] and ultrasound deep heat therapy, which may help improve patients' pain scores.[81]

• A randomized controlled double-blind study of acupuncture (using press tack needles) integrated with conservative therapy in 60 patients with primary FSS reported immediate pain reduction; subsequently, classical needle acupuncture treatments over 10 weeks produced faster improvement in pain compared with conservative therapy only.[82]  This approach may be beneficial in the early painful stages of the disease. 

• Preliminary reports indicate a benefit from intra-articular injection of platelet-rich plasma.[83, 84, 85]

• In a randomized study in 29 patients with early FSS that compared the efficacy of different intra-articular injections, the combination of a low-dose corticosteroid (triamcinolone, 20 mg) with hyaluronidase (1 mL) proved superior to that of low-dose corticosteroid alone and equivalent to that of high-dose corticosteroid (triamcinolone, 40 mg).[86]

• Collagenase clostridium histolyticum (CCH) is an injection treatment that is approved by the US Food and Drug Administration for Dupuytren contracture in adult patients with a palpable cord. An early trial in patients with FSS found that extra-articular injections of CCH were well tolerated and effective compared with exercise. ^[87] In a subsequent trial, however, CCH injection failed to provide a statistically significant improvement in function, and the authors recommended against its use for FSS, in view of its adverse effects and potential risks. ^[88]

Any of the following instruments can be used for long-term monitoring:

• Shoulder Pain and Disability Index (SPADI)
• Simple Shoulder Test (STT)
• Constant-Murley Shoulder Score (CMS)
• Oxford Shoulder Score (OSS)
• Visual Analogue Scale (VAS) 
• UCLA shoulder scale