Adhesive capsulitis (AC), is also known as frozen shoulder an insidious painful condition of the shoulder persisting more than 3 months. This inflammatory condition that causes fibrosis of the glenohumeral joint capsule is accompanied by gradually progressive stiffness and significant restriction of range of motion (typically external rotation). However, the patients may develop symptoms suddenly and have a slow recovery phase. The recovery is satisfying in most of the cases, even though this may take up to 2 to 3 years. 
The etiology of frozen shoulder is not yet fully understood. However, some plausible risk factors have been identified:
Frozen shoulder is usually described as fibrotic, inflammatory contracture of the rotator interval, capsule, and ligaments. However, the development of AC remains not fully understood. Although disagreements exist, the most recognized pathology is cytokine-mediated synovial inflammation with fibroblastic proliferation based on arthroscopic observations. Additional findings include adhesions around the rotator interval caused by increased collagen and nodular band formation.
The structure usually affected first is the coracohumeral ligament the roof of the rotator cuff interval. Contraction of the coracohumeral ligament limits external rotation of the arm, which is usually first affected in early AC. In advanced stages, thickening and contraction of the glenohumeral joint capsule develop, further limiting the range of motion in all directions.
The studies of histopathology for the glenohumeral capsule have confirmed a significant increase in fibroblasts, myofibroblasts, and inflammatory cells, like B-lymphocytes, mast cells, and macrophages.
Patients suffering from early AC usually present with a sudden onset of unilateral anterior shoulder pain. The typical symptoms comprise passive and active range of motion restriction, first affecting external rotation and later abduction of the shoulder. In general, depending on the stage and severity, the condition is self-limiting, interfering with activities of daily living, work, and leisure activities. Functional impairments caused by frozen shoulder consist of limited reaching, particularly during overhead (e.g., hanging clothes) or to-the-side (e.g., fasten one's seat belt) activities. Patients also suffer from restricted shoulder rotations, resulting in difficulties in personal hygiene, clothing and brushing their hair. Another common concomitant condition with frozen shoulder is neck pain, mostly derived from overuse of cervical muscles to compensate the loss of shoulder motion.
The physical findings are essential for a frozen shoulder diagnosis, although pain and stiffness make it difficult for patients to comply with a complete set of physical examination.
Two physical examinations are commonly used for diagnosing AC, including tests of combined motion, as touching the scapula from behind the neck and from behind the back.
However, the most pathognomonic feature for AC is a loss of passive ROM. Practically, in cases of significant restriction of passive ROM, an examination of active motion can be skipped. Nevertheless, as an undetectable limitation of shoulder motion may be present in the early stage, AC diagnosis should be reconsidered in patients who present with a gradual restriction of range of motion at follow-ups.
In general, patients with frozen shoulder usually demonstrate significant restriction in active and passive range of motion, particularly in external rotation and abduction movement. Restricted motion in every direction not only indicates the presence of a developed frozen shoulder, but it may be a “red flag” for possible underlying malignancy or fracture.
Frozen shoulder is a clinical diagnosis made by medical history, physical examination, and imaging modalities (ruling out another condition, rather than confirming the diagnosis of AC). No specific test (laboratory or imaging) alone provides the definitive confirmation of the AC diagnosis.
Diagnostic imaging of AC can be challenging because as the findings based on currently available methods (such as radiographs, ultrasound, plain magnetic resonance imaging, and computed tomography) are usually unremarkable. Imaging is therefore limited to ruling out concurrent pathologies, like rotator cuff tendon tears and glenohumeral joint osteoarthritis. The imaging tool mostly applied to patients with AC is high-resolution musculoskeletal ultrasonography (MUS), which has emerged to be the first line to scrutinize shoulder pathology. Nevertheless, until now, there is lack of specific ultrasound findings for diagnosis of AC. To be more comprehensive, several investigators reported thickening of the coracohumeral ligament to be a sonographic characteristic in patients with AC. Another commonly referred ultrasound finding is the presence of fluid accumulation around the long head of the biceps tendon. Although biceps peri-tendinous effusion is prevalent in shoulders with AC, it is specific to AC because it might be a result of other shoulder pathology (e.g., rotator cuff disorders or biceps tenosynovitis). Furthermore, ultrasound is less useful in the pathology associated with instability or SLAP (superior labrum anterior posterior) lesion. A plain radiograph is of limited diagnostic values in patients with frozen shoulder. Nevertheless, it is reasonable to obtain routine shoulder radiographs to rule out other etiologies (e.g., tumors, acromioclavicular and glenohumeral osteoarthritis). MRI may show thickening of the coracohumeral ligament and glenohumeral joint capsule. MRI arthrography may show a volume reduction of the joint space.
The “lidocaine test” is subacromial injection test that may be helpful in establishing the diagnosis in ambiguous clinical scenarios, to rule out subacromial conditions. In patients with AC, passive movement limitation persists after injection of local anesthetics into the subacromial space. On the other hand, patients suffering from subacromial impingement syndrome (e.g., pathology of the rotator cuff or bursa) usually experience improved passive range of motion after injection. The injection can easily be performed with ultrasound guidance.
Despite the number of published literature on the AC, there is no consistent consensus about management of AC. The majority of treatment options for AC are non-operative and include pharmacological management and physical therapy.
Early Frozen Shoulder
An early stage of AC is often managed as subacromial pathology. The early “freezing” AC mentioned above can be considered as inflammatory. On the other hand, the inflammation becomes less accentuated in the later stages, where ROM limitation is predominant, and inflammation-related pain is not as much pronounced. In the light of above differences, we must consider the disease stage when planning the treatment strategy. The correct recognition of the clinical stage may help tailor treatment plans more specifically. The aim of treatment in the “freezing” stage should focus on pain control, reduction of inflammation and patient education. Initial treatment options for adhesive capsulitis may include acetaminophen or NSAID. Although evidence regarding NSAID for the treatment of frozen shoulder is limited, they can be prescribed to provide short-term relief from the night pain if present. However, in severe cases, opioid analgesics may be required. Physical therapy is important for pain control and restoration of normal shoulder mobility. Those comprise manual therapies based on soft tissue mobilization and gentle stretching. Regarding physical modalities, no particular agent has shown to be superior. The patient can be prescribed, e.g., therapeutic ultrasound, cryotherapy or transcutaneous electrical nerve stimulation (TENS) unit. Physical therapy management should focus on therapeutic exercise. Although not all patients can tolerate mobilization exercise within the initial stage of the frozen shoulder due to severe pain, a supervised therapeutic exercise should be conducted to slow down ROM restriction. Furthermore, a home exercise program should be given to the patients on a daily basis. In patients suffering from moderate to severe pain who are not responsive to non-operative treatments, intra-articular injection of corticosteroid should be considered. The injection should be performed under ultrasonographic or fluoroscopic guidance to ensure the correct needle placement. Last but not least, rehabilitation exercise should be prescribed after injection.
Developed Frozen Shoulder
After the inflammation-related painful period subsides, the condition progresses to a “frozen” and subsequently into a “thawing” phases. Treatment objectives in the advanced stages should focus on regaining ROM limitation. The physical therapists should provide more intensive (compared, e.g., to subacromial pathologies) mobilization exercise to restore joint mobility. In patients who do not respond well to non-operative treatments, a more invasive therapy should be considered. The addition of suprascapular nerve or interscalene brachial plexus blockage may result in further improvement. In patients with refractory cases of frozen shoulder who do not improve after 6 months of non-operative treatment, more aggressive treatments such as capsular hydrodilatation (stretching the joint capsule by the saline injectate pressure), manipulation under anesthesia (tearing of the contracted capsule), and arthroscopic capsular release (particularly in the rotator interval) can be considered.
Adhesive capsulitis, particularly in early (freezing) stage might be a diagnostic challenge as it may mimic subacromial pathology and rotator cuff tendinopathy. Presentations mentioned above may result in the delay in diagnosis of AC in the early phases. Regarding shoulder impingement and rotator cuff pathology, patients report predominantly pain with less pronounced passive range of motion. However, several facets help to distinguish frozen shoulder from other shoulder disorders. Regarding the causes other than AC, patients often state lifting a heavy object or performing repetitive overhead movements. In contrast, frozen shoulder patients usually describe spontaneous onset without an apparent cause or a history of overuse activity. Extra precaution should be paid in case of the history of malignancy.
Common conditions that may mimic early adhesive capsulitis:
Later in the course of frozen shoulder, as severe restriction of motion comes to predominate, the diagnosis becomes more apparent. However, glenohumeral joint arthritis should also be considered, which can be ruled out by free shoulder movement following lidocaine injection to the glenohumeral joint.
Age of onset provides additional clues to diagnose AC. Frozen shoulder is unlikely in patients younger than 40 years of age, and patients older than 70 are more likely to develop rotator cuff tears or glenohumeral osteoarthritis instead of AC.
Gradual restriction of passive shoulder motion characterizes a natural course of AC. The development is commonly described as progressing through 3 overlapping phases (4 stages classification can also be found in the literature). However, from a practical point of view, we recommended using 2-stage scheme: early and developed frozen shoulder.
An initial, painful phase with predominant pain that is worse at night, with gradually increased glenohumeral joint ROM restriction.
The second phase with stiffness and persisted glenohumeral joint motion limitation, but with less pain than that at the “Freezing” stage.
The third (recovery) phase with the gradual return of range of motion.
The duration of AC is from 1 to 3.5 years with a mean of 30 months. In about 15% of patients, the contra-lateral shoulder becomes affected within 5 years.
Considering the diagnostic accuracy of frozen shoulder, researchers should keep investigating the pathomechanism of AC. Some studies have recently reported the application of contrast-enhanced ultrasonography in the diagnosis of frozen shoulder. Application of the microbubble-based ultrasound contrast agents (increasing a liquid substance echogenicity) in musculoskeletal medicine has already been adopted for selected indications. Looking ahead, the utility of contrast agents in a frozen shoulder diagnosis seems to be promising particularly in ambiguous cases.
The management of frozen shoulder is usually done by a team of healthcare professionals that include the orthopedic surgeon, a rehabilitation specialist, and a pain consultant. In addition, the pharmacist must educate the patient on the management of pain. In addition, patients managed with corticosteroids will need to be monitored for adverse side effects of the drug. For most patients, enrolling in a physical therapy program is the key to recovery. Some patients may benefit from supervised home physical therapy. Finally, patients have to be told that recovery will occur but it is gradual and may take several years. (Level V)
Frozen shoulder does recover in most people but the recovery may take 1-3 years. In most cases, physical therapy and arm exercise will gradually result in diminishing symptoms. So far, data do not show that diabetics have worse outcomes compared to non-diabetics. About 10% of patients will have residual shoulder stiffness and disability. After arthroscopic surgery, there is a gradual improvement in symptoms with slow recovery. However, postoperative physical therapy is a must after surgery to ensure recovery. (Level V)