Adhesive capsulitis and frozen shoulder syndrome (FSS) are two terms that have been used to describe a painful and stiff shoulder. The loss of passive range of motion (ROM) is a critical element in establishing the diagnosis of a true frozen shoulder. Although conditions such as subacromial bursitis, calciifc tendinitis, and partial rotator cuff tears can be associated with significant pain and loss of active ROM, passive ROM is preserved. Therefore, patients with those conditions should not be classified as having a frozen shoulder. Most patients with frozen shoulder can be managed with conservative treatments including regular shoulder exercises and oral analgesia. Suprascapular nerve block and Suprascapular nerve ablation techniques may be employed in patients who fail to respond to conservative measures.
At Pain Spa Dr Krishna is very experienced in interventional treatments. Dr Krishna always performs shoulder injections and suprascapular nerve block under ultrasound guidance for greater accuracy and improved safety. Ultrasound gives the added advantage of visualizing the surrounding tendons and muscles, which can be contributory to pain.
The prevalence of shoulder pain has been reported to be between 2.4% and 26%. Primary adhesive capsulitis is reported to affect 2% to 5.3% of the general population. The prevalence of secondary adhesive capsulitis related to diabetes mellitus and thyroid disease is reported to be between 4.3% and 38%.
The glenohumeral joint is a synovial joint containing a syno- vial membrane lining the interior joint capsule and encasing the long head of the biceps tendon into the biceps groove. The glenohumeral capsule, coracohumeral ligament, and gleno- humeral ligaments (superior, middle, and inferior) comprise the capsuloligamentous complex. This complex surrounds the glenohumeral joint inserting onto the humerus (superior to the lesser tuberosity and surgical and anatomic necks), from the coracoid and glenoid rim via the labrum and glenoid neck. The capsuloligamentous complex and rotator cuff tendons create an intimate static and dynamic constraining sleeve around the glenohumeral joint.
The rotator cuff interval forms a triangular-shaped tissue bridge between the anterior supraspinatus tendon edge and the upper subscapularis border. The rota- tor cuff interval is primarily composed of the superior glenohumeral ligament and the coracohumeral ligament.
Adhesive capsulitis is marked by the presence of multiregional synovitis, consistent with inflammation, yet focal vascularity and synovial angiogenesis (increased capillary growth) rather than synovitis are described by others. Accompanying angiogenesis, there is evidence of new nerve growth in the capsuloligamentous complex of patients with adhesive capsulitis, which may explain the heightened pain response. Regardless of the synovial pathology being angiogenesis or synovitis, significant pain can result at rest or with motion.
Significant capsuloligamentous complex fibrosis and contracture are consistently observed upon open or arthroscopic shoulder surgery and histologic examination. The entire capsuloligamentous complex can become fibrotic, but the rotator cuff interval and specifically the capsuloligamentous complex are predominantly involved. The rotator cuff interval is part of the anterosuperior complex, which functions as a superior hammock. With the arm at the side, the anterior limb restricts external rotation while the posterior limb restricts internal rotation. Coracohumeral ligament release in patients with adhesive capsulitis resulted in a dramatic increase in shoulder external rotation motion. Others have noted significant subacromial scarring, loss of the subscapular recess, inflammation of the long head of the biceps tendon and its synovial sheath and musculotendinous contracture.
Clinicians should assess for impairments in the capsuloligamentous complex and musculotendinous structures surrounding the shoulder complex when a patient presents with shoulder pain and mobility deficits (adhesive capsulitis). The loss of passive motion in multiple planes, particularly external rotation with the arm at the side and in varying degrees of shoulder abduction, is a significant finding that can be used to guide treatment planning.
Although the aetiology of adhesive capsulitis has not been identified, there are a number of associated factors. Recent evidence implicates elevated serum cytokine levels as causing or resulting in a sustained intense and protracted inflammatory/fibrotic response affecting the synovial lining and capsuloligamentous complex in patients with adhesive capsulitis. To date, the relationship between cytokines and the causative factor, whether it is insidious or related to minor trauma, is unknown.
Individuals with type 1 or 2 diabetes mellitus have a greater propensity of developing adhesive capsulitis. Patients with Dupuytren’s disease or type 1 diabetes mellitus for 10 or more years have a greater incidence of primary adhesive capsulitis.
Thyroid disease is a risk factor associated with adhesive capsulitis. Milgrom et al reported that 13.4% of patients with adhesive capsulitis had thyroid dysfunction. The majority of the patients with thyroid disease who developed adhesive capsulitis were women.
Age can be considered a risk factor because ad- hesive capsulitis more commonly occurs in individuals between 40 and 65 years of age, with the reported peak incidence occurring, on average, between 51 and 55. Females appear to be affected more commonly than males. Having adhesive capsulitis on 1 side places an individual at risk (5%-34%) for opposite-arm involvement in the future, and adhesive capsulitis can occur bilaterally simultaneously up to 14% of the time.
Other associated risk factors include prolonged immobilization, myocardial infarction, trauma and autoimmune disease.
Four stages of adhesive capsulitis, reflecting a continuum, have been described.
Stage 1 may last up to 3 months, and during this stage patients describe sharp pain at end ranges of motion, achy pain at rest, and sleep disturbance. During this stage, arthroscopic examination reveals diffuse synovial reaction without adhesions or contracture. Subacromial shoulder impingement is often the suspected clinical diagnosis early in this stage because there are minimal to no ROM restrictions. Early loss of external rotation motion with an intact rotator cuff is a hallmark sign of adhesive capsulitis and may be seen in this stage.
Stage 2, known as the “painful” or “freezing” stage, presents with a gradual loss of motion in all directions due to pain and can last from 3 to 9 months. Arthroscopic examination reveals aggressive synovitis/angiogenesis and some loss of motion under anesthesia.
Stage 3, known as the “frozen” stage, is characterized by pain and loss of motion and lasts from 9 to 15 months. In stage 3, the synovitis/angiogenesis lessens but the progressive capsuloligamentous fibrosis results in loss of the axillary fold and ROM when tested under anesthesia.
Stage 4, known as the “thawing” stage, is characterized by pain that begins to resolve, but significant stiffness persists from 15 to 24 months after onsets of symptoms. This stage often progresses to pain resolution, but motion restrictions may persist that are unchanged even when examined under anesthesia. Arthroscopy reveals capsuloligamentous complex fibrosis and receding synovial involvement.
Although adhesive capsulitis was initially considered a 12- to 18-month self-limited process, mild symptoms may persist for years, depending on the extent of fibroplasia and subsequent resorption. Patients with diabetes mellitus may have a protracted recovery and worse outcomes.
The diagnosis of shoulder pain and mobility deficits associated with primary or secondary adhesive capsulitis is determined from the history and physical examination. Patients typically present with a gradual and progressive onset of pain, likely sleep-disturbing night pain and pain at end ranges of movements. Patients also present with painful and restricted active and passive ROM in both elevation and rotation that occurs for at least 1 month and has either reached a plateau or worsened. Functional activities such as reaching overhead, behind the back, or out to the side become increasingly difficult due to pain and/or stiffness.
Patients with adhesive capsulitis present with a number of impairments, but most characteristically have a global loss of both active and passive shoulder ROM. Generally, ROM loss of greater than 25% in at least 2 planes and passive external rotation loss that is greater than 50% of the uninvolved shoulder or less than 30° of external rotation have been used to define adhesive capsulitis.
Diagnosing adhesive capsulitis is primarily determined by history and physical examination, but imaging studies can be used to rule out underlying pathology. Radiographs are typically normal with adhesive capsulitis but can identify osseous abnormalities, such as glenohumeral osteoarthritis. Arthrographic findings associated with adhesive capsulitis include a joint capsule capacity of less than 10 to 12 mL and variable filling of the axillary and subscapular recess.
Magnetic resonance imaging (MRI) may help with the differential diagnosis by identifying soft tissue and bony abnormalities. MRI has identified abnormalities of the capsule and rotator cuff interval in patients with adhesive capsulitis. Findings include a thickened coracohumeral ligament and joint capsule in the rotator cuff interval and a smaller axillary recess volume.
Ultrasound can identify thickened coracohumeral ligament in patients with adhesive capsulitis. Homsi et al performed ultrasound examinations of the coracohumeral ligament on 306 individuals with painful shoulders, 121 asymptomatic shoulders and 17 shoulders with arthrographic evidence of adhesive capsulitis. The aver- age thickness of the coracohumeral ligament was 3 mm in the adhesive capsulitis group, 1.34 mm in the asymptomatic group, and 1.39 mm in the non–adhesive capsulitis painful- shoulder group. Coracohumeral ligament thickness was significantly greater (P = .0001) in the adhesive capsulitis group compared to the asymptomatic group and the non–adhesive capsulitis painful-shoulder group.
Multiple interventions have been described for the treatment of adhesive capsulitis, and there is emerging evidence from high-quality randomized clinical trials regarding both short- and long-term efficacy of these interventions. Successful treatment does not require the patient to achieve full ROM. Instead, a successful outcome may be defined as a significant reduction of pain, improved function, and high levels of patient satisfaction. These are often the short-term outcomes of conservative treatment. A successful long-term outcome could be defined as a continual improvement in shoulder motion and improved function over months as tissue remodels from thickened fibrotic tissue to more normal collagen tissue.
Patient education is central to each patient-physical therapist interaction and critical to the rehabilitative management of patients with adhesive capsulitis. The insidious nature of adhesive capsulitis is perplexing to patients, who often have concerns about serious medical conditions. Patients generally experience exquisite pain in the early stages of adhesive capsulitis, yet their recovery follows a fairly predictable course. Describing the pathology (synovitis/angiogenesis progressing to fibrosis) can allay fears and prepare them for the staged progression of the condition and recovery. Encouraging ac- tivity modification, while emphasizing functional pain-free ROM, is important to prevent self-imposed immobilization. Patients need to understand that exercises should be performed without significant pain.
Several studies have examined the effect of joint mobilization in patients with adhesive capsulitis. Although there is evidence that it may be beneficial, there is little evidence to support superior efficacy over other interventions.
Roubal et al described an alternative treatment method to standard shoulder manipulation for patients with unresponsive adhesive capsulitis. A single session of translational manipulations was performed on 8 patients with recalcitrant adhesive capsulitis following an interscalene brachial plexus block administered by an anaesthetist. This study provides an alternative option to commonly performed manipulation.
Stretching exercises appear to influence pain and improve ROM, but not necessarily more than other interventions. Results are inconsistent across multiple studies, demonstrating that stretching results in minimal or no difference in out- comes (at 3-6 months) in patients treated with a therapist- directed home exercise program (HEP) or other interventions.
Clinicians should instruct patients with adhesive capsulitis in stretching exercises. The intensity of the exercises should be determined by the patient’s tissue irritability level.
Corticosteroids are administered to dampen the inflammatory response and reduce pain in patients with adhesive capsulitis. Evidence shows that intra-articular corticosteroid injections combined with shoulder mobility and stretching exercises are more effective in providing short-term (4-6 weeks) pain relief and improved function compared to shoulder mobility and stretching exercises alone.
Because subacromial tissue may be involved in primary frozen shoulder, subacromial injections may be added as a potential intervention strategy.
Suprascapular nerve block under ultrasound guidance can be used to treat patients with adhesive capsulitis. This may enable patients to engage more effectively with the physiotherapists.
Suprascapular nerve ablation under ultrasound guidance can provide sustained pain relief, enabling patients to engage more effectively with physical therapies to help improve range of motion.