Adhesive Capsulitis (Frozen Shoulder)

                                Dr. KS Dhillon

Introduction

The two terms that have been used to describe a painful and stiff shoulder are adhesive capsulitis and frozen shoulder syndrome (FSS). The consensus definition of a frozen shoulder by the American Shoulder and Elbow Surgeons is "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" [1].  The American Academy of Orthopaedic Surgeons has defined this condition as: "A condition of varying severity characterized by the gradual development of global limitation of active and passive shoulder motion where radiographic findings other than osteopenia are absent."

In frozen shoulder there is a loss of passive range of motion (ROM). This passive loss of motion is a critical element in establishing the diagnosis of a true frozen shoulder. Conditions such as subacromial bursitis, calcifying tendinitis, and partial rotator cuff tears can be associated with significant pain and loss of active ROM, passive ROM is usually preserved. 

Lundberg divided patients with frozen shoulder into two groups: primary and secondary [2]. In patients with primary frozen shoulder there is no known cause for motion loss and pain. Patients with secondary FSS describe an event that preceded the onset of shoulder symptoms. Symptoms of primary frozen shoulder have been divided into three phases: namely freezing (painful), frozen (stiffening), and thawing.

The initial painful phase is marked by a gradual onset of diffuse shoulder pain lasting 9 months. The stiffening phase is characterized by a progressive loss of ROM that may last from 4 months to 20 months. Most of the patients lose glenohumeral external rotation, internal rotation, and abduction during this phase. The final, thawing phase is from 5 months to 26 months. It constitutes a period of gradual motion improvement. Once in this phase, the patient may require up to 9 months to regain a functional shoulder ROM [3-6].

Younger patients and patients with diabetes may be more likely to develop contralateral idiopathic adhesive capsulitis [7].

Unlike patients with primary FSS, patients with secondary FSS describe an event that preceded the onset of shoulder symptoms. These include:

• Upper extremity trauma (eg, proximal humerus fracture, shoulder surgery, rotator cuff tear)

• Immobilization (eg, neurosurgery, cardiothoracic surgery)

•  Metabolic/endocrine (eg, diabetics, thyroid disease, autoimmune disease, hyperlipidemia)

• Neurologic (eg, Parkinson disease, stroke)

• Cardiac disease (eg, hypertension, ischemic heart disease) 

• Drugs (eg, antiretrovirals, immunizations, protease inhibitors, fluoroquinolones)

• Malignancy

Etiology

Duplay was the first physician to present the concept of periarticular tissue pathology rather than periarticular arthritis as the cause of frozen shoulder [8]. There is no evidence linking frozen shoulder to any specific etiology.  However, various triggers that may predispose patients to FSS appear to exist. Some of these etiologic agents include:

• Trauma

• Inflammatory disease

• Diabetes

• Regional surgery 

• Regional conditions

• Various shoulder maladies

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 as compared to controls [9,10]. DePalma was of the opinion that muscular inactivity was a major etiologic factor [11]. Bridgman identified an increased incidence of FSS in patients with diabetes mellitus [12]. Frozen shoulder  has been associated with the following disorders:

• Parkinson disease [13]

• Hyperthyroidism [14]

• Hypothyroidism

• Cervical spine disease

• Ischemic heart disease

Most patients with FSS have undergone a period of shoulder immobilization for various reasons. Reasons for immobilization can be diverse. The common finding in all of these patients is a period of restricted shoulder motion. Bruckner in a study of neurosurgery patients who immobilized their shoulder for varying periods found that the incidence of frozen shoulder was 5 to 9 times greater than that found in the general population [15].

Epidemiology

Frozen shoulder syndrome (FSS) usually affects patients aged between 40 to 60 years. Although the precise incidence of FSS is not known, it is estimated that 2% to 5% of the general population develops the disease during their lifetime [16]. Men are usually less affected than women, and there is no predilection for race. Bilateral shoulder involvement is rarely simultaneous. It occurs sequentially.

Diabetes mellitus is a risk factor for FSS. Diabetic patients are 5 times more likely to develop adhesive capsulitis as compared to non-diabetic controls. There is a 13.4% overall mean prevalence of adhesive capsulitis in patients with diabetes and there is a 30% mean prevalence of diabetes in a population with adhesive capsulitis. There is 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 [17].

Pathophysiology

In frozen shoulders, there is fibrotic and inflammatory contracture of the rotator interval, capsule, and ligaments. The development of adhesive capsulitis (AC) remains poorly understood. Although there are disagreements, the most recognized pathology is cytokine-mediated synovial inflammation with fibroblastic proliferation. In addition, there are adhesions around the rotator interval caused by increased collagen and nodular band formation.

The structure that is usually first affected is the coracohumeral ligament which forms the roof of the rotator cuff interval. Contraction of this ligament limits external rotation of the arm, which is usually first affected in early AC. In later stages, thickening and contraction of the glenohumeral joint capsule occurs which further limits the range of motion in all directions [18].

Histopathology

Histopathology studies have shown a significant increase in fibroblasts, myofibroblasts, and inflammatory cells, like B-lymphocytes, mast cells, and macrophages in the glenohumeral capsule.

History and Physical Examination

Patients having early AC usually present with a sudden onset of unilateral anterior shoulder pain. The typical symptoms include limitation of both passive and active range of motion. First external rotation and later abduction of the shoulder is affected. In general, depending on the stage and severity, the condition is self-limiting. It interferes with activities of daily living, work, as well as leisure activities. Functional impairments caused by a frozen shoulder consist of limiting reach, particularly during overhead or to-the-side activities. 

Patients also have restricted shoulder rotations, resulting in difficulties in personal hygiene, brushing their hair, and wearing their clothes. Patients with frozen shoulder often have neck pain because of overuse of cervical muscles to compensate for the loss of shoulder motion.

A physical examination is essential for the diagnosis of a frozen shoulder. 

Two physical examinations are commonly used for diagnosing AC. These include tests of combined motion, such as touching the scapula from behind the back and from behind the neck. The most pathognomonic feature of AC is the loss of passive ROM. 

Generally, patients with frozen shoulder usually demonstrate significant restriction in active and passive range of motion, especially external rotation and abduction movement. On palpation, there is diffuse tenderness. Resisted movements of the shoulder produces pain and marked limitation in movement mimicking a rotator cuff tear.

Evaluation

The diagnosis of a frozen shoulder is clinical. The diagnosis is made by taking a history and doing a physical examination. Imaging modalities are not needed to make a diagnosis. Imaging modalities are used to rule out other conditions. No specific laboratory test or imaging provides definitive confirmation of the diagnosis of AC [19-21].

Imaging is of not much value in the diagnosis of AC. Radiographs, ultrasound, plain magnetic resonance imaging, and computed tomography are usually unremarkable. Imaging is limited to ruling out concurrent pathologies such as rotator cuff tears and glenohumeral osteoarthritis. The imaging tool most often used in patients with AC is high-resolution musculoskeletal ultrasonography (MUS). There is, however, a lack of specific ultrasound findings for the diagnosis of AC. In patients with AC, several investigators have reported thickening of the coracohumeral ligament to be a sonographic characteristic. Another ultrasound finding is the presence of fluid accumulation around the long head of the biceps tendon. Biceps peritendinous effusion can be seen in other shoulder pathologies such as rotator cuff disorders or biceps tenosynovitis. Plain shoulder X-rays are useful to rule out other pathologies such as tumors, and acromioclavicular and glenohumeral osteoarthritis. MRI may show a thickening of the glenohumeral joint capsule and coracohumeral ligament. MRI arthrography may show a reduction of the joint space.

Treatment

There is no consistent consensus about the management of AC. The majority of treatment options for AC are non-operative. They include physical and pharmacological therapy [22-24].

Early Frozen Shoulder

The aim of treatment in the early stage should focus on pain control, reduction of inflammation, and patient education. The pain is treated with acetaminophen or NSAIDs. Severe pain may require the use of opioid analgesics.

Oral corticosteroids can be prescribed in lieu of NSAIDs. They provide a stronger anti-inflammatory effect, however, they should not be given routinely due to their potential adverse effects. Low-dose oral corticosteroids are recommended only in cases of severe refractory frozen shoulder that has either been present for an extended period i.e. longer than 2 months or is causing significant pain. Although oral corticosteroids provide significant short-term benefits, the effect may not be maintained after 6 weeks.

Physical therapy is important for pain control and restoration of shoulder movements. Physical therapy includes soft tissue mobilization and gentle stretching exercises. Therapeutic ultrasound, cryotherapy, or transcutaneous electrical nerve stimulation (TENS) can also be used. A home exercise program should be provided to the patients. Exercises are done at home on a daily basis. In patients with moderate to severe pain who are not responding to non-operative treatments, intra-articular injection of corticosteroid can be done. The injection can be performed under ultrasonographic or fluoroscopic guidance. 

Developed Frozen Shoulder

Once the inflammation-related painful period subsides, the condition progresses to a frozen and then into a thawing phase. Treatment objectives in the advanced stages are to regain movements. Intensive mobilization exercises are provided to restore joint mobility. In patients who do not respond well to non-operative treatments, a more invasive therapy is provided. A suprascapular nerve or interscalene brachial plexus blockage may provide further improvement. In patients who do not improve after 6 months of non-operative treatment, more aggressive treatments are needed. Capsular hydrodilatation i.e. stretching the joint capsule by the saline injection pressure, manipulation of the shoulder under anesthesia, and arthroscopic capsular release, particularly in the rotator interval can be done.

Differential Diagnosis

Adhesive capsulitis especially in the early stage might be a diagnostic challenge. It can mimic subacromial pathology and rotator cuff tendinopathy. Patients with shoulder impingement and rotator cuff pathology usually report predominantly pain with less pronounced loss of passive range of motion. Several facets help to distinguish a frozen shoulder from other shoulder disorders. In patients with other shoulder disorders there often is a history of lifting a heavy object or performing repetitive overhead movements. In patients with frozen shoulder, there is spontaneous onset without an apparent cause or a history of overuse activity. 

Conditions that can mimic early adhesive capsulitis include:

• Post-stroke shoulder subluxation

• Subacromial pathology and rotator cuff tendinopathy

• Referred pain from the cervical spine or malignancy such as Pancoast tumor.

Glenohumeral joint arthritis should also be considered. It can be ruled out by free shoulder movement following lidocaine injection to the shoulder joint.

Age of onset provides clues to diagnose AC. Frozen shoulder is unlikely in patients younger than 40 years and patients older than 70 years are more likely to develop rotator cuff tears or glenohumeral osteoarthritis.

Staging

The natural course of AC is a gradual restriction of passive shoulder motion. The development progresses through 3 overlapping phases. A 4 stages classification can also be found in the literature. From a practical point of view, a  2-stage scheme i.e. early and developed frozen shoulder is used. The three overlapping phases include:

• Freezing (2 to 9 months): Early

• Frozen (4 to 12 months): Developed

• Thawing (12 to 42 months): Developed

Freezing

The early phase is known as the freezing phase. It is a painful phase with predominant pain that is worse at night. There is a gradual increase in glenohumeral joint movement restriction.

Frozen

The second phase is the frozen phase with stiffness and persistent glenohumeral joint motion limitation. The pain, however, is less than that in the “Freezing” stage. 

Thawing

The third phase is the thawing phase. Here there is a gradual return of the range of motion.

Prognosis

Adhesive capsulitis lasts from 1 to 3.5 years with a mean of 30 months.  The contra-lateral shoulder becomes affected within 5 years in about 15% of the patients.

Complications

In patients with adhesive capsulitis, there can be several complications. These include:

• Residual stiffness

• Residual pain

• Fracture of the humerus

• Rupture of the biceps tendon during shoulder manipulation

Outcomes

Frozen shoulder recovers in most people. The recovery, however, may take 1 to 3 years. Physical therapy and shoulder exercises will gradually result in diminishing symptoms in most patients. There is no data to show that diabetics have worse outcomes as compared to non-diabetics. There will be residual shoulder stiffness and disability in about 10% of the patients. After arthroscopic surgery, there is a gradual improvement in symptoms but the recovery is slow. Postoperative physical therapy is a must after surgery to ensure a good recovery [7,22].

Conclusion

The two terms that have been used to describe a painful and stiff shoulder are adhesive capsulitis and frozen shoulder syndrome. It is 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. A frozen shoulder can be primary or secondary to trauma, inflammatory disease, etc. Patients having early AC usually present with a sudden onset of unilateral anterior shoulder pain. The typical symptoms include limitation of both passive and active range of motion. The diagnosis of a frozen shoulder is clinical. X-rays are used to exclude other pathologies.

There is no consistent consensus about the management of AC. The majority of treatment options for AC are non-operative. They include physical and pharmacological therapy. In patients who do not respond well to non-operative treatments, a more invasive therapy is provided including 

nerve blocks, capsular hydrodilatation i.e. stretching the joint capsule by the saline injection pressure, manipulation of the shoulder under anesthesia, and arthroscopic capsular release.

Frozen shoulder recovers in most people. The recovery, however, may take 1 to 3 years. There will be residual shoulder stiffness and disability in about 10% of the patients.

References

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