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Introduction
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. [1][2]
Etiology
The etiology of frozen shoulder is not yet fully understood. However, some plausible risk factors
have been identified:
Epidemiology
Adhesive capsulitis occurs in up to 5%. Females are 4 times more often affected than men, while
the non-dominant shoulder is more prone to be affected.[3][4]
Pathophysiology
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.[5]
Histopathology
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.
Evaluation
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.[6][1][2]
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.
Treatment / Management
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.[7][8][9]
Early 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.
Differential Diagnosis
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.
Staging
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.
Frozen
The second phase with stiffness and persisted glenohumeral joint motion limitation, but with less
pain than that at the “Freezing” stage.
Thawing
The third (recovery) phase with the gradual return of range of motion.
Prognosis
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.
Complications
Residual pain
Residual stiffness
Fracture of the humerus
Rupture of the biceps tendon after shoulder manipulation
Consultations
Physical therapy
Pain specialist
Orthopedic surgeon
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, nurse practitioner, pharmacist, 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.[10][11]
[12] (Level V)
Outcomes
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. [13][7](Level V)