Adhesive Capsulitis, also known as frozen shoulder, is an inflammatory condition characterized by shoulder stiffness and pain. The American Academy of Orthopedic Surgeons defines adhesive capsulitis 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.”
The majority of patients have a significant loss of passive range of motion, a feature that is crucial for diagnosis.[rx][rx][rx]
Causes of The Adhesive Capsulitis
Adhesive capsulitis can be classified as either primary or secondary. The primary disease typically has an insidious onset and is idiopathic and is often associated with other diseases such as diabetes mellitus, thyroid disease, drugs, hypertriglyceridemia, or cervical spondylosis.[rx][rx]
- Fractures
- Proximal Humerus Fracture
- Humeral Shaft Fracture
- Clavicle Fracture
- Scapula Fracture
- First Rib Fracture (traumatic or atraumatic)
- Dislocations & Separations
- Acromioclavicular Joint Separation
- Glenohumeral Dislocation (Acute)
- Sternoclavicular Joint Dislocation
- Glenohumeral Instability (Chronic)
- Arthropathies
- Glenohumeral Arthritis
- Acromioclavicular Joint Arthritis
- Muscle & Tendon Injuries
- Pectoralis Major Injuries
- Pectoralis Minor Injuries
- Proximal Biceps Tendon Injuries
- Scapular Dyskinesis
- Rotator Cuff
- Rotator Cuff Tear
- Rotator Cuff Tendonitis
- Calcific Tendinitis of the Rotator Cuff
- Subcoracoid Impingement Syndrome
- Bursopathies
- Subacromial Bursitis
- Scapulothoracic Bursitis
- Ligament Injuries
- Glenoid Labral Tears
- Neuropathies
- Suprascapular Nerve Injury
- Parsonage-Turner Syndrome
- Quadrilateral Space Syndrome
- Winged Scapula
- Other
- Adhesive Capsulitis
- Paget-Schroetter Syndrome
- Pediatrics
- Coracoid Avulsion Fracture
- Humeral Head Epiphysiolysis (Little League Shoulder)
The secondary disease typically follows trauma or injuries to the shoulder. Common injuries include rotator cuff tears, fractures, surgery, or immobilization.
Pathophysiology
The exact pathophysiology is unknown. The most commonly accepted hypothesis states that inflammation initially occurs within the joint capsule and synovial fluid. The inflammation is followed by reactive fibrosis and adhesions of the synovial lining of the joint. The initial inflammation of the capsule leads to pain, and the capsular fibrosis and adhesions lead to a decreased range of motion.
During arthroscopy, the following may be seen:
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Subacromial fibrosis
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Proliferative synovitis
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Capsular thickening
Symptoms
- History
- Onset is most often insidious
- Patients typically report shoulder pain followed by loss of range of motion
- Boyle-Walker et al: 90.6% of patients develop pain before loss of ROM
- Physical: Physical Exam Shoulder
- External rotation is often the first motion most commonly affected
- Pain is worse at extremes of motion when the capsule is under tension
- Firm endpoints in passive ROM suggest mechanical rather than pain-related restriction
- Special Tests
Diagnosis of The Adhesive Capsulitis
History and Physical
Patients with adhesive capsulitis usually present with progressively worsening shoulder pain over weeks to months followed by significant limitation in shoulder motion. Disease progression is described in 3 clinical phases:
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Phase 1: The painful phase. Development of diffuse and disabling shoulder pain that is initially worse at night but then progresses to pain at rest. Associated with increasing stiffness. Can last from two to nine months.
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Phase 2: The frozen or adhesive phase. This period is characterized by progressive limitation in ROM in all shoulder planes but with the pain gradually becoming less pronounced. Can last from four to 12 months.
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Phase 3: The thawing or regression phase. The recovery phase is where there is a gradual return of the range of motion. It takes 12 to 24 months for the complete return of ROM.
Evaluation
During a physical exam, patients will often have a decreased glenohumeral range of motion and associated pain with testing. Pain will often limit a complete and thorough physical exam. Typically, there is a significant reduction in the active and passive range of motion in 2 or more planes of motion compared to the unaffected side. Usually, the range of motion is lost in the following order: external rotation, abduction, internal rotation, forward flexion. Often, when using special tests of the shoulder, the Neer and Hawkins tests for impingement and the Speed’s test for biceps tendinopathy, are positive. Diagnosis is clinical and based on history and physical exam findings as described above.[7]
There is no laboratory testing indicated for diagnosis. If there is a concern for underlying systemic disease, test as needed.
Imaging is not indicated. The diagnosis of adhesive capsulitis is primarily clinical. If there is a concern of an alternative diagnosis, such as evaluating for a fracture, then imaging such as a shoulder X-ray may be useful.
The injection test can be performed if a clinician is uncertain of the etiology of shoulder pain based on history and exam. The subacromial space is injected with an anesthetic, typically 5 ml of 1% lidocaine. In patients with adhesive capsulitis, the ROM limitations and pain will persist after the injection. In patients with subacromial pathology (rotator cuff tendinopathy or subacromial bursitis) will show an improvement of pain and improved range of motion.
Clinical Stages
- Per Neviaser and Neviaser
- Stage I (Freezing/ Painful): Gradual onset of diffuse shoulder pain pain (6 wks to 9 mos)
- Worse at night, motion preserved, synovitis on arthroscopy
- Stage II (Frozen/Stiff): Decreased ROM affecting activities of daily living (4 to 9 mos or more)
- Characterized by early adhesion formation, capsular contraction
- Stage III: Global loss of ROM, extreme pain
- Synovitis resolved, axillary fold obliterated
- Stage IV (chronic): persistent stiffness, no pain
- Can see thawing, gradual return of motion (5 to 26 mos)
Treatment of The Adhesive Capsulitis
In most cases, adhesive capsulitis is a self-limited disease with high rates of spontaneous recovery within 18 to 30 months. Treatment is focused on symptomatic relief and improving ROM.[rx][rx] There are limited studies that guide treatment management. The following are some viable treatment options:
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NSAIDs – During the initial phase NSAIDs can be used to aid with pain control.
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Physical therapy – Therapy has limited evidence supporting its benefit but patients often in the recovery phase may benefit from a gentle range of motion exercises, stretching, and graded resistance training. These have been shown to reduce pain and increase function. Patients and providers should not allow vigorous rehab as that can lead to worsening symptoms.
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Oral corticosteroids – These provide short-term pain relief for improved ROM and function. The benefits often do not last longer than a few weeks, and the clinician should be cognizant of the side effects associated with oral steroid use.
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Intra-articular steroid injection – Injections have been shown to improve function, decrease pain, and increase ROM. Like oral steroids the duration of effects of steroid injections are limited as providers must be cognizant of side effects. Often patients who receive injections early in their disease course are more likely to obtain a benefit. Multiple injections can be given to provide symptomatic relief.
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Hyaluronic Acid – Improves ROM, constant scores, and pain at short term follow up Rovetta et al: Hyaluronic acid, corticosteroids, and physical therapy is superior to corticosteroids and physical therapy alone
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Suprascapular Nerve Block (SSNB) – The suprascapular Nerve provides sensory innervation in up to 70% of the Glenohumeral Joint. Dahan et al: SSNB improved pain but not function and Jones et al: when combined with triamcinolone, SSNB offered greater pain control and ROM at 3 months compared to intra-articular corticosteroid injection[20]
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Hydrodilation – Quraishi et al: superior constant score, VAS score compared to manipulation under anesthesia + intra-articular corticosteroids. Cochrane review: Improved pain at 3 weeks, disability at 12, however no difference compared to steroids alone[22]
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Whole Body Cryotherapy – Improved VAS, active ROM when combined with physical therapy when compared to physical therapy alone.
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Botulinum Toxin Injection – No difference in pain, range of motion compared to triamcinolone but may be an option for those where steroids are contraindicated.
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Hydrosilation – In this treatment modality, the joint is injected with saline and steroid to dilate the glenohumeral capsule. This has been shown to reduce pain and improve ROM and function in the short term. Current evidence shows no significant difference in outcomes when comparing hydrodilatation to intra-articular steroid injection.
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Manipulation under anesthesia – this is reserved for more refractory cases that do not respond to the modalities mentioned above. There is an increased risk of homers fractures.
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Surgical capsular release – This is reserved for refractory cases. Typically, if symptoms do not improve with conservative measures within 10 to 12 months referral to an orthopedic surgeon is recommended.
Indications for Surgery
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The patient fails a trial of prednisone or NSAIDs
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Does not respond to glenohumeral or subacromial injections
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Does not respond to physical therapy
Contraindications for Surgery
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The patient has had an inadequate course of steroids or NSAIDs
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The patient has not had any attempt at conservative therapy
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There is an acute infection
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The patient has a concomitant malignancy in the shoulder
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The patient has a neurological deficit or nerve complaint originating from the cervical spine
Differential Diagnosis
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Cervical radiculopathy
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Fracture
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Calcifying tendinitis/synovitis
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Malignancy
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Rotator cuff impingement
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Polymyalgia rheumatica
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Shoulder impingement syndrom
Complications
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Residual shoulder pain and/or stiffness
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Humeral fracture
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Rupture of the biceps and subscapularis tendons
