Adhesive Capsulitis (Frozen Shoulder)
- Adhesive capsulitis (AC) or frozen shoulder:
- Presents as progressive painful restriction in range of movement of the glenohumeral (GH) joint (1)
- Course usually involves diminishment of pain but can have residual pain and limits of active and passive range of motion (ROM) (1).
- Primary AC:
- Usually associated with diabetes mellitus (DM) (1)
- Typically resolves in 9 to 18 months (2)
- Secondary AC:
- Typically due to prolonged immobilization
- Most commonly due to a complication of rotator cuff impingement syndrome (rotator cuff tendonitis) that remains incompletely treated
- Sometimes called “shoulder-hand-syndrome,” which is a complex regional pain syndrome (or reflex sympathetic dystrophy), if it is characterized by shoulder pain, diffuse swelling, and decreased ROM (2)
- Clinical course:
- Phase 1 (2 to 9 months): painful phase. Pain is constant. Diagnosis may be difficult if restricted movement is not present in early disease.
- Phase 2 (4 to 12 months): stiffening or freezing phase. Movement becomes restricted, especially with external rotation.
- Phase 3 (12 to 42 months): resolution or thawing phase; gradual return to normal shoulder mobility (2)
2.4/1,000 people per year (2)
2–5% in the general population, 10–20% among diabetes (2),(3)
Etiology and Pathophysiology
Underlying fundamental processes:
- Inflammation: Mast cells, T cells, B cells, and macrophages have been identified histologically, suggesting an inflammatory process. Studies confirm presence of elevated inflammatory cytokines such as IL-1, IL-6, TNF-α, COX-1, and COX-2 (3).
- Elevated markers for neoangiogenesis (CD34) and neoinnervation (GAP43, PGP9.5, NGFRp75) have been associated with AC which helps explain the acute painful phase. Additionally, one study showed that over expression of TGF-β led to the development of AC in rats (3).
- Scarring: Fibroblasts and myofibroblasts have been identified histologically. Capsular contracture reduces the joint volume to 3 to 4 mL compared to the normal 10 to 15 mL. Intracellular adhesion molecule-1 (ICAM-1) facilitates leukocyte endothelial transmigration. It is elevated in both AC and DM.
- This scarring primarily effects the rotator interval (coracohumeral ligament [CHL], biceps tendon, and GH capsule). A contracted CHL is an essential finding in AC (3).
- Contracture of the GH capsule from loss of synovial layer, capsular adhesions, and loss of capsular volume are seen in AC.
- Shoulder immobilization; often due to impingement syndrome (most significant risk factor)
- Increasing age (1)
- Female gender (1)
- Diabetes (1)
- Thyroid disease (1)
- Atherosclerotic cardiovascular disease (ASCVD): cerebrovascular accident (CVA)/myocardial infarction (MI)/hyperlipidemia (2)
- Antiretroviral medication use
- Parkinson disease
- Trauma/surgery (1)
- Prior history of AC in contralateral shoulder
- Active lifestyle, while avoiding shoulder injury
- Control of diabetes, atherosclerotic disease, thyroid, and autoimmune conditions
Commonly Associated Conditions
DM, autoimmune disorders, Parkinson disease, highly active antiretroviral therapy (HAART) use, CVA/MI, cervical disc disease, thyroid disorders (1)
- Identify possible risk factors.
- Progressive and worsening stiffness of the GH joint
- Majority will have diffuse shoulder pain, especially at the beginning of the disease.
- On the late phase of the disease, stiffness becomes predominant.
- Rule out other pain invoking conditions such as fractures, osteoarthritis (OA), subacromial pathologies such as bursitis and rotator cuff tendinopathy, cervical radiculopathy, and GH arthrosis (3).
- Limitation in both active and passive ROM due to true mechanical restriction
- Capsular pattern of ROM restriction is demonstrated, with external rotation most affected, followed by abduction, and then flexion (1).
- Pain with rotator cuff impingement tests
- Inability to reach overhead or back pocket
- Scapular substitution frequently accompanies active shoulder movement.
- Loss of arm swing with gait
- Rotator cuff strain/tear/impingement syndrome
- GH or acromioclavicular joint OA
- Cervical strain/radiculopathy/OA
- Subacromial bursitis
- Parsonage-Turner syndrome: brachial plexus inflammation secondary to a trigger, such as an infection, trauma, or autoimmune condition
- Myofascial pain syndrome
- Calcific tendonitis
- Shoulder subluxation/dislocation
- Bony neoplasm/metastasis
Diagnostic Tests & Interpretation
AC is a clinical diagnosis that can further be guided by labs and images if needed. No single lab or imaging alone can make the diagnosis.
Initial Tests (lab, imaging)
- No labs are required for idiopathic AC. Blood tests can be used to check for associated/related conditions, such as diabetes, thyroid disease, a stroke, autoimmune diseases, and, in rare cases, Parkinson disease (e.g., thyroid-stimulating hormone, hemoglobin A1C, erythrocyte sedimentation rate).
- Plain radiographs of the affected shoulder (posteroanterior, external rotation, axillary, and supraspinatus outlet views)
- Preferred initial tests
- In most cases, will be negative
- Used primarily to rule out other pathologies such as GH OA, fractures, dislocation, or tumors (2)
- Magnetic resonance imaging (MRI)
- Not indicated unless there is a concomitant pathology in the shoulder or neurologic deficit
- May show thickening of the joint capsule and the coracohumeral ligament along with edema and increased joint fluid (2)
- Rotator interval/axillary joint capsule enhancement and inferior GH and/or coracohumeral ligament hyperintensity are the most diagnostic signs with sensitivity and specificity >80% (4).
- Ultrasound (US)
- Indications similar to those for MRI
- Selection depends on individual cases and clinician’s preference.
- Can also reveal thickening of the coracohumeral ligament and soft tissues of the joint capsule and increased joint fluid
- Doppler can show increased vascularity around the intra-articular portion of the biceps tendon and coracohumeral ligament.
Follow-Up Tests & Special Considerations
- Shared decision-making regarding treatment
- Pain referral for CRPS
Injection test can be helpful in differentiating AC from subacromial pathologies such as rotator cuff tendinopathy (which should improve with injection of local anesthetics, in contrast to AC). This should only be done if the diagnosis is still uncertain after a thorough history and physical.
- In most cases, self-limited
- Physical therapy with exercises within the limits of pain
- Manage patient expectations; resolution often takes 18 months of medication and rehabilitation (2).
- Treat any underlying medical conditions associated with AC such as DM and thyroid disorders.
- Medication should be used in conjunction with physical therapy to provide symptomatic relief.
- Acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) are first line of treatment.
- Glucocorticoid injections:
- Single intra-articular corticosteroid injections and multisite injections showed great statistical and clinical outcomes for pain when used in the beginning of the disease (5). Intra-articular corticosteroid injections in patients with frozen shoulder for <1 duration showed greater benefits compared to other interventions and such benefits were shown to last as long as 6 months (5).
- A course of physical therapy after an injection, for 4 to 6 weeks, with or without intra-articular corticosteroid appeared to be associated with short-term benefits of improving pain and ROM.
- Injection may be diluted with a local anesthetic such as lidocaine. Triamcinolone 20 to 40 mg or methylprednisolone 20 to 40 mg can be used.
- Hydrodilatation with normal saline combined with intra-articular corticosteroid injection may expedite ROM recovery compared to corticosteroid injection alone (3).
- Although a short course of oral glucocorticoid can temporarily provide pain relief and improved mobility, the benefits were not greater than a few weeks. Studies have shown that intra-articular corticosteroid injections are more effective than oral steroid treatment (3).
Issues For Referral
Surgical referral can be considered if patients fail to make progress with conservative management for one year.
- Exercise and physical therapy:
- Gentle ROM exercises should be offered to every patient.
- Exercises should be performed daily and as tolerated. A structured plan should be given to the patient (6).
- Physical therapy has been found to be beneficial especially in phases 2 and 3 of AC. Best data supports its use in conjunction with other treatment such as corticosteroid injections.
- Laser has been suggested as a possible treatment, particularly for pain relief; not enough evidence for support
- Suprascapular nerve block can provide temporary pain relief and may be a therapeutic option for AC refractory to intra-articular corticosteroid injections; however, there is a lack of high-quality evidence for support (3).
- Other therapies that have been studied include whole-body cryotherapy and intra-articular injection of botulinum toxin type A, both of which have demonstrated to improve pain and ROM but with limited evidence (3).
- Should be reserved for patients who do not respond to conservative measures for at least 1 year or is not showing any improvement conservatively
- Some of the most common procedures include manipulation under anesthesia (MUA), arthroscopic capsular release (ARC), distension arthrogram, among others (2). One study comparing ARC, MUA, and physiotherapy showed that although all three treatments led to substantial improvements in pain and function, none of the treatments were clinically superior to another (7).
- After establishing a diagnosis, assess the need for pain control and start the patient on NSAIDs, in combination with a gentle exercise program with guidance with physical therapy.
- Follow up in 3 to 4 weeks: if no significant improvement, may consider intra-articular corticosteroid injections (5)
- Physical therapy should be concurrently used because it can hasten the rate of recovery and increase ROM (5).
- For secondary AC, consider evaluation by a multidisciplinary team.
- If no improvement, consider surgical intervention (2).
- Patient education is important; explain prognosis and ensure compliance with treatment.
- Climbing the wall: Face a wall and place the hand from the affected shoulder flat on the surface of the wall; use the fingers to “climb” the wall; pause 30 seconds every few inches. Repeat the exercise after turning the torso 90 degrees to wall (abduction).
- In case of secondary AC, address the importance of treating underlying causes.
- Recovery is dependent on onset of treatment, symptoms, and comorbidities in patient.
- Variable duration, lasting 1 to 3 years without intervention (1)
- Patients with idiopathic frozen shoulder have a good rate of recovery (5).
- M75.00 Adhesive capsulitis of unspecified shoulder
- M75.01 Adhesive capsulitis of right shoulder
- M75.02 Adhesive capsulitis of left shoulder
- 726.0 Adhesive capsulitis of shoulder
- 15635961000119100 Bilateral adhesive capsulitis of shoulders (disorder)
- 301971000119109 Adhesive capsulitis of right shoulder (disorder)
- 301981000119107 Adhesive capsulitis of left shoulder (disorder)
- 399114005 adhesive capsulitis of shoulder (disorder)
- 430474001 Secondary adhesive capsulitis (disorder)
- Frozen shoulder or AC is generally a self-limiting global restriction in ROM of the shoulder joint. Up to 15% will have disability long-term.
- Natural course consists of a painful phase, freezing phase, and thawing phase. It occurs mostly in older women; total prevalence is 2–5% of the general population and roughly 10–20% of the diabetic population.
- An active and passive ROM restriction will be present. Most common is an inability to externally rotate the shoulder. Other signs include pain on provocation of subacromial space and inability to reach overhead or for back pocket.
- Plain x-rays are the preferred initial imaging modality. MRI and US are done only if there is concomitant pathology or neurologic deficit.
- Treatment includes pain control and physical therapy; can progress to glucocorticoid therapy with a consideration for surgery
- Resolution of symptoms often takes ≥18 months.
Edwin Y. Choi, MD, MS, FAAFP, DFPHM
Daniel Jordan Whitaker, MD
Lea S. Choi, DO
- Zreik NH, Malik RA, Charalambous CP. Adhesive capsulitis of the shoulder and diabetes: a meta-analysis of prevalence. Muscles Ligaments Tendons J. 2016;6(1):26–34. [PMID:27331029]
- Rangan A, Goodchild L, Gibson J, et al. Frozen shoulder. Shoulder Elbow. 2015;7(4):299–307. [PMID:27582992]
- Le HV, Lee SJ, Nazarian A, et al. Adhesive capsulitis of the shoulder: review of pathophysiology and current clinical treatments. Shoulder Elbow. 2017;9(2):75–84. [PMID:28405218]
- Suh CH, Yun SJ, Jin W, et al. Systematic review and meta-analysis of magnetic resonance imaging features for diagnosis of adhesive capsulitis of the shoulder. Eur Radiol. 2019;29(2):566–577. [PMID:29978436]
- Challoumas D, Biddle M, McLean M, et al. Comparison of treatments for frozen shoulder: a systematic review and meta-analysis. JAMA Netw Open. 2020;3(12):e2029581. [PMID:33326025]
- Jain TK, Sharma NK. The effectiveness of physiotherapeutic interventions in treatment of frozen shoulder/adhesive capsulitis: a systematic review. J Back Musculoskelet Rehabil. 2014;27(3):247–273. [PMID:24284277]
- Rangan A, Brealey SD, Keding A, et al. Management of adults with primary frozen shoulder in secondary care (UK FROST): a multicentre, pragmatic, three-arm, superiority randomised clinical trial. Lancet. 2020;396(10256):977–989. [PMID:33010843]
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Adhesive Capsulitis (Frozen Shoulder)
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