Adhesive Capsulitis (Frozen Shoulder)
Basics
Description
- Adhesive capsulitis (AC) or frozen shoulder:
- Presents as progressive painful restriction in range of movement of the glenohumeral (GH) joint
- Course usually involves diminishment of pain, but can have residual pain and limits of active and passive range of motion (ROM).
- Subtypes:
- Primary AC:
- Idiopathic
- Usually associated with diabetes mellitus (DM)
- Commonly resolves in 9 to 24 months
- Secondary AC:
- Commonly 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”
- A complex regional pain syndrome (CRPS) or reflex sympathetic dystrophy (RSD) characterized by shoulder pain, diffuse swelling, and decreased ROM
- Primary AC:
- 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
- Phase 1 (2 to 9 months): painful phase
Epidemiology
Incidence
- 2.4/1,000 people per year
- Female:male ratio (1.4:1)
Prevalence
2–5% in the general population, 10–20% among diabetes (1)
Etiology and Pathophysiology
Underlying fundamental processes:
- Idiopathic
- 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 (1).
- Elevated markers for neoangiogenesis (CD34) and neoinnervation (GAP43, PGP9.5, NGFR p75) 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 (1).
- Scarring:
- Fibroblasts and myofibroblasts have been identified histologically.
- Capsular contracture reduces the joint volume to 3 to 4 mL (normal 10 to 15 mL).
- Intracellular adhesion molecule-1 (ICAM-1) facilitates leukocyte endothelial transmigration (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 (1).
- Contracture of the GH capsule from loss of synovial layer, capsular adhesions, and loss of capsular volume are seen in AC.
Risk Factors
- Shoulder immobilization; often due to impingement syndrome (most significant risk factor)
- Increasing age
- Female gender
- Diabetes
- Thyroid disease
- Atherosclerotic cardiovascular disease (ASCVD): cerebrovascular accident (CVA)/myocardial infarction (MI)/hyperlipidemia
- Antiretroviral medication use
- Parkinson disease
- Trauma/surgery
- Prior history of AC in contralateral shoulder
General Prevention
- Active lifestyle, while avoiding shoulder injury
- Optimization 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
Diagnosis
History
- Identify possible risk factors.
- Progressive and worsening stiffness of the GH joint
- Most patients will experience diffuse shoulder pain at disease onset, followed by progression to shoulder stiffness.
- 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 (1).
Physical Exam
- Limitation in both active and passive ROM due to true mechanical restriction
- Capsular pattern of ROM restriction is demonstrated.
- External rotation most affected, followed by abduction and flexion, respectively
- 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
Differential Diagnosis
- Rotator cuff strain/tear/impingement syndrome
- GH or acromioclavicular (AC) 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
- Fracture
- Shoulder subluxation/dislocation
- Bony neoplasm/metastasis
Diagnostic Tests & Interpretation
AC is a clinical diagnosis that can further be guided by labs and imaging if needed. No single lab or imaging alone can make the diagnosis.
Initial Tests (lab, imaging)
- No labs are required for diagnosis of idiopathic AC.
- If risk factors for an associated condition are present, laboratory evaluation is indicated for further workup (diabetes, thyroid diseases, stroke, autoimmune disease, Parkinson disease) consider obtaining appropriate labs (thyroid-stimulating hormone (TSH), hemoglobin A1C (HbA1c), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP).
- Imaging
- Plain radiographs of the affected shoulder are the preferred initial test in order to rule out other pathologies such as GH, OA, fractures, dislocation, or tumors (posteroanterior, external rotation, axillary, and supraspinatus outlet views)
- Magnetic resonance imaging (MRI)
- Not indicated unless there is a concomitant pathology in the shoulder or neurologic deficit
- Thickening of the joint capsule and the CHL along with edema and increased joint fluid may be visualized
- Rotator interval/axillary joint capsule enhancement and inferior GH and/or CHL hyperintensity are the most diagnostic signs with sensitivity and specificity >80% (2).
- Ultrasound (US)
- Indicated if there is neurologic deficit on exam or concomitant pathology in shoulder, should be performed on case-by-case basis.
- May reveal thickening of the CHL, thickening of soft tissues of the joint capsule, and increased joint fluid
- Doppler may show increased vascularity surrounding the intra-articular (IA) portion of the biceps tendon and CHL.
Follow-Up Tests & Special Considerations
- Shared decision-making regarding treatment
- Pain referral for CRPS/RSD
Diagnostic Procedures/Other
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.
Treatment
- Self-limited condition in most patients
- Physical therapy with exercises within the limits of pain
- Manage patient expectations; resolution often takes 18 months of medication and rehabilitation.
- Treat any underlying medical conditions associated with AC such as DM and thyroid disorders.
Medication
- Medication can be used to provide symptomatic relief.
- Acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) are first line of treatment.
- Glucocorticoid injections:
- Single IA corticosteroid injections and multi-site injections showed great statistical and clinical outcomes for pain when used in the beginning of the disease.
- IA corticosteroid injections in patients with frozen shoulder for <1 year duration showed greater benefits compared to other interventions and such benefits were shown to last as long as 6 months.
- A course of physical therapy after an injection, for 4 to 6 weeks, with or without IA 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.
- Hydrodilation with normal saline combined with IA corticosteroid injection may expedite ROM recovery compared to corticosteroid injection alone (1).
- Single IA corticosteroid injections and multi-site injections showed great statistical and clinical outcomes for pain when used in the beginning of the disease.
- 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 IA corticosteroid injections are more effective than oral steroid treatment (1).
First Line
- Conservative treatment
- Home exercises including “climbing the wall”
- 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).
- Patients may perform home exercises/physical therapy in conjunction with NSAIDs or glucocorticoid injections.
- Oral steroids are usually not recommended.
- Home exercises including “climbing the wall”
Second Line
If there is no improvement in 6 to 8 weeks of conservative treatment, more invasive treatment may be indicated.
- Hydrodilatation:
- Injection of 10 to 20 mL of saline or 1% lidocaine along with glucocorticoid
- Continuation of physical therapy
Issues for Referral
Surgical referral can be considered if symptoms have been present for >1 year and patients fail to make progress with appropriate management for 3 months.
Additional Therapies
- 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.
- 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.
- Gentle ROM exercises should be offered to every patient.
- 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 IA corticosteroid injections; however, there is a lack of high-quality evidence for support (1).
- Other therapies that have been studied include whole-body cryotherapy and IA injection of botulinum toxin type A, both of which have demonstrated to improve pain and ROM but with limited evidence (1).
Surgery/Other Procedures
- Should be reserved for patients who do not respond to conservative measures for at least 1 year.
- Some of the most common procedures include manipulation under anesthesia (MUA), arthroscopic capsular release (ARC), distension arthrogram, among others. One study comparing ARC, MUA, and physiotherapy showed that while all three treatments led to substantial improvements in pain and function, none of the treatments were clinically superior to another.
Ongoing Care
Follow-up Recommendations
- 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 IA corticosteroid injections
- Physical therapy should be concurrently used because it can hasten the rate of recovery and increase ROM.
- For secondary AC, consider evaluation and management of underlying condition.
- If no improvement, consider surgical intervention.
Patient Education
- Patient education is important; discuss prognosis and reinforce that patient will likely see improvement in symptoms with treatment compliance.
- 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.
Prognosis
- Recovery is dependent on onset of treatment, symptoms, and comorbidities in patient.
- Variable duration, lasting 1 to 3 years without intervention
- Patients with idiopathic frozen shoulder have a good rate of recovery.
Authors
Erin L. Trolley, MD
References
- , , , et al. Adhesive capsulitis of the shoulder: review of pathophysiology and current clinical treatments. Shoulder Elbow. 2017;9(2):75–84. [PMID:28405218]
- , , , 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]
Codes
ICD-10
- M75.00 Adhesive capsulitis of unspecified shoulder
- M75.01 Adhesive capsulitis of right shoulder
- M75.02 Adhesive capsulitis of left shoulder
SNOMED
- 399114005 adhesive capsulitis of shoulder (disorder)
- 301971000119109 Adhesive capsulitis of right shoulder (disorder)
- 301981000119107 Adhesive capsulitis of left shoulder (disorder)
- 15635961000119100 Bilateral adhesive capsulitis of shoulders (disorder)
- 430474001 Secondary adhesive capsulitis (disorder)
Clinical Pearls
- Frozen shoulder or AC is generally a self-limiting global restriction in ROM of the shoulder joint. Up to 15% will have long-term disability.
- 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 commonly, patients will have 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 may take up to 24 months.
- Given the prevalence in patients who are middle-aged, it is also referred to as the “50-year-old shoulder.”
Last Updated: 2027
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