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)
    • Typically resolves in 9 to 24 months
  • 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 (CRPS) or reflex sympathetic dystrophy (RDS), if it is characterized by shoulder pain, diffuse swelling, and decreased ROM
• 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

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, NGFRp75) have been associated with AC which helps explain the acute painful phase. Additionally, one study showed that overexpression 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 compared to the normal 10 to 15 mL. Intercellular 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 (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
• 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

History

• 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 (1).

Physical Exam

• 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.
• 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 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 images if needed. No single lab or imaging alone can make the diagnosis.

Initial Tests (lab, imaging)

• No labs are required for idiopathic AC. If other risk factor for a particular associated condition are present, then blood tests can be used to check for these conditions. This includes diabetes, thyroid disease, a stroke, autoimmune diseases, and, in rare cases, Parkinson disease.
  • For example, thyroid-stimulating hormone, hemoglobin A1C, erythrocyte sedimentation rate, C-reactive protein.
• Imaging
  • 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
  • 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 CHL along with edema and increased joint fluid
    • 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)
    • Indications similar to those for MRI
    • Selection depends on individual cases and clinician’s preference.
    • Can also reveal thickening of the CHL and soft tissues of the joint capsule and increased joint fluid
    • Doppler US can show increased vascularity around 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

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.

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 multisite 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).
• 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 using 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).
• Can also be used along with NSAIDs or glucocorticoid injections
• Oral steroids are usually not recommended.

Second Line
If there is no improvement in 6 to 8 weeks of conservative treatment, then more invasive treatment may be indicated.

• Hydrodilatation:
  • Injection of 10 to 20 mL of saline or 1% Lidocaine along with glucocorticoid
• Physical therapy should be continued.

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.
• 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 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. 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.

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; 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.

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.

ICD-10

• M75.00 Adhesive capsulitis of unspecified shoulder
• M75.01 Adhesive capsulitis of right shoulder
• M75.02 Adhesive capsulitis of left shoulder

SNOMED

• 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)