> Table of Contents > Adhesive Capsulitis (Frozen Shoulder)
Adhesive Capsulitis (Frozen Shoulder)
Brandon David Hecht, DO
image BASICS
DESCRIPTION
  • Painful, gradual loss of both active and passive glenohumeral (GH) motion due to progressive fibrosis/contracture of the GH joint capsule
  • The clinical course of adhesive capsulitis (AC) follows a predictable progression
    • Stage 1, freeze/pain: subacute onset of diffuse vague pain, lasting 2 to 9 months
    • Stage 2, frozen/adhesive: insidious onset of stiffness, lasting 4 to 12 months
    • Stage 3, thaw/recovery: gradual resolution over 5 to 24+ months. Resolution may be protracted (symptoms lasting >36 months) and incomplete but rarely results in a functional limitation.
  • AC categorized as primary (idiopathic) and secondary (underlying or associated condition)
  • System(s) affected: musculoskeletal
  • Synonym(s): pericapsulitis; scapulohumeral periarthritis
EPIDEMIOLOGY
  • Predominant age: 40 to 60 years
  • Predominant sex: female > male
Prevalence
  • General population: 2-5%
  • Diabetics type 1 and type 2: 10-20%
ETIOLOGY AND PATHOPHYSIOLOGY
  • Synovial inflammation and capsular fibrosis resulting in contracture of the rotator cuff, coracohumeral ligament, and anterior shoulder capsule restricting movement of the shoulder
  • A poorly understood chronic inflammatory response with fibroblastic proliferation, possibly immunomodulated
Genetics
No known genetic predispositions
RISK FACTORS
  • Sedentary vocation or lifestyle
  • Age ≥40 years
  • History of AC: 20-30% will develop the condition in contralateral shoulder.
  • Minor injury: 20-30% of those with AC will report recent minor trauma to the shoulder.
  • Systemic diseases: endocrinopathies, autoimmune disorders, atherosclerotic disease (see “Commonly Associated Conditions”)
GENERAL PREVENTION
No current evidence regarding prevention
COMMONLY ASSOCIATED CONDITIONS
  • Idiopathic AC associated with a history of Dupuytren contractures
  • Secondary AC is associated with diabetes, thyroid disease, autoimmune diseases, rotator cuff injury or minor shoulder trauma, shoulder immobilization, history of stroke, or myocardial infarction.
image DIAGNOSIS
PHYSICAL EXAM
  • Limited active and passive shoulder range of motion (ROM) in >1 plane of motion: Document ROM for forward flexion, abduction, and external and internal rotation at each visit.
  • Diffuse shoulder tenderness with deep palpation
  • Loss of natural arm swing with gait
  • Normal strength (weakness may be present if pain inhibits effort, but objective strength testing typically reveals 5/5 strength in all planes)
  • Special tests (Neer, Hawkins, etc.) are not diagnostic.
  • No neurovascular deficits.
DIFFERENTIAL DIAGNOSIS
  • Rotator cuff strain/tear/impingement syndrome
  • GH or acromioclavicular joint osteoarthritis (OA)
  • Cervical strain/radiculopathy/OA
  • Myofascial pain syndrome
  • Calcific tendonitis
  • Fracture, dislocation
  • Bony neoplasm/metastases
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
No lab is diagnostic for primary (idiopathic) AC. Labs may help rule out underlying systemic diseases associated with secondary AC: Hbg A1C, TSH, and ESR.
  • Plain radiograph (anteroposterior [AP], axillary, supraspinatus outlet views) to rule out OA, calcific tendinitis, avascular necrosis, osteomyelitis, fracture, dislocation, and tumor
  • Radiographs are typically normal but may demonstrate disuse osteopenia of the proximal humerus in late AC.
  • In secondary AC, MRI demonstrates characteristic thickening of the axillary pouch and helps to rule out other shoulder disorders.
Follow-up Tests & Special Considerations
  • Serial exams in patients who present with nonspecific shoulder pain and normal radiographs. At follow-up visits, the diagnosis of AC is supported if progressive motion restriction is identified in >1 plane of motion.
  • Early in stage 1, pain is the predominant feature and restriction of motion may be difficult to identify. At 8-week follow-up, the patient may not complain of stiffness, but the loss of passive ROM may be easier to identify on exam.
  • Early on, AC is difficult to distinguish from subacromial bursitis. The loss of passive external rotation may be the only finding that differentiates early AC from subacromial bursitis. The only other condition that may cause insidious loss of passive external rotation is GH arthritis.
Diagnostic Procedures/Other
Diagnostic subacromial anesthetic injection can help to differentiate AC from rotator cuff pathologies:
  • Resolution of pain and restoration of ROM after subacromial injection suggests rotator cuff pathology or other cause of subacromial bursitis.
  • Intact muscle strength with persistent active and passive ROM deficits and a firm mechanical end point are consistent with AC.
Test Interpretation
If performed, arthroscopy demonstrates capsular thickening and synovial inflammation with adhesions to the humerus.
image TREATMENT
  • Treatment is guided by the stage of AC at presentation. Conservative therapy is recommended initially (the first 4 to 6 months).
  • Therapy includes combination of physical therapy, oral medications, and joint/bursal injections (1)[A].
  • Structured physical therapy is superior to home exercises (2)[A].
  • Patient education should include the following:
    • Expectations for a protracted recovery (months to years) characterized by resolution of pain prior to the return of function
    • Full ROM may never be recovered; however, functional limitations are uncommon.
GENERAL MEASURES
  • Control pain, preserve mobility, and allow for restful sleep.
  • Codman pendulum exercises: Lean forward onto table or chair with unaffected arm bending at the waist; let the affected arm dangle. Swing the affected arm slowly by moving the torso. Try smaller and then bigger circles (clockwise and counterclockwise).
  • Climbing the wall: Put the hand flat on a wall in front of you; use the fingers to “climb” the wall; pause 30 seconds every few inches. Repeat the exercise after turning 90 degrees to wall (abduction).
  • Heat and/or ice: may temporarily improve pain and secondary spasm
  • Address underlying causes of secondary AC (see “Commonly Associated Conditions”).
  • Patient reassessment must be ongoing to reinforce expectations and determine patient's goals.
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MEDICATION
First Line
  • NSAIDs: widely used in the treatment of AC and thought to be most beneficial in stage 1 when pain is the predominant feature. If contraindicated, alternatives include acetaminophen or opioid analgesics. Concomitant use of NSAIDs with oral or injectable corticosteroids has no added benefit.
  • Oral corticosteroids: rarely used in clinical practice, may have short-term improvement in pain and ROM (up to 6 weeks early in the course of the disease (stage 1 and early stage 2)
    • Prednisolone: 30 mg/day for 3 weeks (alternatively 10 mg × 4 weeks, then 5 mg × 2 weeks)
  • Subacromial (SA) corticosteroid injection: At any stage, SA injection in conjunction with physical therapy provides short-term (16 weeks) benefit in pain and ROM.
  • Intra-articular (IA) corticosteroid injection short-term (16 weeks) improvement in pain and ROM if used in conjunction with physical therapy
    • No additional benefit with ultrasound guidance (3)[A]
    • Equal efficacy to scheduled NSAID therapy (4)[A]
Second Line
Tricyclic antidepressants (amitriptyline) have been used as neuromodulators. No evidence exists to support use in AC.
ISSUES FOR REFERRAL
  • Some cases do not respond to nonoperative treatment.
  • Orthopedic referral should be considered if patient has not responded adequately to conservative treatment within 4 to 6 months.
ADDITIONAL THERAPIES
  • Physical therapy: additive effect when used in conjunction with other treatments (NSAIDs, injections, manipulation under anesthesia [MUA], surgical release), but there is no evidence to support the use of physical therapy alone in the treatment of AC (1,2)[A].
  • Iontophoresis (electromotive drug administration) is generally not recommended in this condition.
  • Although not commonly used, supervised neglect is a plausible treatment option for some patients as condition can resolve spontaneously over time.
  • Capsular hydrodilation (arthrography distention): IA injection of large-volume saline with steroid or hyaluronic acid has demonstrated some short-term improvements (12 weeks) in pain and function (5)[A].
  • IA hyaluronic acid: A systematic review showed no benefit when compared to IA corticosteroid when used in conjunction with physical therapy (6)[A].
  • Suprascapular nerve block: may help with short-term pain relief
  • Low-power laser therapy: superior to placebo (1)[A]
  • Botox: Evidence suggests no benefit.
SURGERY/OTHER PROCEDURES
  • Arthroscopic capsular release: most common surgical method for treating recalcitrant AC
    • Short-term benefits: improved pain and function
    • Long-term benefits: superior to conservative therapies in recalcitrant cases (5)[A]
  • MUA: Outcomes are similar to those with conservative, noninvasive therapies; contraindicated in posttraumatic/postsurgical AC (5)[A]
  • Transcatheter arterial embolization: Early evidence suggests benefit (7)[B].
COMPLEMENTARY & ALTERNATIVE MEDICINE
  • Acupuncture: Insufficient evidence exists regarding the effectiveness of acupuncture for AC.
  • Osteopathic manipulative technique: Evidence is equivocal.
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
Outpatient care
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Reinforce the natural course of the disease. Many patients are more likely to request invasive procedures (injections, capsular distension, MUA, surgery) when stiffness starts to affect ADLs.
Patient Monitoring
A multidisciplinary team approach helps reinforce the natural history of AC and provides patient encouragement.
DIET
No restrictions
PATIENT EDUCATION
Long-term course of treatment until resolution of symptoms; stretching and ROM exercises daily during and after improvement
PROGNOSIS
  • Although AC is considered self-limiting, up to 50% of patients will have permanent restrictions of ROM (usually external rotation).
  • Rare functional disability results
REFERENCES
1. 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.
2. Russel S, Jariwala A, Conlon R, et al. A blinded, randomized, controlled trial assessing conservative management strategies for frozen shoulder. J Shoulder Elbow Surg. 2014;23(4):500-507.
3. Prestgaard T, Wormgoor ME, Haugen S, et al. Ultrasound-guided intra-articular and rotator interval corticosteroid injections in adhesive capsulitis of the shoulder: a double-blind, sham-controlled randomized study. Pain. 2015;156(9):1683-1691.
4. Dehghan A, Pishgooei N, Salami MA, et al. Comparison between NSAID and intra-articular corticosteroid injection in frozen shoulder of diabetic patients; a randomized clinical trial. Exp Clin Endocrinol Diabetes. 2013;121(2):75-79.
5. Uppal HS, Evans JP, Smith C. Frozen shoulder: a systematic review of therapeutic options. World J Orthop. 2015;6(2):263-268.
6. Lee LC, Lieu FK, Lee HL, et al. Effectiveness of hyaluronic acid administration in treating adhesive capsulitis of the shoulder: a systematic review of randomized controlled trials. Biomed Res Int. 2015;2015:314120.
7. Okuno Y, Oguro S, Iwamoto W, et al. Short-term results of transcatheter arterial embolization of abnormal neovessels in patients with adhesive capsulitis: a pilot study. J Shoulder Elbow Surg. 2014;23(9):e199-e206.
Additional Reading
  • Ewald A. Adhesive capsulitis: a review. Am Fam Physician. 2011;83(4):417-422.
  • Maund E, Craig D, Suekarran S, et al. Management of frozen shoulder: a systematic review and cost-effectiveness analysis. Health Technol Assess. 2012;16(11):1-264.
  • Rill BK, Fleckenstein CM, Levy MS, et al. Predictors of outcome after nonoperative and operative treatment of adhesive capsulitis. Am J Sports Med. 2011;39(3):567-574.
  • Smith CD, Hamer P, Bunker TD. Arthroscopic capsular release for idiopathic frozen shoulder with intraarticular injection and a controlled manipulation. Ann R Coll Surg Engl. 2014;96(1):55-60.
Codes
ICD10
  • M75.00 Adhesive capsulitis of unspecified shoulder
  • M75.01 Adhesive capsulitis of right shoulder
  • M75.02 Adhesive capsulitis of left shoulder
Clinical Pearls
  • Early-stage AC is difficult to distinguish from rotator cuff pathology. Restriction of external ROM suggests AC.
  • Diagnostic subacromial bursa injection may help differentiate early AC from impingement syndrome. In AC, ROM deficits persist and strength is intact after injection.
  • Normal radiographs in the setting of progressive restriction of motion in >1 plane confirms AC.
  • Initial AC treatment is conservative.
  • Invasive treatment options (capsular distention, MUA, and arthroscopy) can be considered after 4 to 6 months of conservative therapy. This is necessary in only about 10% of cases.