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Disease/Disorder

Definition

Also known as “frozen shoulder,” adhesive capsulitis (AC) is an insidious inflammatory condition characterized by a painful, gradual loss in passive or active glenohumeral range of motion (ROM) resulting from progressive fibrosis and ultimate contracture of the glenohumeral joint capsule.1

Etiology

In 1872, the first physician to describe this pathology was Simon-Emmanuel Duplay who named the pathology as “scapulohumeral periarthritis”, an entity separate from arthritis with radiographic preservation of the joint. The term “frozen shoulder” was later established by Earnest and Codman in 1934 to demonstrate the loss of shoulder motion in patients affected with this disease. The disease was redefined as “adhesive capsulitis” by Julius Neviaser in 1945 with the establishment of inflammatory and fibrotic changes observed in the capsule and adjacent bursa.2

AC has been described to be either primary or secondary. Primary (Idiopathic) disease can occur spontaneously without any specific inciting event. Primary adhesive capsulitis is often associated with other conditions such as diabetes mellitus, thyroid dysfunction, dyslipidemia, Dupuytren’s contractures, autoimmune disease, and operative procedures (e.g., axillary dissection for malignancy).1,3 

The secondary form of the disease usually follows trauma or direct injury to the shoulder such as surgical interventions, fractures, rotator cuff tears or other severe articular trauma.3

Conditions such as calcific tendonitis, bicipital tenosynovitis, glenohumeral and acromioclavicular arthritis, and rotator cuff tears can also potentially lead to a stiff and painful shoulder4-5 causing apparent limitation of active ROM, but they lack pathognomonic features of true capsular contracture with subsequent restriction in passive ROM. These conditions are distinct from AC and, therefore, should not be diagnosed as such. Given that the treatment differs between these conditions, an accurate diagnosis is essential.4

Epidemiology including risk factors and primary prevention

The prevalence of AC in the general population is reported to be 3-5% and upwards of 20% in individuals with diabetes.5,6 AC has a peak incidence between 40 to 60 years of age.5 Females are four times more often affected than males.7 The non-dominant shoulder is most often involved, although bilateral involvement has been reported up to 40-50% of cases.6

Twenty to 30% of patients will report a history of trauma to the shoulder,8,9 and one study reported that more than 60% of patients with AC had supraspinatus pathology.10

Despite its prevalence, the etiology of AC is poorly understood although many risk factors have been established. Well cited conditions associated with AC include both diabetes mellitus type I and II, thyroid disorder, cerebrovascular disease and Dupuytren’s disease. A meta-analysis demonstrated that diabetic patients with diabetes were five times more likely to develop AC, with about 30% of the patients with AC having some form of diabetes.11 An association has also been found between AC and thyroid disease with an increased risk of 2.69 times that of patients without thyroid disease. Those with the highest association were hypothyroidism and the presence of benign thyroid nodules.12 Recently, Prodromidis, et al. suggested a genetic predisposition to AC, noting a higher predilection of the condition in Caucasian patients, positive family history and HLA-27 positivity.13 A 2022 genome wide association study consisting of 500,000 patients identified 3 loci (WNT7B, POU1F1, and MAU2) that carried nearly a six-fold increase in developing adhesive capsulitis.14 There also appears to be an association between AC and depression but likely not a causal relationship.15 Recent studies have found a significant association between diabetes and Parkinson’s disease and the diagnosis of AC in the elderly.16

Patho-anatomy/physiology1,2,17

AC involves an inflammatory process and subsequently a reactive fibroblastic proliferation of the joint capsule leading to thickening and contracture of the joint capsule, a hallmark of the disease. An initial release of inflammatory cytokines (Interleukins, TNF-a, COX-1&2) and cells (T cells, B cells, Mast cells) play a crucial role in the later fibrotic process of the disease. Intercellular adhesion molecules (ICAM-1), which is elevated in diabetes mellitus, are increased in the serum of patients with frozen shoulders. Markers for blood vessels and nerve growth factor receptor are elevated as well as suggesting neoangiogenesis and neoinnervation.18 Histological features demonstrate a mix of type I and type II collagen and an imbalance between extracellular matrix tissue degradation, remodeling, and regeneration.

Anatomical findings include a loss of synovial layer of the capsule and an overall decreased capsular volume. Key structures involved include the coracohumeral ligament (CHL) and the rotator cuff interval. The rotator interval is a triangular region between the anterior border of the supraspinatus and the superior border of the subscapularis that contains the superior glenohumeral ligament and CHL. The structure usually affected first is the CHL at the roof of the rotator cuff interval. Contraction of the CHL can limit external rotation of the arm that may be seen early on in AC. In later stages, thickening and contracture of the glenohumeral joint capsule itself can limit range of motion in additional planes. The thickened, tight glenohumeral joint capsule with adhesions can lead to obliteration of the axillary fold. The fibrotic capsule adheres to itself and to the anatomic neck of the humerus. This leads to a minimal synovial fluid in the joint, and the overall joint volume is diminished.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Four stages of the disease have been described, based on the arthroscopic appearance of the joint capsule as it progresses from capsular inflammation to fibrosis.19 These have been summarized in Table 1.

 Stage 1Stage 2Stage 3Stage 4
StagePre-adhesiveAdhesiveMaturationChronic
Disease processFibrinous inflammation reaction without adhesionsSynovium proliferates, early adhesionsMature adhesionsScarred capsule
ROMFullMild loss of ROMSignificantly restricted ROMLimited ROM
SymptomsPain at night, non-specific symptoms that may be easily misdiagnosedPain is prominent with active and passive movementLess pain than stage 1 and 2May have painless ROM, but pain with sudden movement beyond scarred capsule

Table 1. Stages of Adhesive Capsulitis. ROM = range of motion. Reference: Neviaser, et al.19

The clinical presentation of AC is generally described in three phases. The first clinical phase, “Freezing Stage” often lasts 2-6 months and is characterized by pain as the primary symptom. During this phase, patients will begin to lose end ranges of motion. The second phase, “Frozen Stage” may last for 4-12 months and is characterized by worsening stiffness. While pain is still present, the stiffness beings to predominate. The third clinical phase, “Thawing Stage” may last for 6-26 months and is characterized by the gradual return of range of motion.20

Specific secondary or associated conditions and complications

Patients with AC may demonstrate residual stiffness. Axillary nerve injuries are possible with a capsular release depending on the technique used. Patients are prone to proximal humerus fractures, dislocations, rotator cuff tears and brachial plexopathy with manipulation in the setting of osteopenic bone. Evaluation may present significant increases in scapular upward rotation on the affected side as compared to their non-affected side. Secondary conditions might include cervical pain or thoracic pain.

Essentials of Assessment

History

In early stages, patients complain of shoulder pain and stiffness with both passive and active movement. This rapidly progresses to joint global stiffness actively and passively. In some cases, there is no glenohumeral motion at all, just scapulothoracic motion. In other cases, loss of ROM is only at the shoulder end ranges. It is important to extrapolate associated conditions, especially diabetes mellitus which has shown to have worse outcomes.

Physical examination

Inspection for muscle atrophy and scars denoting prior surgery at the start of the examination given this may be a risk factor for the development of AC. Point tenderness is unlikely and non-specific for AC. Examination does not reveal a specific point of tenderness. Occasionally, the long head of the biceps tendon is tender because its synovium is confluent with the synovium of the glenohumeral joint. Rotator cuff strength is usually normal in the preserved range of motion. Both passive and active ROM of the shoulder is restricted with loss of external ROM with the arm at the patient’s side a hallmark of this condition. Loss of passive external ROM is the single most important finding on examination and helps to differentiate the diagnosis from rotator cuff pathology, since the latter does not result in loss of passive ROM.21 The International Society of Arthroscopy, Knee Surgery and Orthopedic Sports Medicine (ISAKOS) defined ROM less than 100o of flexion, less than 10o of external rotation and less than L5 internal rotation as typical for the frozen phase of frozen shoulder.22 Rotator cuff testing may be limited given the loss of range of motion. Impingement sign, superior labrum anterior and posterior (SLAP) tear and biceps exam maneuvers may appear positive. An additional physical examination sign with good sensitivity is the shrug sign.23 The shrug sign is classically described as the inability to lift the arm to 90° abduction without elevating the whole scapula or shoulder girdle.

An injection test can be used as a diagnostic tool to determine adhesive capsulitis vs subacromial pathology, such as rotator cuff tendinopathy or subacromial bursitis. In adhesive capsulitis, ROM limitations and discomfort persist after injection with a local anesthetic while in the latter these symptoms may improve.24

Functional assessment

Patients are often asked to actively demonstrate the limits of shoulder motion. If loss of motion is observed, the physician may assist passively, with scapular stabilization to ensure an accurate measurement of movement. The most widely accepted method for measuring internal rotation is the Apley scratch test, usually expressed in terms of the highest vertebral level reached. Full ROM in all planes suggests another diagnosis. It is important to compare these maneuvers on the affected and unaffected sides to accurately assess deficits.25

Patients may experience sleep disturbances due to pain or inability to sleep on their affected side. It might prevent them from performing activities of daily living (such as reaching for a wallet in the back pocket, combing the hair, fastening a bra in the back). It also might affect activities at work, particularly, those that require reaching. Furthermore, it may affect recreational activities that feature significant use of the upper extremity such as swimming, throwing a ball, etc.21 There is a significant correlation between functional disability related to lack of shoulder ROM and quality of life.26

Laboratory studies

Usually, no lab studies are needed unless there is a need to evaluate for an underlying condition that is known to be a high-risk factor such as diabetes mellitus (Hemoglobin A1C), thyroid dysfunction (Thyroid Stimulating Hormone), rheumatological disorders.

Imaging

Although radiographs are typically normal, they are important to exclude other causes and evaluation of osteoarthritis and dislocations. Recommended views include anterior-posterior in neutral position, scapular-Y and axillary lateral. The most common finding on radiographic imaging is disuse osteopenia.19

Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) may reveal thickening of the joint capsule, a contracted glenohumeral joint space and diminished filling of the axillary pouch.27,28 Emig, et al. found thickness of the capsule >4 mm and of the synovium adjacent to the axillary recess to be highly specific for AC.29

Most common features found on ultrasonography include an increase in the coracohumeral ligament (CHL) thickness, an increase in the thickness of the axillary pouch and an increase in the soft tissue and/or vascularity in the rotator interval (RI).30 Of these findings, an increased CHL thickness has most consistently been found to be found in patients with AC. The consistency of these findings is demonstrated in intraoperative visualization of the primary thickening of the rotator interval and coracohumeral ligament (CHL).31

Supplemental assessment tools32

Recommended validated functional outcome measures include the Disabilities of the Arm, Shoulder and Hand (DASH), the American Shoulder and Elbow Surgeons shoulder scale (ASES) and the Shoulder Pain and Disability Index (SPADI) are commonly utilized before and after interventions.33

The Constant-Murley Shoulder Outcome Score is one of the most commonly used outcome measures for assessing the treatment of shoulder disorders. It is the recommended scoring system of the European Society of Shoulder & Elbow Surgery (SECEC/ESSE) and has the benefit of including the pain score, functional assessment, range of motion and strength measures.33

DASH

  • 30-question patient self-report questionnaire
  • Score range: 0 to 100
  • 0 indicates no disability

ASES

  • Self-report patient scale
  • Range 0 to 100
    • 50 point maximum scale for pain (1 Question)
    • 50 point maximum scale for activities/participation (10 Questions)
  • 100 indicates maximum shoulder use

SPADI

  • 13-item patient self-report tool
  • 2 domains:
    • Pain (5 items)
    • Disability (8 items)
  • Score range 0 to 100
  • 0 indicates no pain or difficulty

Early predictions of outcomes

Risk factors for the disease process particularly diabetes mellitus and thyroid disease have been identified to have poor prognostic value for patients with primary AC receiving nonsurgical or conservative treatments.34

Surgical review has corroborated that patients with diabetes had a higher failure rate of conservative management and increasing needs for multiple surgeries.35

The literature has originally suggested that AC is a self-limited disease. In 1934, Codman counseled his patients that their symptoms would gradually subside over time without treatment on an average of 2 years.17 However, clinicians have reported patients with residual pain and dysfunction beyond 2 years of disease as demonstrated by a survey by Kim, et al.36 in 2020 on 234 patients who received conservative treatment.

A recent study by Yang et. Al34 revealed CHL thickness to represent a predictor of outcomes. The investigators reported that a CHL of less than 3 mm on ultrasound highly correlated with a greater short-term improvement and these patients had a tendency of achieving a minimal detectable change in the Shoulder Pain and Disability Index (SPADI) scores in patients with primary AC after receiving hydrodilatation with corticosteroids.34 

Environmental

AC is more common in those with sedentary vocations than in manual laborers.1

Professional issues

It is important when examining the shoulder to expose the entire shoulder; not all clinicians do. This will rule out atrophy, winging scapulae and other asymmetries.

Rehabilitation Management and Treatments

Available or current treatment guidelines

The goal of treatment of AC is to relieve pain and restore mobility of the shoulder joint. Several treatments are available for AC depending on the phase of the disease. However, few of them have a high level of evidence to support them. A recent appraisal article reviewed the available treatments and assigned a level of confidence based on the criteria from the Centre for Evidence-Based Medicine in Oxford, UK. The strongest recommendation was for intraarticular corticosteroid injections combined with mobility and stretching exercises to provide short-term (i.e., 4-6 weeks) relief and improved mobility.37,38 There is further evidence that early intra-articular corticosteroid injections may allow for faster recovery, especially if provided in the first (freezing) stage.39 Limited evidence was available for other modalities such as short wave diathermy, ultrasound, and electrical stimulation combined with stretching and mobilization to help reduce pain and increase motion.37

Medical treatments include non-steroidal anti-inflammatory drugs, physical therapy, and oral corticosteroids. Injection type treatments include glenohumeral joint injection of corticosteroids, hydrodilatation, suprascapular nerve blocks (SSNB), manipulation under anesthesia, arthroscopic release, and open release.1,40 A recent randomized double-blind placebo controlled trial showed that SSNB reduced the symptoms of adhesive capsulitis by an average of 6 months.41 There has been some thought that intra-articular injection of viscosupplementation may improve outcomes with AC of the shoulder, but research has not shown additive benefits compared to conventional therapy.42

Treatment options

The cornerstone for treatment of adhesive capsulitis involves patient education, oral NSAIDs, intraarticular injections, and stretching exercises.43

When combined with other treatments, rehab therapy can result in better outcomes.25 The goals are to minimize capsular adhesions and restrictions of motion and to reduce pain and inflammation.25 Optimal intervention should be individualized to the patient, depending on disease stage, symptoms, adjunctive therapies, sex, and complex comorbid conditions such as diabetes that portend a poor outcome.44

Proprioceptive neuromuscular facilitation (PNF) involves rotational and diagonal movements along a single plane such as flexion, abduction, or rotation. Hold-relax and contract-relax exercises in upper limb D2 flexion pattern (shoulder flexion, abduction and external rotation, forearm supination, wrist and finger extension) were shown to reduce pain, reduce disability, improve ROM, and improve function.45 Additionally, dynamic scapular recognition exercises using a wireless biofeedback mechanism shows improved scapular upward rotation and shoulder flexion and abduction.46

A systematic review and network meta-analysis by Kitridis, et al.47 showed that intraarticular administration of corticosteroids alone and with distension of the shoulder capsule produced statistically significant and clinically meaningful improvements in the short term. There was no significant difference over placebo in the other pharmacological interventions, including subacromial corticosteroid injection, oral corticosteroids, platelet-rich plasma, subcutaneous adalimumab, intraarticular hyaluronate, collagenase clostridium histolyticum, shoulder joint distension with corticosteroids and hypertonic saline, distension with sodium hyaluronate, and NSAIDs administered orally and transcutaneously. Although the effect sizes of some of these interventions were large, none were statistically significant.47

  • Capsular Distension
    • Hydraulic distension/Hydrodilatation: there have been some conflicting reports regarding the use of hydraulic distension with corticosteroids, saline and anesthetic, however most studies have shown improvement in pain and ROM after distension.
      • Hydraulic distension with steroids provides pain relief and an immediate improvement in the range of motion, but the greatest clinical improvement is in capsule-preserved hydraulic distension compared to capsule-ruptured hydraulic distension48
      • When performing hydrodilatation it is recommended that a total volume of approximately 18mL of combined fluid can help ensure that the capsule integrity is maintained.48
      • Capsule-preserving distension with hypertonic saline has been shown to decrease tissue edema and superior to normal saline when measuring shoulder passive ROM as well as assessing pain scores.49
    • A retrospective review found that additional stretching of the preserved capsule using a “pumping technique” during hydraulic distension with steroids improved SPADI disability score and improved ROM.50
    • Another 10-year retrospective review found that there was a low rate of repeat intervention following distension arthrography in patients with adhesive capsulitis, and greater volumes of distension were correlated with lower rates of recurrence of capsule rupture.51
    • Jellad, et al.52 concluded that intra-articular distension before physical therapy is more beneficial than intra-articular distension after physical therapy. They also concluded that intra-articular distension alone does not significantly improve pain compared to physical therapy alone – this is in contrast to the studies previously cited.
  • Extracorporeal Shockwave Therapy.
    • Chen, et al.53 believe that ESWT stimulates soft-tissue healing, increases blood flow to the treated site, and induces an inflammatory-mediated healing process.
    • Shown to improve functional outcome in patients with diabetes and a potentially desirable alternative to corticosteroids.54
  • Laser Therapy
    • Low-level and high-intensity laser therapy (HILT) have been used for pain relief with some evidence of improving mobility and minimal adverse effects. In a 2020 publication, Atan, et al.55 demonstrated HILT plus therapeutic exercises were found beneficial for pain and quality of life compared with sham-laser plus therapeutic exercises and therapeutic exercises alone in the treatment of AC. Disability and ROM of shoulder joint were comparable between the groups after the intervention and follow up.

Surgical Interventions56-58

Surgical management is indicated when nonsurgical management, including NSAIDs, PT and injections have failed to provide relief of symptoms by 6 to 12 months. Those who undergo surgical options have been cited to be a younger age (mid-50s) with no difference in sex. Surgical options include manipulation under anesthesia (MUA) or arthroscopic capsular release with or without MUA. Evidence for the indication and timing of operative treatment or ideal technique is limited. Complications of manipulation include fractures, dislocations, rotator cuff or labral tears and brachial plexus palsies. Axillary nerve injury as well as postoperative capsulitis may be complications of capsular release.

Coordination of care

A stage-based approach and treatment in conjunction with physical therapy is the best approach. Treatment failures will require an orthopedic surgeon’s input. Continuous communication with the patient, explaining of the course of the disease and treatment plan, along with a well-prepared and guided home exercise program, will provide better results.

Patient & family education

As mentioned previously, home therapy is one of the pillars of treatment. In order to have better results, the patient has to understand his role in the recovery process, as well as the importance of his active participation from the beginning of treatment.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Designing the appropriate treatment plan depends on recognition of the clinical stage. Because immobilization should be avoided, physical therapy and a guided home exercise program will be the pillars of treatment, in conjunction with a clear communication with the patient. Medical and rehabilitation treatments will be the first step, progressing to more invasive treatments, depending on the patient’s response.

Cutting Edge/Emerging and Unique Concepts and Practice

Targeting inflammatory cytokines in early stages (1 and 2) and decreasing fibrosis as well as enhancing capsular remodeling in late states (3 and 4) are the main goals of new agents.16 For better results with intra-articular corticosteroid injection, hydrodilatation, and SSNB in early stages, the use of ultrasound or radiographically guided procedures is recommended.1 Manipulation under anesthesia was formerly the standard of care for recalcitrant cases, however, arthroscopy has shown good and sustained results.59,60 Additionally, the use of ultrasound to assess the thickness of the coracohumeral ligament (CHL) as a diagnostic imaging modality to determine CHL thickness in adhesive capsulitis of the shoulder has been shown to be effective in diagnosing AC given that a thickened CHL is suggestive of adhesive capsulitis and a thickness less than 3 mm may show a positive outcome with certain therapies.34 Below are newer treatment strategies that are developing to present positive results at different stages of the disease process or combined with physiotherapy.

  • Whole-body cryotherapy (WBC)61
    • Administered for two to three minutes on the surface of the body in minimal clothing at −110°C to −140°C. Ma et al. hypothesized that WBC could have a positive effect on the rate of post-injury recovery after conservative AC treatment.
    • Their study suggested that WBC provided a significant improvement in all outcome measures and ROM measures from pre to post treatment.
    • This therapy along with joint manipulation demonstrated to be more effective in shoulder mobility, pain and ASES scores. Further RCTs suggested to enhance these conclusions for AC of the shoulder.
  • Neuromodulation Techniques
    • Pulsed Radiofrequency
      • Stimulation lesioning of the suprascapular nerve demonstrated for shoulder pain control.44
    • Peripheral Nerve Stimulation (PNS)
      • Case report demonstrating improved pain and shoulder ROM in all planes at 3-month follow-up period after permanent implantation of a suprascapular nerve stimulator. Authors proposed a nerve block may help select patients who may respond to peripheral stimulation.62
      • Axillary Nerve Stimulation Mansfield and Desai demonstrated a small retrospective case series supporting the evidence of the use of axillary (PNS) therapy for management of chronic shoulder pain although higher-level studies are required to further support its use.63
  • Collagenase Injections
    • Subacromial collagenase injections in rats by Karahan, et al.64 demonstrated an effective result in shoulder abduction angle compared to steroid and saline. The authors suggest a potential for adhesive capsulitis treatment in patients with an intact rotator cuff.
    • Recently, Fitzpatrick, et al.65 refuted the use of this treatment due to a lack of statistical significance and adverse events and potential risk of the procedure. The authors recommended against this treatment for AC of the shoulder unless further studies demonstrated more significant results.
  • Role of Platelet Rich Plasma (PRP)
    • Demonstrated positive outcomes in shoulder pain and ROM in a case report by Aslani, et al.66 using PRP for frozen shoulder. The authors suggest future randomized control trials using this therapy for frozen shoulder.
  • Calcitonin
    • Studies with salmon calcitonin have demonstrated that outcomes are better than physical therapy and NSAIDs alone. Further research is required to validate the use of calcitonin.67
  • Wearable Motion Sensor Device to Facilitate Rehabilitation
    • Advancing technology has demonstrated to have benefits in the rehabilitation community. Chen, et al.68 demonstrated shoulder ROM measured using a motion sensor device, exhibited positive results in shoulder mobility, functional recovery and exercise completion rate during and after 3 months of rehabilitation. This treatment strategy may be beneficial for the telerehabilitation model overcoming obstacles of home-based physiotherapy.
  • Adhesive capsulitis embolization
    • A recent systematic review of articles showed that arterial embolization is a safe and effective treatment with no major adverse effects or recurrent symptoms.69

Gaps in the Evidence-Based Knowledge

There is a need for high-level evidence studies on different treatment alternatives for each stage of the disease. Information on the number, type, and timing and stages of targeted treatment of office-based injections and procedures is needed to best optimize participation in therapy and improve functional outcomes. Intra-articular injection techniques including capsular distension and steroid injections are currently prevailing nonsurgical treatments for frozen shoulders Non-invasive strategies include ESWT and laser therapy show promising outcomes in pain relief and shoulder ROM. Neuromodulation techniques including peripheral nerve stimulation require larger scale studies. Technological advancements for rehabilitation provide a means of gaining and measuring progressive functional gains. Interventions at the different stages of the AC of the shoulder are required to decide the most effective treatment algorithm. The difficulty of individualized treatment continues to depend on factors such as comorbid conditions, particularly diabetes, symptoms, disease stage and other demographic characteristics.

References

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Original Version of the Topic

Erik Hoyer, MD, MA. Critical illness myopathy. 11/27/2012

Previous Revision(s) of the Topic

Jason L. Zaremski, MD. Adhesive Capsulitis. 8/18/2016

Mooyeon Oh-Park, MD, Mohammad Zaidi, MD, Safwan Zar, MD. Adhesive Capsulitis. 12/10/2020

Author Disclosures

Mooyeon Oh-Park, MD
Nothing to Disclose

Atinder Nijjar DO
Nothing to Disclose

Michael Lew DO
Nothing to Disclose