Adhesive Capsulitis

Adhesive Capsulitis, also known asFrozen ShoulderorArthrofibrosis, is a condition of The Shoulder Girdle marked by the Pain ful and gradual loss of motion in many or all directions (SOURCE-25). Conceptualised as a contraction of the Glenohumeral Joint Capsule where the Head of the Humerus and the Glenoid of the Scapula become progressively bound (SOURCE-21). The condition is considered either primary or secondary depending on the context of its onset:Primary- also known as idiopathic capsulitis. No findings from history or examination can be attributed to onset.Secondary- the capsulitis is a sequela of trauma, surgery or another related condition. These predisposing factors can be further classified into three main categories (SOURCE-6):

Pathomechanics

Given its progressive nature, Adhesive Capsulitis is often described in four stages (SOURCE-4+6):

  • Stage I- known as theInflammatory Stage, typically occurs in the first 3 months, with notable loss of GH Joint - External Rotation despite full Rotator Cuff Strength that is reasonably specific to Capsulitis. The gradual onset of Pain is often local to the Deltoid Tuberosity and is achy at rest or sharp with movement. Pain is often worse at night, particularly when sleeping on the symptomatic side which may disturb sleep. Assessment at this stage reveals an empty joint End-Feel and Pain on palpation of Glenohumeral Joint Capsule or during passive stretch. Tissue samples reveal a normal Glenohumeral Joint Capsule but hypervascular, hypertrophic (thickened) Synovial Membrane , known as Synovitis

  • Stage II- known as theFreezing Stage, usually occurs between 3 and 9 months and is marked by acute Synovitis and progressive Glenohumeral Joint Capsule Contracture formation. Pain symptoms resemble stage I but can be severe at night. A partial loss of theAxillary Pouchleads to joint stiffness and the restriction of most Glenohumeral Joint ranges, most notably GH Joint - Flexion , GH Joint - Abduction , GH Joint - Internal Rotation , GH Joint - External Rotation . While motion can be improved with anaesthesia it cannot be restored. Synovitis at this stage is increasingly thickened and hypervascular and begins to resemble a Christmas Tree. A tissue biopsy can reveal Subsynovial Capsular Scars

  • Stage III- known as theFrozen Stage, typically occurs between months 9-15 and is characterised by significant stiffness and loss of motion due to a complete loss of theAxillary Pouchand Contracture formation. Assessment may reveal Pain exclusively at end ranges which is paired with a blocked joint End-Feel . Anaesthesia no longer improves restrictive symptoms. In lieu of the previously abundant Synovitis is dense, hypercellular Collagen with a thin synovial layer that resembles other fibrotic conditions

  • Stage IV- known as theThawing Stage, occurring usually beyond 15 months, is marked by significant stiffness and loss of motion with little-to-no Pain . At this stage Contractures are fully mature and make identification of intra-articular structures difficult. A gradual improvement in motion may occur naturally

Stimulation of Synovitis through Cytokines such as Tumor Necrosis Factor ɑ, transforming growth factor ß, platelet-derived growth factor, Interleukins 1ß leads to synovial hyperplasia and a fibrotic cascade which results in the formation of Contractures (SORUCE-4+5). Fibroblasts of Type I and Type III Collagens appear most vulnerable to tranformation into Myofibroblasts which are thought to cause contractures (SOURCE-25). Increased Vascular Endothelial Growth Factor -derived neo-vascularisation of the Synovium and Glenohumeral Joint Capsule and high levels of Inflammatory Mediators / Cytokines produced by the Subacromial Bursa may play a role in Adhesive Capsulitis pathogenesis (SOURCE-2). Relevant vulnerable structures include:

  • Coracohumeral Ligament - In almost all Adhesive Capsulitis cases, the ligament was significantly thicker than both the asymptomatic and painful shoulders from other causes (SOURCE-5). This thickened and highly vascular fibrous scar tissue consists of type-III Collagen composed predominately of Fibroblasts and Myofibroblasts (SOURCE-20)

  • Anterior and Inferior Glenohumeral Joint Capsule (SOURCE-6)

  • Rotator Interval - significant increase in thickness/ density displayed in the majority of Adhesive Capsulitis cases when compared to asymptomatic and painful shoulders from other causes (SOURCE-5). Many Rotator Intervals also displayed increased vascularity (SOURCE-5)

Either a predisposing factor or sequela of adhesive capsulitis is altered positioning and Motor Control of the Scapula (SOURCE-1 (10)) which may present as areverse Scapulohumeral Rhythm .

Prevalence

Establishing an estimated prevalence of Adhesive Capsulitis is difficult. On one hand, its insidious onset and ambiguous symptoms may deter individuals from seeking professional help (SOURCE-3). On the other, many studies are conducted on specific populations with unusually high incidence when compared to the general population (SOURCE-3). Best estimates suggest Adhesive Capsulitis occurs in 2-5% of the population (SOURCE 3+4+6+21). This condition is also more common in females and those between the ages of 40-70 (SORUCE-3+4+6+21).

Risk Factors

Diabetes - a strong association between Diabetes and Adhesive Capsulitis has been established, where those with the condition have displayed ~5 fold the incidence compared to those without (SOURCE-3 (12) +14). These individuals were also more likely to experience the condition bilaterally (SOURCE-3 (2, 40, 102). While a consensus is yet to be reached, it has been postulated this phenomenon is due to an excess concentration of glucose increasing the rate of Collagen glycosylation and cross-linking in The Shoulder Girdle (SOURCE-5).

Pathology

While Adhesive Capsulitis is often idopathic, it may also result from trauma, surgery or prolonged immobilisation. The following lists pathologies that predispose Adhesive Capsulitis occur concomitantly or are a common sequela:

Subacromial Bursitis - may play a role in the onset of Frozen Shoulder and/ or cause Pain leading to apprehensive movement (SOURCE-2).

Scapular Dyskinesis - insufficient movement at the Glenohumeral Joint is compensated for with excessive Scapulothoracic Joint - Upward Rotation , leading to Dyskinesis (SOURCE-18).

Proximal Humerus Fracture - an extrinsic factor that may lead to secondary adhesive capsulitis

Rotator Cuff Tear - considered a major intrinsic predisposing factor for secondary Adhesive Capsulitis (SOURCE-6)

Rotator Cuff Tendinopathy - considered a major intrinsic predisposing factor for secondary Adhesive Capsulitis (SOURCE-6)

Long Head of Biceps Tear / Tendinopathy - considered a major intrinsic predisposing factor for secondary Adhesive Capsulitis (SOURCE-6)

Cervical Spine Pathology - with nervous innervation linking the neck to The Shoulder Girdle , poor Cervical posture or motion causing Radiculopathy provides an avenue by which Cevical Pathology could predispose Adhesive Capsulitis. While Cevical pathologies often occur comcomitantly with Adhesive Capsulitis, some attempts have been made to investigate their role as a risk factor. One study found a significant association between C5 Foraminal Spinal Stenosis and ipsilateral frozen shoulder, apparent in ~1/4 of patients (SOURCE-23)

Diabetes Mellitus - those with Diabetes Mellitus are 5x more likely to develop Adhesive Capsulitis than non-diabetic controls and the disease course is typically more severe and less responsive to treatment (SOURCE-28). 13.4% of those with Diabetes had Adhesive Capsulitis, while 30% of those with Adhesive Capsulitis had Diabetes (SOURCE-28).

Thyroid Disease - Thyropathies are strongly associated with Adhesive Capsulitis, with some suggesting a 2.6x increased development risk (SOURCE-29). While Hyperthyroidism appears to share a similar relationship, Hypothyroidsim is suggested to be a more profound risk factor for the development of Adhesive Capsulitis (SOURCE-29).

Differential Diagnosis

The following pathologies share symptoms with Adhesive Capsulitis and may serve as an alternative diagnosis (SOURCE-32):

Assessment

Observation

Range of Motion

While all Glenohumeral Joint motions may be compromised, the most notable and consistent restrictions are seen in:

  • Active GH Joint - Abduction - one study found this to be restricted in all instances of Adhesive Capsulitis; however, it was also restricted in the vast majority of painful shoulders, making it sensitive but not specific (SOURCE-5)

  • Active GH Joint - External Rotation - often the first motion to be compromised in Adhesive Capsulitis yet rarely affected in other painful shoulder patholgies, making it a sensitive and specific diagnostic tool (SOURCE-5+14+25). If External Rotation is only restricted when performed actively a Rotator Cuff pathology should be suspected

  • Active GH Joint - Flexion

In the majority of Adhesive Capsulitis patients Pain precedes a loss of motion (SOURCE-25). Insufficient movement at the Glenohumeral Joint is compensated for at the Scapulothoracic Joint , leading to a disturbed Scapulohumeral Rhythm with increased Scapulothoracic Joint - Upward Rotation (SOURCE-18). The practitioner may manually aid stabilisation of the Scapula through movement to better isolate the Glenohumeral Joint (SOURCE-21). Full Range of Motion in any direction would challenge Adhesive Capsulitis diagnosis (SOURCE-21).

Manual Muscle Testing

While compromised positioning of the Scapula may bear an effect, in Adhesive Capsulitis the dynamic stabilises remain largely unaffected. This would indicate at less compromised ranges, Manual Muscle Testing should remain within normal limits.

Palpation

Imaging

Although the diagnosis of Adhesive Capsulitis is based predominately on clinical findings, imaging may be used to exclude concomitant pathology (SOURCE-27):

  • Radiographs (X-Rays)- while soft-tissue not visible can rule out differentials or in concomitant pathologies such as Calcific Tendonitis , early stage Osteoarthritis , Fracture (SOURCE-4+21)

  • Magnetic Resonance Imaging (MRI)- although capsular thickening may be observed on MRI’s they are not considered diagnostic for Adhesive Capsulitis (SOURCE-21). Akin to X-Rays, MRIs can evaluate for other differentials such as Rotator Cuff Tendinopathy or Subacromial Bursitis (SOURCE-4+21)

Blood Test

  • Fasting Glucose Test - an absence of Diabetes diagnosis (SOURCE-21)

  • Erythrocyte Sedimentation and C-reactive protein - may be elevated with primary Adhesive Capsulitis but non sensitive nor specific (SOURCE-21)

Treatment

A consensus on an appropriate protocol for Adhesive Capsulitis is yet to be established, with some authors arguing the condition naturally recovers over the course of a few years (SOURCE-4+6). Conversely, several papers have reported symptoms such as Pain and immobility persisting for as long as 7 years (SOURCE-4+6). A consistent finding among many of the papers discussed in this section is combination therapies are more effective in the treatment of Adhesive Capsulitis than any stand alone therapy. For most patients, nonsurgical treatment is effective (SOURCE-21+30). As a general trend, the focus for each stage should be as follows (SOURCE-14):

  • Stage-I- Disrupt the cycle of Inflammation and relieve Pain . ADL modification/ patient education

  • Stage-II- Physical therapy and Stretching , particularly of the Glenohumeral Joint to improve mechanics. Pain intensity should dictate treatment intensity

Stretching

Both supervised and self-guided Stretching has been supported in the treatment of Adhesive Capsulitis (SOURCE-3+6+7+8+9).Techniques:

  • Stretching

    • One six week study applied a progressive stretching technique (stretch held for a few seconds and repeated 10-15 times with increasing intensity) to GH Joint - Flexion , Scaption, GH Joint - External Rotation (in Scapula plane) and GH Joint - Internal Rotation (in half side-lying) three times a week. They reported a significant effect on symptoms of Adhesive Capsulitis such as range of motion, functional status and patient satisfaction (SOURCE-10)

    • A highly generalised stretching/ strengthening program was found to be as effective as the the same program with added mobilisations after 3 sessions a week for 5 weeks. Findings included reduced Pain and increased ranges of motion (SOURCE-11)

  • Proprioceptive Neuromuscular Facilitation

    • A sequence of Glenohumeral Joint and Scapulothoracic Joint motions performed in a 5-8 second contract-relax manner provided additional benefit for night pain and certain ranges of motion than conventional physical therapy alone (SOURCE-7)

    • A sequence of anterior elevation, posterior depression, posterior elevation and anterior depression was applied to the Scapula . While all groups (PNF and physiotherapy, exercise and physiotherapy and physiotherapy alone) effective for improving shoulder function and range of motion in a single hour session, the PNF group had a greater analgesic effect (SOURCE-8)

    • A conventional group of stretching and strengthening techniques was compared to conventional treatment with proprioceptive closed chain exercises in the quadruped position for 16 sessions over a 4 week period. While both were effective in treating Pain and range of motion in patients with Adhesive Capsulitis, the proprioceptive group showed significantly greater reductions in Pain (SOURCE-9)

Structures - stretching of the following muscles and structures have been supported (SOURCE-9+10+11+13):

Strengthening

Strength training within Pain -free ranges has been supported in the treatment of Adhesive Capsulitis (SORUCE-3). Reported benefits include reduced Pain and increased Range of Motion (SOURCE-11). While strengthening many of The Shoulder Girdles Muscles may be of benefit, the following muscles have been supported as a treatment for Adhesive Capsulitis:

  • Rotator Cuff - isometric and Isotonic exercises have improved symptoms of Pain , range of motion and function (SOURCE-9+8+11+12). A combined protocol of Rotator Cuff strengthening with joint Mobilisations and TENS provided further alleviation to Adhesive Capsulitis symptoms (SOURCE-12). Exercises progressed from isometric to isotonic Muscle Contractions over 12 sessions in 4 weeks (SOURCE-12)

  • Middle and Lower Trapezius - isometric and Isotonic exercises have improved symptoms of Pain , range of motion and function (SOURCE-9+13). As a specific example, improving function of the lower fibres has been shown to reduce Scapula tilting in those with diabetic Adhesive Capsulitis (SOURCE-13). Akin to the Rotator Cuff, the addition of isotonic and isometric Lower Trapezius exercises to Mobilisations reduced the presence of Scapular Dyskinesis in those with Adhesive Capsulitis (SOURCE-13)

  • Serratus Anterior - direct Serratus training as part of a generalised strength program was shown to significantly improve symptoms of Adhesive Capsulitis including Range of Motion , functional status and patient satisfaction (SOURCE-10)

Initial Phase - starting with isometrics (SOURCE-12)

Mid-Phase

Late Phase

Mobilisations

Manual Mobilisations have been supported in the treatment of Adhesive Capsulitis (SOURCE-3+15+11+16+17). End-Range mobilisations may be of greater benefit to those with Adhesive Capsulitis. (SOURCE-16) compared End-Range with Mid-Range mobilisations in tandem with a conventional therapeutic approach (heat therapy, TENS and home-exercise) over 10 sessions in two weeks. While both groups boasted significant results on Pain , mobility and function, the End-Range mobilisations were superior in treating range of motion and function. Interestingly, the paper did also report Mid-Range mobilisations were better for improving Pain . Joint Play - a regimen of general stretches/ exercise and the addition of Maitland’s Joint Play techniques which included AP, PA and Inferior glides to the Glenohumeral Joint improved measures of Pain , range of motion and disability over a 5 week period. Grade I-II mobilisations were performed at a rate of 2-3 oscillations a second for 30 seconds and repeated 5 times each, for 3 sessions a week over 5 weeks. These findings weren’t significantly greater than the general stretches/ exercise control (SOURCE-11). The following mobilisation techniques may be relevant:

Mobilisation with Movement - one study (SOURCE-15) compared a conventional progressive Stretching strategy (end-range Scaption, GH Joint - Flexion and Rotations with arm straight), heat therapy and TENS against an intervention group which added mobilisations (3 sets of 15 Shoulder - MWM Techniques in GH Joint - Flexion , GH Joint - Abduction and GH Joint - Internal Rotation ). While both groups were effective in alleviating symptoms of Adhesive Capsulitits, the mobilisation group had additional Pain reduction and increased range of motion and function benefits. This study was conducted on individuals who were at least at the Freezing Stage (3 months +). The following Mobilisation with Movement techniques may be relevant:

Dry Needling

There is some evidence to suggest Dry Needling may be used for Adhesive Capsulitis to improve symptoms such as Range of Motion and Pain (SOURCE-22). Interestingly, one study found bee venom acupuncture in conjunction with phyiotherapy to be more effective and non-steroidal injections at 3 month follow-up with a continued benefit displayed at 12 months (SOURCE-6). Another study used needling techniques at myofascial “trigger points” (SOURCE-22). The support for dry needling as a treatment for adhesive capsulitis remains in its infancy (SOURCE-21). The following structures may be relevant to needling in cases of Adhesive Capsulitis:

Surgery

A minimum of 6 months of structured conservative treatment is recommended before surgical intervention is considered, with some suggesting this number should be high as 12 months (SOURCE-3+14+21+30+31):

  • Manipulation Under Anaesthesia (MUA)- patient is placed under anaesthesia while the practitioner manipulates the Humerus to forcefully break up adhesions/ the Contracture d Glenohumeral Joint Capsule . Some findings suggest MUA may be effective as a standalone treatement for reducing symptoms of Pain and restoring Range of Motion in those with Adhesive Capsulitis; however, as it is a “blind” (without direct visualisation) procedure it may carry a greater risk of iatrogenic injuries such as Fractures or Tears of the Glenoid Labrum or Rotator Cuff . While contended, postoperative GH Joint - External Rotation may be more favorable with MUA when compared to arthroscopic release

  • Arthroscopic Capsular Release- the thickened/ Contracture d Glenohumeral Joint Capsule and any associated adhesions are surgically cut to release tension. Cuts may be a full 360º capsule or limited release and with direct visualisation may reduce the risk of iatrogenic complications. Both Range of Motion and Pain assocaited with Adhesive Capsulitis have displayed improvement following this procedure even at multi-year follow-ups

While both MUA and Arthroscopic Capsular Release have individually shown promise, studies have found that combining the two procedures does not appear to provide added benefit over either standalone procedure (SOURCE-30). Although postoperative recommendations remain nebulous, there appears a consensus that rehabilitation is integral for preventing recurrence (SOURCE-33). Some authors advocate immediate/ early intervention to maintain the newly found ranges, while others recommend commencing rehabilitaion when Pain subsides roughly 1-2 weeks following surgery (SOURCE-33). Rehabilitative techniques include many of those listed in this section for conservative management, including (SOURCE-33):

Medication

With Inflammation playing a key role in the onset of Adhesive Capsulitis it’s reasonable to suggest anti-inflammatory interventions may be of benefit, particularly in the early stages of the condition.

  • Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)- while these drugs make an appearance in several studies, there is a paucity of literature comparing it as an intervention against a control (SOURCE-4). Various NSAIDs revealed a decrease in Pain compared to baseline; however, these drugs failed to significantly alter other symptoms such as range of motion deficits (SOURCE-4 (61)). NSAIDs are most likely to be of benefit in Stage-II (SOURCE-14)

  • Oral Steroids- these drugs show some capacity to catalyse recovery in the early phases of treatment; however, at long-term follow-up these interventions fail to display any benefit over physical therapy controls (SOURCE-4)

  • Intra-Articular Steroid Injections- Akin to oral steroids, intra-articular injections may catalyse recovery in the short-term but fail to provide significant benefit over other interventions such as physical therapy (SOURCE-4). Intra-Articular Steroid Injections are most likely to be of benefit in Stages I + II (SOURCE-14)

Other

  • Extracorporeal Shockwave Therapy - may be better than a placebo at 5 months and oral steroids (SOURCE-6)

  • Laser Therapy - at at week follow up has displayed significant improvement in Pain and Range of Motion in diabetic frozen shoulder (SOURCE-6)

  • Cryotherapy - whole body cryotherapy has displayed additional benefit to physiotherapy and joint mobilisations (SOURCE-6)

References

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