New York Physical Therapy Ebook Continuing Education

While reviewing the classification system for FS and associated conditions, it is evident that there is a high correlation between these diagnoses and two comorbidities in particular: diabetes and thyroid diseases. The incidence of frozen or adhesive capsulitis rises to 10% - 38% with diabetes and thyroid problems (Kelley (2009); Milgrom (2008); Pandey (2022); Ryan (2016); Shah (2015) and Zreik (2016). External rotation and elevation were found to be more restricted in patients with diabetes compared to those without. This can put this population at risk for increased pain and functional deficits with daily activities (Shah, 2015). The recognized higher incidence of thyroid disease in women (8-9x than that of men) may also explain the higher incidence of FS in women vs. men (Chiavato, 2019). Thus, it is important for clinicians to screen for any pre- existing conditions during an evaluation with new patients experiencing shoulder dysfunctions. common symptoms noted are: greater than 25% loss of motion in two planes, passive external rotation loss greater than 50% of non-involved shoulder and/or less than 30 degrees of active external rotation on the involved side. Along with these common symptoms, radiographs are negative for related shoulder conditions, such as osteoarthritis or osteophytes (bone spurs). (Zappia, 2016). This faulty movement pattern can be seen during active elevation of the shoulder. This common mobility deficit pattern is described by the classic capsular pattern of Cyriax- where the greatest limitation occurs in external rotation, followed by restriction of elevation and then restriction of internal rotation. Unlike many shoulder dysfunctions and injuries, strength deficits do not dominate the clinical profile for FS or adhesive capsulitis. When strength deficits are present, weakness is usually noted in shoulder internal rotation (inflammation/tightness of a prime mover- the subscapularis) and elevation. Weakness is typically dependent on the length of recovery time. Strength deficits can emerge due to the combined effects of disuse atrophy, prolonged positions in a shortened lever arm and/or pain suppression factors. Special tests for shoulder impingement, labral involvement, and glenohumeral instability (i.e., the relocation test) are not predictive in the initial assessments. These tests can provoke end-range stress on the restricted shoulder capsule, leading to painful response and therefore a false-positive result. Frequent primary functional impairments include difficulty with daily activities such as sleep positions, routine dressing/ grooming and overhead lifting/reaching. Unexpected or quick movements can cause pain, described by some patients as a level 10 on the visual analog scale (VAS). These intense pain responses are more common during the freezing phase of FS. However, this pain may be presents with functional activities for months after the initial onset despite overall decreased pain at baseline and improved ROM. With worsened mobility restrictions in the frozen phase of FS, difficulty and pain with additional daily activities such as reaching across the body and behind the back (like reaching to the back pocket for a wallet) may also arise. In early onset of frozen shoulder, the presence of B-lymphocytes and macrophages can represent an initial immunologic reaction, which leads to inflammation and fibrosis (Ryan, 2016). This irritation results in increased fibroblasts, inflammatory cytokines and interleukins. In addition, increased vascularity and angiogenesis are present with inflammation and a proliferation of nerve cells in the anterior synovium (Pandey, 2022). These changes explain the pain during the initial onset of FS and provide the rationale for pain relieving medication and joint

Multiple frozen shoulder and adhesive capsulitis studies show the societal prevalence is between 2%-5% (Pandey 2022; Kelley, 2009) and that number is projected to increase over the next several decades. These dysfunctions in daily activities have led to a loss of work productivity that estimated at about twelve billion dollars in costs in 2000 (Johnson, 2005). It is noted that women are more prone to shoulder stiffness problems, particularly idiopathic frozen shoulder. This could be related to women having a higher degree of capsular hyper-mobility and decreased protective upper body strength (Sheridan 2006). These conflicting presentations eventual lead to inflammation changes and capsular micro- traumas in older women, specifically women around sixty years old. Frozen shoulder and additional shoulder stiffness problems typically appear between ages forty to sixty. Unfortunately, treatments for these problems are less effective in people over sixty years old. The occurrence of frozen shoulder increases the likelihood of the problem in the contralateral shoulder by 5-34%. Classification system & associated impairments The major categories of shoulder stiffness are primary, secondary, and post-traumatic. ● Primary: Primary shoulder stiffness relates to idiopathic FS, with no known cause or associated history of disease. With primary shoulder stiffness, there are no definitive sources of past trauma to the shoulder complex or noted activity or overuse of shoulder that can sometimes lead to latent micro- trauma pathways. ● Secondary : This category can be sub-divided into systemic, extrinsic, and intrinsic. Secondary Systemic stiffness causes include history of comorbidities, such as the previously mentioned conditions of diabetes and thyroid diseases. Secondary extrinsic stiffness causes include varied pathologies not related specifically to the shoulder – such as cervical disc disease, self-imposed immobilization, cerebrovascular accident, and post- mastectomy. Finally, secondary intrinsic stiffness relates to other common orthopedic shoulder injuries, such as rotator cuff syndrome, glenoid osteo-arthritis and calcific tendonitis. These injuries can lead to inflammatory responses within the shoulder that can lead to a FS diagnosis. ● Post-traumatic : Post-traumatic shoulder stiffness relates to causes such as deep contusions, post-surgical contracture following acromioclavicular decompression or labral repairs, humeral fractures and excessive immobilization time after capsular stabilization procedures. In capsular shift surgeries specifically, where there is minimal post op immobilization (10 days or less in a sling), there is an increased risk of post-traumatic shoulder stiffness. Another type of post- traumatic cause for FS has been recently identified following a COVID-19 vaccination. This may be related to mechanical irritation from the depth of injection or a biochemical response to the vaccine (Demyttenaere (2022); Sahu (2022)). Healthcare Consideration: Shoulder dysfunction of any etiology will routinely alter a patient’s ability to move in their own plane of scapula through full elevation. The most critical indicators of FS or adhesive capsulitis are the loss of active and passive range of motion (ROM). The most Pathophysiology The joint capsule demonstrates thickening with inflammatory changes centered at the rotator cuff. The deltoid insertion, adjacent to the long head of the biceps and/or the insertion of the subscapularis tendon are typically the areas where the earliest reports of pain are noted. This area is a common point of pain shared by many shoulder dysfunctions. When patients are asked to point to their area of pain with one finger, it usually focuses on this spot and is tender to palpation.

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Book Code: PTNY1024

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