Notes
5
Adhesive Capsulitis
Adhesive capsulitis, or frozen shoulder, is an inflammatory condition that results in pain, stiffness, and loss of range of motion in the shoulder. It is a relatively common problem and affects approximately 3 to 5 percent of the general population.1 The condition is more common in individuals with diabetes mellitus and thyroid disease.2-4 Notably, adhesive capsulitis most commonly affects women and individuals between fifty and seventy years of age.1
The progression of adhesive capsulitis can be classified into three distinct stages: freezing (painful), frozen (stiff), and thawing.1,5,6 In the freezing (painful) stage, there is the gradual onset of diffuse shoulder pain over the course of several weeks to several months. Next, in the frozen (stiff) stage, there is an improvement in shoulder pain, but a gradual loss of active and passive range of motion in all planes. This stage can last between four and twelve months. Lastly, in the thawing stage, which lasts between five and twenty-six months, there is a gradual improvement in active and passive range of motion.1,5,6 While it was previously believed that the course of adhesive capsulitis was self-limiting and that patients would make a full functional recovery, recent evidence has disputed this claim.7 Several studies that examined long-term follow-up in patients with adhesive capsulitis demonstrated that some patients had persistent pain and lasting restrictions in range of motion of the shoulder,8,9 and surgical intervention or manipulation may be needed to minimize these deficits.
Pathophysiology
Adhesive capsulitis may be categorized as primary or secondary.10 In primary idiopathic adhesive capsulitis, the pain and functional limitations of the shoulder have no underlying cause. In contrast, in secondary adhesive capsulitis, the symptoms result from previous trauma, previous surgery, or associated medical conditions, including diabetes and thyroid disease.10 Regardless of etiology, the pathophysiology of adhesive capsulitis is not well understood. It is believed that an inflammatory process contributes to thickening, fibrosis, and contracture of the glenohumeral joint capsule, including the coracohumeral ligament.6,11 Biopsies of the shoulder joint capsule in patients with adhesive capsulitis have identified both chronic inflammatory cells, including B cells, T cells, and mast cells, and dysregulated cytokines, including IL-1β, IL-6, and TNF-α. These cellular changes contribute to the hallmark histologic changes of fibroblast proliferation in Type I and Type III collagen. Notably, the fibroblasts change into smooth muscle fibroblasts (myofibroblasts), which causes the contraction of the joint capsule.6,12 Altogether, these processes contribute to a mechanical restriction of motion, which results in the classical symptoms of adhesive capsulitis.
History
The diagnosis of adhesive capsulitis is made clinically, so it is essential to first obtain a thorough history of the present illness.1,11,13 Patients typically present with an insidious onset of pain progressing over the course of several months. The pain often is deep and diffuse but also may localize to the anterior rotator interval.14 Pain can be present at night, at rest, or with activity. Patients may report the loss of both active and passive range of motion of the shoulder. This deficit notably affects activities of daily living, including dressing, overhead activities, and reaching to the side or behind the back. In addition to gathering details about the presenting symptoms, it is important to gather information about hand dominance, occupation, recent shoulder injury or surgery, and comorbid medical conditions, such as diabetes, thyroid disease, or endocrine disorders. Notably, the presence of diabetes, in addition to increasing the likelihood of adhesive capsulitis, portends a worse prognosis in patients with this condition.15,16
Physical Examination
The next step in evaluation and diagnosis of adhesive capsulitis is a thorough examination involving inspection, palpation, and range of motion of the bilateral shoulders. The bilateral shoulders are examined with careful attention to signs of previous surgery. Further, palpation may elicit tenderness in the region of the bicipital groove, as the synovium of the long head of the biceps tendon is continuous with that of the glenohumeral joint.11 Following inspection and palpation, it is important to assess and compare the range of motion in both shoulders. Specifically, forward elevation, abduction, external rotation at the side, and internal rotation to vertebral height should be documented. Careful examination is required as adhesive capsulitis is commonly mistaken for glenohumeral arthritis and vice versa. Importantly, OA of the glenohumeral joint has several distinguishing features such as a grinding sensation or crepitation. Additionally, radiographs will be normal in adhesive capsulitis, while the presence of osteophytes and joint space narrowing will confirm the presence of arthritis. With respect to timing, adhesive capsulitis typically progresses over a shorter period of time than glenohumeral arthritis, which progresses over a span of months to years.
In patients with adhesive capsulitis, a loss of both active and passive range of motion is observed in all planes. The distinguishing feature in this condition is the loss of passive range of motion, especially in external rotation at the side.11,13 Video 5.1 illustrates the loss of passive range of motion in a patient with left-sided adhesive capsulitis, while video 5.2 illustrates the loss of active range of motion in a different patient with left-sided adhesive capsulitis. Notably, figure 5.1 demonstrates the deficit in forward elevation, external rotation, and internal rotation compared to the contralateral, unaffected side. In addition, there may be pain at the extremes of motion due to stretching of the joint capsule.6 Strength of the rotator cuff should be normal in the absence of additional pathology.
Video 5.1a: Examination of a Supine Patient with Adhesive Capsulitis. The examiner demonstrates a range of motion assessment on the left (affected) shoulder of a supine patient with adhesive capsulitis. In order, the patient demonstrates significant deficits in forward elevation, external rotation at the side, abduction at 90 degrees, external rotation at 90 degrees, and internal rotation at 90 degrees with passive range of motion.
Video 5.1b: Examination of a Supine Patient with Adhesive Capsulities. In the same patient, the examiner demonstrates a range-of-motion assessment on the right (unaffected) shoulder in the supine position. In order, the patient demonstrates normal passive range of motion with respect to forward elevation, external rotation at the side, abduction at 90 degrees, external rotation at 90 degrees, and internal rotation at 90 degrees.
Video 5.2: Examination of a Standing Patient with Adhesive Capsulities. In a different patient with left-sided adhesive capsulitis, the examiner asks the patient to perform active forward elevation, external rotation at the side, and internal rotation to vertebral height in the bilateral shoulders. The patient clearly has significant deficits in all three planes in the left (affected) shoulder compared to the right (unaffected) shoulder.
Key Terminology
Inflammatory condition, also known as frozen shoulder, that results in pain, stiffness, and loss of both active and passive range of motion in the shoulder. ↵
Initial stage in adhesive capsulitis, characterized by the gradual onset of diffuse shoulder pain over the course of several weeks to months. ↵
Second stage in adhesive capsulitis, characterized by improvement in shoulder pain, but a gradual loss of active and passive range of motion in all planes. ↵
Third and final stage in adhesive capsulitis, characterized by a gradual improvement in active and passive range of motion lasting between five and twenty-six months. ↵
References
Manske RC, Prohaska D. Diagnosis and management of adhesive capsulitis. Curr Rev Musculoskelet Med. 2008;1(3-4):180-189. ↵
Huang SW, et al. Hyperthyroidism is a risk factor for developing adhesive capsulitis of the shoulder: a nationwide longitudinal population-based study. Sci Rep. 2014;4:4183. ↵
Kingston K, et al. Shoulder adhesive capsulitis: epidemiology and predictors of surgery. J Shoulder Elbow Surg. 2018;27(8):1437-1443. ↵
Wang JY, et al. Hyperlipidemia is a risk factor of adhesive capsulitis: real-world evidence using the Taiwanese national health insurance research database. Orthop J Sports Med. 2021;9(4):2325967120986808. ↵
Neviaser RJ, Neviaser TJ. The frozen shoulder: diagnosis and management. Clin Orthop Relat Res. 1987(223):59-64. ↵
Le HV, et al. Adhesive capsulitis of the shoulder: review of pathophysiology and current clinical treatments. Shoulder Elbow. 2017;9(2):75-84. ↵
Wong CK, et al. Natural history of frozen shoulder: fact or fiction? a systematic review. Physiotherapy. 2017:103(1):40-47. ↵
Hand C, Clipsham K, Rees J, Carr AJ. Long-term outcome of frozen shoulder. J Shoulder Elbow Surg. 2008; 17(2):231-236. ↵
Shaffer B, Tibone JE, Kerlan RK. Frozen shoulder: a long-term follow-up. J Bone Joint Surg Am. 1992;74(5):738-746. ↵
Date A, Rahman L. Frozen shoulder: overview of clinical presentation and review of the current evidence base for management strategies. Future Sci OA. 2020;6(10):FSO647. ↵
Neviaser AS, Neviaser RJ. Adhesive capsulitis of the shoulder. J Am Acad Orthop Surg. 2011;19(9):536-542. ↵
Akbar M, McLean M, Garcia-Melchor E, et al. Fibroblast activation and inflammation in frozen shoulder. PLoS One. 2019;14(4):e0215301. ↵
Mezian KR, Coffey R, and Chang KV. Frozen Shoulder. Treasure Island, FL: StatPearls; 2021. ↵
D’Orsi GM, Via AG, Frizziero A, Oliva F. Treatment of adhesive capsulitis: a review. Muscles Ligaments Tendons J. 2012;2(2):70-78. ↵
Cinar M, Akpinar S, Derincek A, Circi E, Uysal M.Comparison of arthroscopic capsular release in diabetic and idiopathic frozen shoulder patients. Arch Orthop Trauma Surg. 2010;130(3):401-406. ↵
Griggs, SM, Ahn A, and Green A. Idiopathic adhesive capsulitis: a prospective functional outcome study of nonoperative treatment. J Bone Joint Surg Am. 2000:82(10):1398-1407. ↵