Stiff Shoulder

Pain

Pain is usually the patient's chief presenting complaint. Patients less often report stiffness, although the two frequently coexist. To understand how a painful, stiff shoulder is affecting one's daily life, several descriptors of pain must be established with explicit questioning adapted to each response given by the patient ( Box 51.1 ). Pain is a difficult parameter to analyze because it is a wholly subjective complaint that, despite numerical scales, cannot be compared between individuals. It is the physician's perception of the patient's pain that often guides management. The two most common reasons that pain drives a patient to seek medical attention are severity and timing ( Box 51.2 ).

Severe pain brought on acutely by trauma generally mandates medical care soon after the injury occurs. Underlying differential diagnoses include fracture, dislocation, rotator cuff tear, biceps tendon (long head or distal/elbow) tear, pectoralis major tear, and labral tear. Further examination with or without imaging can typically lead to an accurate diagnosis in this situation. The pain attributed to adhesive capsulitis is usually minimal at rest but can become severely disabling at the end extremes of arc of motion (the freezing stage). With time, this pain usually minimizes to being present at just the extremes of motion while stiffness prevails in the frozen stage. However, by this point, many patients have been dealing with this for some time, and have grown frustrated. Intermittent severe pain is also common with compressive joint loads in persons with osteoarthritis and with calcific tendonitis (which is sometimes even referred to as the “kidney stone of the shoulder”). Patients who sustain an injury with minimal pain may not seek care for several weeks to months, if at all. Some patients do not even recall a clearly identifiable event that precipitated pain. However, in this situation, mild pain may lead to unappreciated chronic disuse or underuse of the extremity (“pseudoimmobilization” of the shoulder) and possibly incite a stiffness response that may eventually warrant medical attention (e.g., rotator cuff tear and impingement).

Other Findings (Stiffness, Weakness, Crepitus)

When pain is mild, other factors that limit function are usually stiffness, weakness, or crunching/grinding at the shoulder. Weakness is a common symptom in patients with a rotator cuff tear and neuromuscular dysfunction (e.g., cerebrovascular disease, a cervical spine disorder, Parsonage-Turner syndrome, a burner/stinger, and myasthenia gravis). Crepitus is commonly reported after surgery (especially after rotator cuff repair) and with rotator cuff tendonitis, subacromial bursitis, snapping scapula (i.e., scapulothoracic bursitis, a space-occupying mass, or dyskinesis), arthrosis, and instability.

One of the primary goals in diagnosing the stiff shoulder is determining the direction of motion loss. This determination allows the location of the pathologic process that is responsible for the motion deficit to be deduced, thereby pointing to the methods necessary to treat it. For example, global loss of both active and passive motion reflects idiopathic adhesive capsulitis. Early in the disease process, loss of external rotation in the adducted arm is attributable to rotator interval contracture. The shoulder of an athlete whose sport involves throwing may lose internal rotation with the arm abducted (GIRD), which is attributable to tightness of the posterior capsule. The latter two conditions are only two among many shoulder and non–shoulder-related pathologies contributing to a stiff shoulder ( Box 51.3 ).

Primary/Idiopathic Adhesive Capsulitis

In 1934, Codman described a clinical condition of glenohumeral stiffness that he called “frozen shoulder.” The term idiopathic adhesive capsulitis was then coined by Neviaser in 1945 to describe pathologic conditions in stiff shoulder capsules. Neviaser described findings of fibrosis, chronic inflammation, and capsular contracture that were responsible for the pathologic loss of motion. The terms frozen shoulder and adhesive capsulitis are used interchangeably, leading to confusion and ambiguity in shoulder stiffness nomenclature literature. Inconsistencies in disease classification, diagnosis, staging, and treatment have led to further uncertainty in the literature. Although the disease is commonly believed to be self-limiting, the true natural history is not definitively known. Adhesive capsulitis may affect up to 5% of the population, with a greater preponderance in women. The condition tends to affect middle-aged patients in their nondominant arm with a variable history of minor trauma (up to 30%). A link between adhesive capsulitis and lower body mass index and positive family history has also been described. Development of adhesive capsulitis in the contralateral shoulder will occur in approximately one third of patients. The disease does not seem to recur in the same shoulder.

Adhesive capsulitis has been associated with other systemic conditions that have an apparent lack of innate relation to the shoulder. The most commonly associated systemic disease is diabetes mellitus. In a large retrospective review of diabetics with adhesive capsulitis, Yian et al. showed a correlation between adhesive capsulitis and the use of insulin or oral glycemic agents, suggesting that diabetics requiring more aggressive glycemic management tend to be predisposed to an increased risk of adhesive capsulitis; however, hemoglobin (Hgb)A1c, in and of itself, did not appear to have a direct correlation. Importantly, patients with adhesive capsulitis and diabetes tend to be more difficult to manage, with less clinical improvement and higher rates of recurrence, especially in patients with peripheral neuropathy, patients who have had a longer duration of time since the diagnosis of diabetes, and older patients. Both hypothyroidism and hyperthyroidism have also been observed with adhesive capsulitis, with some suggestion that higher thyroid stimulating hormone (TSH) levels may be independently linked with bilateral and more severe cases. Dupuytren contracture, an inherited condition of the hand characterized by digital flexion contracture and adhesions, has also been associated with adhesive capsulitis. Although autoimmune disease has been suggested to be an associated condition, autoimmune serology testing has proved to be inconclusive.

The true cause of adhesive capsulitis remains unknown. Nevertheless, a progression of stages (freezing, frozen, and thawed stages) has been cited and is often used in the literature. Initially the instigation of a fibrinous hypervascular, hypertrophic synovitis leads to capsular scarring and loss of the axillary fold (the freezing stage). The precipitating factor may be related to a fibrotic cascade involving inflammatory cytokines, including transforming growth factor-β, tumor necrosis factor α, interleukins, or cyclooxygenase 1 or 2. These various cytokines have been found to be markedly elevated in the subacromial space and capsular tissue in patients with adhesive capsulitis.

Pain is often moderate to severe, especially at night. Once resolution of the synovitis occurs, a dense hypercellular collagenous fibrotic capsule remains, which exhibits significant stiffness (frozen stage). Pain is improved and is generally present only at the ends of motion and at night. Adhesions and stiffness variably persist, both in severity and in duration. Pain eventually minimizes or resolves completely (thawed stage). Despite the lack of a well-defined natural history, Grey reported that 96% of patients with a minimum of 2 years of follow-up had normal function with reassurance and use of oral pain medication. At 4-year follow-up, Miller et al. reported that 100% of patients had normal function and minimal pain with home-based therapy and use of oral antiinflammatory medications. In contrast, O'Kane et al. reported that up to 40% of patients could not lift an 8-lb object onto a shelf or a 20-lb object at their side at 2-year follow-up. Further, Binder et al. reported on 16 patients with residual mild to severe limited motion at 3.5-year follow-up. At longer follow-up (more than 4 years), residual pain and lost motion has also been reported in up to half of patients.

Secondary/Acquired Causes of Shoulder Stiffness

Postoperative loss of motion is the most common acquired cause of shoulder stiffness. The incidence of stiffness after arthroscopic and open-shoulder surgery is variable but nonetheless is an ever-present risk that must be discussed with patients before undertaking elective shoulder surgery. Intraarticular arthroscopic shoulder surgery (e.g., labral repair for instability or superior labral anterior to posterior [SLAP] repair) generally leads to intraarticular adhesions and capsular contracture, but not extraarticular contracture. Rotator cuff repair (both open and arthroscopic) and fracture fixation may result in subacromial adhesions in addition to capsular contracture. Huberty et al. reported that after arthroscopic rotator cuff repair, patient dissatisfaction due to stiffness was observed in 4.9% of nearly 500 repairs. Further, patients with Workers’ Compensation status (9%) and who were younger than 50 years (9%) were more likely to be dissatisfied as a result of stiffness. A systematic review by Denard et al. reported stiffness outcomes after arthroscopic rotator cuff repair for seven Level I through IV evidence studies. In this review it was found that the incidence of transient stiffness that was responsive to nonoperative treatment and resistant stiffness requiring surgical release was 10% and 3.3%, respectively. Further, the outcomes of patients requiring a repeat operation were successful in that their motion improved to a level comparable with that of the persons who did not require a repeat operation. Stiffness after instability surgery (anterior and posterior ) is also common, especially in cases that involve loss of external rotation, although to some degree, this is the goal of the surgery: to prevent instability. This treatment requires a balance of safe immobilization for healing but early enough motion to prevent stiffness. Nevertheless, if postoperative immobilization is continued for too long or the capsule is overtightened intraoperatively, patients are at risk for stiffness. After SLAP repair, stiffness is a common cause of pain and dissatisfaction.

Patients with shoulder arthrosis (e.g., primary glenohumeral arthritis or rheumatoid arthritis) also have a tendency toward stiffness. Joint capsule thickening, especially anteriorly and in the rotator interval in persons with osteoarthritis, correlates to motion loss, especially with external rotation. In addition, early findings in persons with primary glenohumeral osteoarthritis include loss of internal rotation as a result of posterior capsular contracture. In these situations, stiffness often leads to unsatisfied patients who are experiencing pain. In patients with osteoarthritis who underwent arthroplasty (total shoulder and hemiarthroplasty) in four randomized clinical trials, stiffness improved significantly at final follow-up, with a greater degree of motion improvement, especially forward elevation, in patients who underwent total shoulder arthroplasty. In a subset of patients with shoulder stiffness after arthroplasty, it must be ascertained whether loss of motion is due to true adhesion formation or component malpositioning. In patients with component malpositioning, stiffness surgery is likely to be unsuccessful unless the underlying reason, the malaligned prosthesis, is addressed.

Patients undergoing surgical intervention for subacromial impingement and acromioclavicular joint arthritis have also been shown to develop secondary stiff shoulder. Evans et al. found an ~5% risk of developing adhesive capsulitis postoperatively in patients who have had an isolated subacromial decompression or in conjunction with arthroscopic distal clavicle excision. Additionally, it was found that history of contralateral adhesive capsulitis and an age between 46 and 60 years old were independent risk factors for developing secondary stiff shoulder.

In patients who have subacromial impingement without a rotator cuff may have significant posterior capsule tightness (correlating with loss of internal rotation) in their dominant arms and a more global capsule tightness (correlating with loss of internal and external rotation) in their nondominant arms. Athletes with internal impingement whose sport involves throwing have also been shown to have significant GIRD and posterior shoulder tightness. The shoulder used in throwing is an amazing example of adaptation of a joint to the repetitive high forces generated during the throwing motion. The motion disparity (excessive external rotation and loss of internal rotation) has been theorized to be due to both bony (humeral head retroversion) and soft tissue (static capsule and dynamic muscular tightness) adaptations. Further, throwers with GIRD have a higher risk of shoulder injury and need for shoulder surgery, which emphasizes the need for preemptive therapy to increase motion early when minor motion discrepancies are detected. In patients with internal impingement that is treated with physical therapy (posterior capsule stretching), symptom resolution is thought to be related to correction of posterior shoulder tightness (measured via cross-body adduction) but not GIRD correction. For further information regarding this topic, the reader is referred to Chapter 45 , which pertains to throwing injuries.