The structural anatomy of the glenohumeral articulation affords considerable range of motion to the shoulder. The osseous and soft tissue structures provide limited yet sufficient static and dynamic restraints to allow significant motion not only for activities of daily living but also for high-level athletic endeavors. At one end of the motion spectrum is shoulder instability, a pathologic and symptomatic condition in which the humeral head is unable to stay seated on the glenoid. At the other end of the continuum is the stiff shoulder. A vast range of clinical encounters and diagnoses encompass the stiff shoulder, both traumatic and atraumatic.
Patients with a stiff shoulder may present with a brief or long-standing persistent loss of motion. The shoulder may be stiff and/or painful. The treating physician may be the first to evaluate and manage these patients. However, many patients have already seen several clinicians and have undergone both nonoperative and operative treatments that have either been unsuccessful or only partially successful. It is not uncommon to encounter a frustrated and discouraged patient. It is also not uncommon to see patients who are unaware that they are stiff and whose perception of the primary issue is pain and, less commonly, motion loss. Thus the stiff shoulder is a commonly encountered diagnostic and therapeutic challenge. This chapter discusses the framework for evaluation, management, and outcomes of patients with a stiff shoulder.
Overview of Pathologies
Relevant Anatomy and Biomechanics
Motion of the shoulder is derived primarily from the glenohumeral joint and scapulothoracic “joint” in a 2 : 1 ratio, respectively. Three planes of motion are commonly used: axial (internal and external rotation), sagittal (flexion and extension), and coronal (abduction and adduction) or oblique coronal (scapular plane). Stability of the glenohumeral joint is maintained dynamically through concavity-compression forces exerted by the rotator cuff muscles. The glenohumeral ligaments and joint capsule are passive joint restraints that function at the extremes of range of motion to resist abnormal humeral head translation and rotation movements relative to the glenoid. In addition to the glenohumeral joint, the subacromial space and scapulothoracic articulation are interfaces that integrate shoulder motion. Thus one or all of these locations may become involved in the etiology and pathogenesis of a stiff shoulder via scar tissue adhesions or contracture.
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 (glenohumeral internal rotation deficit [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 55-1 ).
Idiopathic adhesive capsulitis
Type I and II diabetes mellitus
Endocrinopathy, including thyroid disorders
Rotator cuff tear
Glenoid labral tear
Thrower’s shoulder (glenohumeral internal rotation deficit)
Primary/Idiopathic Causes of Shoulder Stiffness
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 unfortunately 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%). Adhesive capsulitis will develop in the contralateral shoulder 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. Importantly, the conditions of patients with diabetes tend to be quite difficult to manage, with less clinical improvement and higher rates of recurrence, especially in persons with peripheral neuropathy, persons who have had a longer duration of time since the diagnosis of diabetes, and older persons. Both hypothyroidism and hyperthyroidism have been observed with adhesive capsulitis. 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 is unknown. Nevertheless, a progression of events (freezing, frozen, and thawed stages) has been proposed and 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 transforming growth factor-β. Pain is moderate to severe, especially at night. Once resolution of the synovitis occurs, a dense hypercellular collagenous fibrotic capsule remains, which exhibits significant stiffness. 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. 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 real risk that must be discussed with patients before undertaking elective shoulder surgery. Primarily intraarticular arthroscopic shoulder surgery (e.g., instability labral repair 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 recent 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 high 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 who have subacromial impingement without a rotator cuff tear have been found to 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 aggressive 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 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 50 , which pertains to throwing injuries.
The ability to obtain an accurate history is a key component of establishing a correct diagnosis. Obtaining an accurate history requires not only asking specific questions pertinent to a chief complaint but also actively listening and responding with successive adaptive questions related to the patient’s responses. The treating physician must recognize that the presence of pathology on advanced imaging (radiographs and magnetic resonance imaging [MRI]) is quite common in asymptomatic patients. Thus the history and physical examination are the only way to determine if patients’ complaints are concurrent with imaging findings (“treat the patient and not the MRI”). Time constraints in today’s world of medicine impose limitations on the amount of time spent with each patient, and thus many physicians have already examined images before seeing and examining the patient. This situation may prompt the examiner to make an untoward diagnosis of a condition that is truly asymptomatic (e.g., without obtaining a thorough history and performing a physical examination for a diabetic patient with a frozen shoulder, rotator cuff tendinopathy, and a possible partial tear on MRI, the physician may not discover the lost motion and may improperly formulate a treatment plan of rotator cuff repair). Taking a history and examining the patient before viewing images is advantageous, although this process may not be possible in some busy clinics.
Often the history of a present illness can all but definitively lead to a diagnosis before the patient is even examined or images are reviewed when assessing a stiff shoulder. Characterization of the principal symptoms attributable to the chief complaint should describe seven entities : location, quality, severity, timing (i.e., onset, duration, and frequency), setting, exacerbating and relieving factors, and associated manifestations. Patient demographics and epidemiology also must not be overlooked, especially age and gender, because these factors play a significant role in evaluating the stiff shoulder. More than two thirds of patients with a frozen shoulder are female. Rotator cuff tears are an age-related phenomenon, along with the risk of stiffness associated with their operative or nonoperative management. Symptomatic shoulder instability requiring surgical intervention is also on an age-related continuum, with its inherent risks of postoperative stiffness, as previously discussed.
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 55-2 ). 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 55-3 ).
Location (anterior, posterior, lateral, neck, back, arm, chest wall, or axilla)
Radiation (neck, arm, below elbow, into hand)
Quality (sharp, dull, achy, throbbing, or stabbing)
Severity (mild, moderate, severe, or on a scale of 1 to 10)
Onset (acute, subacute, chronic, acute on chronic, insidious, traumatic, or atraumatic)
Duration (days, weeks, months, years)
Frequency (constant, once daily, weekly, monthly)
Setting (at rest, at night, with activity, with throwing, when reaching behind the back, when lifting overhead)
Exacerbating factors (activity, arm position, day/night)
Relieving factors (activity, arm position, day/night, medications, therapy, injection, surgery)
Associated conditions (weakness, numbness/paresthesias, crepitus, instability)
Trauma (fracture, dislocation, tendon tear)
Shoulder arthrosis (glenohumeral, acromioclavicular)
Posterior capsule tightness/glenohumeral internal rotation deficit
Lateral arm/deltoid insertion (rotator cuff/impingement)
Neck/posterior periscapular (cervical spine, trapezius, adhesive capsulitis, scapular dyskinesis)
Anterior (long head biceps tendon)
“Top of the shoulder” (acromioclavicular joint, cervical spine)
“Deep in the shoulder” (infection, arthrosis, avascular necrosis)
Radiating distal to elbow (cervical radiculopathy)
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 usually lead to an accurate diagnosis in this situation quite readily. 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). This pain usually minimizes to being present at just the extremes of motion while stiffness prevails in the frozen stage. However, by this point, approximately 12 months have passed since the onset of pain and patients are 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).
Pain that awakens the patient from sleep (night pain) often compels the patient to seek care. Differential diagnoses in this situation include malignancy or infection but more commonly entail rotator cuff pathology, impingement, adhesive capsulitis, and shoulder arthrosis (glenohumeral or acromioclavicular arthritis). Pain may not only awaken the patient from sleep but also preclude sleep. Patients with rotator cuff tears often report persistent, unrelenting pain similar to a toothache, making the nighttime miserable. Some patients also report the need to find a comfortable position to gain rest. While lying on the affected side, both the glenohumeral and acromioclavicular joints are compressed, and arthrosis leads to positional pain. Pain associated with adhesive capsulitis also typically prevents a person from sleeping on the affected side. Pain that is present while lying on the unaffected side may be due to the across-body position of stretching the posterior capsule and compressing the acromioclavicular joint. In addition, athletes whose sport entails throwing and who have a tight posterior capsule or GIRD may experience night discomfort related to this phenomenon.
Patients with adhesive capsulitis often present with pain of an insidious onset that is localized around the deltoid insertion; the pain is gradually progressive and is associated with usually underappreciated degrees of shoulder stiffness. Often the pain may not be severe enough to warrant evaluation until it and the associated stiffness preclude performance of activities of daily living (e.g., reaching into the back pocket for a wallet, combing one’s hair, getting dressed, and fastening a brassiere). Although patients with inflammatory shoulder arthropathies (e.g., rheumatoid arthritis) may have severe destructive radiographic disease, they have dealt with the pain and loss of function for such a long time that their description of chronic pain is truly inconsistent with their imaging. In these situations, it is important for the clinician to remember to treat the patient and not the radiograph. Patients with rotator cuff pathology who do not have acute tears often report chronic, dull, boring pain without a discrete time of onset. Often the pain is related to overhead activities or is aggravated by lifting the arm out with an extended elbow (increased moment arm).
The location of pain is an important component in clinical diagnosis. In the shoulder, however, localization is poor, because the patient’s perception of the location of pain often does not coincide with the actual source of pathology. Pain related to the neck (e.g., cervical radiculopathy) may begin proximal to the ear, jaw, or neck and radiate down the trapezius into the posterior periscapular region. True radiculopathy, however, radiates distal to the shoulder, usually to the hand into the appropriate dermatomal distribution. True intrinsic shoulder pathology does not radiate distal to the elbow. Posterior periscapular pain may also be noted in pathology related to glenohumeral joint stiffness (e.g., adhesive capsulitis) because it invokes greater use of the scapulothoracic articulation. Glenohumeral joint pathology is perceived down the arm around the deltoid insertion (e.g., rotator cuff and subacromial bursitis). Pain that is poorly localized or felt “deep in the shoulder” may be ascribed to glenohumeral osteoarthritis, rheumatoid arthritis, avascular necrosis, malignancy, or infection. Anterior shoulder pain may be attributable to long head biceps tendon pathology along the bicipital groove. Pain localized to “on top of the shoulder” is often related to the acromioclavicular joint, with radiation anteriorly and/or medially.
Exacerbating and Relieving Factors
Situational circumstances that aggravate a painful sensation often provide a clue to the diagnosis. Patients with adhesive capsulitis often have sudden worsening of severe pain at the end points of the arc of motion. Overhead motion and lifting with an extended arm worsens pain related to the rotator cuff or subacromial space (impingement). In athletes with GIRD whose sport entails throwing, the loss of internal rotation motion is related to timing during the season: dynamic GIRD early in the season (primarily a muscle spasm) can develop into a posteroinferior capsule contracture later in the season (as a result of repetitive microtrauma from early acceleration through deceleration during the throwing cycle). This pathology tends to manifest as tightness, discomfort, and loss of velocity that becomes greater in severity as the season progresses. Repetitive activity tends to exacerbate intraarticular pathology (e.g., arthrosis). Factors that relieve pain include motions, medications, and procedures. Persons with some conditions (e.g., adhesive capsulitis) report that nothing relieves pain. Patients with rotator cuff tendon pathology often find relief at night by sleeping with their arm over their head, which takes the tensile stress off the rotator cuff. Patients with cervical radiculopathy experience similar relief by reproducing the shoulder abduction relief test. An injection of local anesthetic also is able to localize a pain source depending on the pain relief response to the injection. This technique is especially valuable for the subacromial space and acromioclavicular joint. The response to injection may replicate the response to a surgical intervention, and this possibility should be adequately conveyed to the patient.
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.
The physical examination for a person with a stiff shoulder—as with the physical examination of all shoulders—should be comprehensive and systematic, which allows for consistency and reproducibility while permitting the clinician to consider different causes. As with the questioning involved in obtaining a comprehensive history, the physical examination should be adaptive. When a thorough history indicates that a patient has a stiff, painful, or weak shoulder, the physical examination techniques performed should focus on these subjective symptoms. Physical assessment of any joint requires visual inspection (with men disrobed and women gowned to maintain modesty), palpation, motion, strength, and special testing (e.g., relating to instability, the rotator cuff, and the biceps tendon). To ascertain whether pathology exists in the involved shoulder, the clinician must also thoroughly examine the contralateral shoulder. Extensions of the physical examination of the shoulder may require examination of the cervical spine and elbow, wrist, and hand.
Physical Examination of the Stiff Shoulder
The key physical examination finding to distinguish adhesive capsulitis from other causes of shoulder stiffness is primarily a similar loss of both active and passive range of motion. As discussed in the History section, loss of external rotation commonly results from anterior shoulder tightness (attributed to the anterior capsule, rotator interval, anteroinferior capsule, and glenohumeral ligaments). The most common diagnoses related to the anterior shoulder tightness include adhesive capsulitis, glenohumeral osteoarthritis, postanterior instability surgery stiffness, and postimmobilization (effectively shortening the anterior structures). Stiffness with internal rotation movements are experienced while trying to reach behind the back, toward the back pocket of one’s trousers, and occasionally across the body. Motion loss here may be attributed to the posterior capsule and often the shoulder capsule as a whole. The most common diagnoses related to the latter pathology include adhesive capsulitis, articular-sided partial rotator cuff tears, posterior capsule tightness, and glenohumeral internal rotation deficit. In addition to pathology that is primarily related to the shoulder, stiffness may be present from nonshoulder etiologies including axillary node dissection (especially with perioperative radiation therapy), cervical node dissection, elbow or arm conditions (especially if immobilization is required), and systemic conditions (e.g., diabetes, thyroid, cardiopulmonary, and neuromuscular disease).
Thorough inspection of the shoulder requires observation of the entire upper extremity, neck, and upper thorax ( Fig. 55-1 ). Simultaneous inspection of both shoulders allows immediate comparison for signs of trauma (e.g., ecchymosis, abrasion, laceration, deformity, and bony prominence), atrophy (e.g., the deltoid or rotator cuff) ( Fig. 55-2 ), infection (e.g., erythema), and prior surgical incisions. Often patients may not recall the timing or number of prior surgical procedures (or even their existence, in some situations), but observation of an anterior deltopectoral approach for remote shoulder dislocations may provide a clue to the examiner regarding the open procedure performed. Further, although the patient may not recall why the procedure was performed, a superior shoulder saber incision (relating to the rotator cuff or acromioclavicular joint), an axillary incision (for node dissection), a cervical spine incision (relating to cranial nerve XI or a spinal accessory nerve injury leading to lateral scapular winging), or a chest wall incision/laceration (pertaining to a long thoracic nerve injury leading to medial scapular winging) may assist in evaluation. A prominent acromioclavicular joint may indicate arthrosis. The appearance of a superior fluid bulge may indicate subacromial effusion extension as a sign of a chronic massive rotator cuff tear. Static or dynamic scapular winging may indicate a neurologic injury or dysfunctional muscular coordination. Often the appearance of an atraumatic stiff shoulder without prior shoulder conditions may reveal no obvious pathology.