Intrinsic mechanisms originate in the tendon itself and have a multitude of causes which include natural process of aging (Tempelhof et al. 1999; Milgrom et al. 1995), microvascular blood supply (Biberthaler et al. 2003; Fukuda et al. 1990b), morphology, and mechanical properties (Michener et al. 2003). Age has been shown to have a negative influence on tendon properties including decreased collagen orientation, cellularity, compliance, elasticity, and overall tensile strength (Seitz et al. 2011). There is a decrease in total glycosaminoglycans and proteoglycans in the supraspinatus tendon with age (Riley et al. 1994).

Rotator cuff tendon vascularity may play a role in rotator cuff tendinopathy. Codman described a “critical zone” in the supraspinatus tendon approximately 1 cm from the insertion on the greater tubercle, also the most common site of rotator cuff tendon injury (Petri et al. 1987; Codman 1934). Multiple studies have confirmed this hypovascular zone of the distal 2 cm of the supraspinatus tendon, predisposing the rotator cuff tendon to injury due to poor healing potential (Biberthaler et al. 2003; Brooks et al. 1992; Fukuda et al. 1990b). However, other studies refute this concept and have demonstrated no region of avascularity in the critical zone. The role vascularity plays in rotator cuff tendinopathy therefore remains unclear (Matthews and Fadale 1989; Levy et al. 2008; Longo et al. 2008).

No single test can efficiently diagnose rotator cuff tendinopathy. Diagnosis involves the combination of a thorough history, physical examination, and supporting imaging studies including x-rays and MRI. Pain, weakness, and loss of shoulder motion are common complaints (Fongemie et al. 1998). Pain is generally exacerbated by overhead activities as the rotator cuff passes through the coracoacromial arch, frequently occurs at night, and may radiate into the deltoid and scapular regions (Fongemie et al. 1998). Patients may also complain of pain and difficulty reaching behind the back such as when tucking in shirt or placing a wallet in the back pocket and even when reaching out to the side.

Several key maneuvers are essential to include in the physical examination to aid in the diagnosis of subacromial impingement syndrome. A combination of a positive Hawkins-Kennedy impingement test, painful arc of motion, and a positive infraspinatus test yields a >95% likelihood of a diagnosis of impingement, whereas, when these tests are negative, the likelihood of impingement is <24%.

The Neer impingement sign causes provocation of pain at the anterolateral edge of the acromion when the examiner passively forward flexes the arm greater than 120° with the humerus internally rotated and the scapula stabilized (Fig. 18.2). The Neer sign has a sensitivity and specificity of 72 and 60%, respectively (Hegedus et al. 2012). Hawkins and Kennedy also described an alternative impingement test which elicits symptoms when the arm is placed in 90° forward elevation and then gently internally rotated (Fig. 18.3). The Hawkins-Kennedy sign has a sensitivity and specificity of 79 and 59%, respectively (Hegedus et al. 2012). These impingement tests place the greater tuberosity, rotator cuff, or biceps tendon against the undersurface of the acromion or coracoacromial ligament causing aggravation of an inflamed bursa. A painful arc of motion between 60° and 120° of active forward elevation in the plane of the scapula is also indicative of impingement. The patient often reports pain or painful catching in the shoulder. This test has a sensitivity of 73.5% and specificity of 81.1% (Factor and Dale 2014). Lastly, the infraspinatus muscle test performed with the arm at the side and the elbow flexed to 90° elicits pain when the patient resists against an internal rotation force.

Many disorders of the shoulder present similar to subacromial impingement syndrome. A diagnostic lidocaine anesthetic injection into the subacromial space can improve the accuracy of the diagnosis of subacromial impingement syndrome. We inject 10 mL of 1% lidocaine using a 25-gauge, 1½ in. needle into the subacromial space through an anterior approach. Ultrasound can be used as an adjunct to guide the needle to ensure accuracy. Alternatively, the needle can be placed 1 cm inferior to the posterolateral corner of the acromion directed toward the coracoid. Provocative maneuvers should be performed following the injection to confirm the diagnosis. Alleviation of symptoms on impingement tests is highly indicative of subacromial impingement syndrome. The authors believe that a 1½ in. needle is essential if using a posterior approach to avoid a false-negative result.

The specificity of special tests on physical examination is relatively low; therefore, imaging of the shoulder should also be utilized in the diagnostic process in order to make an accurate and complete assessment of the underlying pathology (Silva et al. 2010). Radiographs can aid in evaluating acromial morphology, assessing for the presence of subacromial spurs and calcific tendinitis and for the presence of degenerative changes at the greater tuberosity, the acromioclavicular joint, or anterior acromion. A supraspinatus outlet view radiograph is best to evaluate acromial shape. The scapular outlet view, on the other hand, best evaluates the anteroinferior acromion (Fig. 18.4). This view is a true scapulolateral with the x-ray tube angled 5–10° caudally. An AP view of the shoulder with the x-ray tube angled 30° caudally can also be used to evaluate the anteroinferior acromion as well as for the presence of a calcified coracoacromial ligament (Fig. 18.5). This AP caudal tilt view has been shown to have the highest interobserver reliability (Kitay et al. 1995).

This radiographic series is extremely useful in surgical planning to determine the amount of resection necessary to establish a flat acromion. A study by Kitay et al. demonstrated that the distance from the acromial cortex to the end of the acromial spur on x-ray significantly correlated with intraoperative spur length (1995). Acromial slope measured on the supraspinatus outlet view, which was shown to have less intraobserver reliability than the caudal tilt view, significantly correlated with intraoperative acromial thickness. Therefore, the authors believe these views should be included in routine radiographic evaluation and surgical planning when presented with suspected subacromial impingement or rotator cuff involvement prior to acromioplasty.

Magnetic resonance imaging (MRI) can also be useful to evaluate soft tissue and bony pathology associated with rotator cuff pathology and assess the subacromial-subdeltoid bursa. MRI evaluation of rotator cuff tendinopathy has a reported sensitivity of 84–96% (Quinn et al. 1995; Balich et al. 1997). Tendinopathy is characterized on MRI as increased intra-substance signal on short TE sequences, not as bright as fluid on T2-weighted images (Buchbinder et al. 2008). Coronal or sagittal oblique cuts are best to evaluate subacromial spurs as well as acromion type (Fig. 18.6) Small spurs appear black (hypointensity) on T2-weighted images, whereas larger spurs appear as high signal on both T1-weighted and T2-weighted images because they contain marrow. Degenerative changes of the acromioclavicular joint can also be visualized on MRI, indicated by hypertrophy of the joint capsule as a medium signal intensity surrounding the acromioclavicular joint on pulse sequences with short repetition time (TR) and short echo time (TE). Changes in the subacromial-subdeltoid bursa and peri-bursal fat are signs of a rotator cuff tear as a complete tear allows extension of intra-articular fluid in the bursa. This is represented as high signal intensity or white within the bursa on T2-weighted images.

The use of ultrasound, computed tomography (CT), and MRI has been shown to be reliable methods for measuring acromiohumeral distance (McCreesh et al. 2013). Normal acromiohumeral distance is approximately 10.5–11 mm and is smaller in females compared to males (Cotty et al. 1988; Kim et al. 2014). The distance is also dependent on arm position and has been shown to be smallest (8.1–9.9 mm), when the arm is flexed to 90° and in neutral rotation and is largest in positions of internal rotation (range, 11.2–12.2 mm) (Kim et al. 2014). Additionally, an acromiohumeral distance less than 7 mm has been correlated with a complete rotator cuff tear (Weiner and Macnab 1970; Fehringer et al. 2008; Henseler et al. 2014).

Oral NSAIDS are commonly utilized as the initial treatment for tendinopathy. Multiple studies have demonstrated the effectiveness of oral and local NSAIDS in the treatment of acute shoulder tendinopathy (Mena et al. 1986; Mazieres et al. 2005; Petri et al. 1987, 2004). Patients who present with a longer duration and greater severity of symptoms are less likely to have a positive response with NSAIDS (Andres and Murrell 2008b).

Physical therapy is also a common treatment for rotator cuff tendinopathy. Physical therapy for rotator cuff tendinopathy generally focuses on rotator cuff strengthening, scapular stabilization, as well as improving the biomechanics of the shoulder. There appears to be moderate evidence that manual physical therapy may decrease pain in rotator cuff tendinopathy; however, it is unclear if it improves overall function (Bang and Deyle 2000; Desjardins-Charbonneau et al. 2015).

Corticosteroid injections, most commonly subacromial injections, have also been a mainstay of treatment for rotator cuff tendinopathy. The mechanism of action is to locally decrease inflammation and improve the ability to perform exercises and improve function (Griffin 2005). Alvarez found no improvement in symptoms with an injection of betamethasone versus Xylocaine in range of motion or improving quality of life (Alvarez et al. 2005). In contrast, multiple studies have demonstrated at least short-term improvement after a corticosteroid subacromial injection (Celik et al. 2009; Yu et al. 2006). In general, it is recommended to attempt conservative treatment of a course of NSAIDS, physical therapy, and possibly a steroid injection prior to any surgical treatment.

Orthobiologics are emerging in the treatment of tendon pathologies. Platelet-rich plasma (PRP) and stem cell injections are two methods of introducing growth factors from autologous or allogeneic sources that can be used in isolation or as adjuvant therapies to augment tendon healing. While still in their infancy, these modalities show promise in addressing the underlying pathologic processes to promote an optimal healing environment (Freitag et al. 2014; Kesikburun et al. 2013; Scapone et al. 2013; Abdulrazzak et al. 2010). These modalities can be introduced via direct injection or intraoperative application to improve the effectiveness of conservative and surgical treatments.