Introduction

• The past 3 decades have witnessed a revolution in our understanding of and treatment options for disorders of the rotator cuff and associated subacromial pathology. Several concepts have emerged as central tenets of the evaluation and management of these disorders.

• Rotator cuff disease is a true syndrome with a constellation of signs and symptoms that are associated with an alteration of normal anatomy. The incriminating anatomic structure or precipitating event that initiates the cascade of events leading to rotator cuff disease may relate not only to pathoanatomy of the anterior acromion and coracoacromial arch, but may also include traumatic events, repetitive overhead activity, or glenohumeral joint imbalance, such as that associated with posterior capsular tightness.

• Poor biologic health of the rotator cuff tissue may hinder the ability of tendon tissue to recover from small injuries.

• An appreciation of the complexity of shoulder anatomy, physiology, and biomechanics is an important part of evaluating and treating patients with suspected disorders of the rotator cuff and subacromial space.

• A thorough understanding of rotator cuff disease is important not only to the orthopedist who may provide surgical treatment, but also to the primary care physicians, physical therapists, and athletic trainers who are well positioned to diagnose and treat these disorders early in the spectrum of disease progression.

Figure 25-1 Normal anatomy: rotator cuff cable.

distribution explains why some patients can maintain reasonable shoulder function in the setting of a painful full-thickness tear of considerable size, if normal balanced kinematics patterns are maintained.8

There is considerable debate regarding the role of the biceps tendon as a humeral head depressor. Reports of the biome-chanical properties9 and clinical behavior10 of the long head of the biceps may suggest its role as a humeral head depressor, but careful clinical analyses have demonstrated that its role as a humeral head depressor may be less than previously thought.9 The tendon of the long head of the biceps traverses the gleno-humeral joint at the rotator cuff interval. At the interval, the cuff is reinforced by the coracohumeral ligament, with extensions to the biceps-restraining sling at the upper biceps groove and to the rotator cuff cable.11 The upper insertion of the sub-scapularis combines with the superior glenohumeral ligament at their insertion on the upper portion of the lesser tuberosity and continues laterally, forming the floor of the bicipital groove. The supraspinatus combines with the coracohumeral ligament infe-riorly to form the roof of the groove. A confluence of these structures forms a ring around the biceps, providing stability.12 Inflammation in this region will produce anterolateral pain similar to rotator cuff impingement, but is often discernible by tenderness directly over the biceps tendon in several arm positions. In the setting of a tear of the subscapularis or a supraspinatus tear that extends into the rotator cuff interval, the integrity of this restraining mechanism is often compromised, and biceps stability must be carefully assessed. Although the rotator cuff interval is a normally appearing gap between the anterior super-spinatus and the superior edge of the subscapularis, the two tendon edges are confluent near the insertion of the myotendi-nous unit onto the humerus. The "critical zone" in this region, located within the supraspinatus tendon insertion just posterior to the biceps tendon, is a common location for rotator cuff pathology.

It is thought that the quality of the blood supply to the cuff insertion on the greater and lesser tuberosity is a factor in the development of rotator cuff disease, particularly in the critical zone. The suprascapular artery is a primary vascular supply to the supraspinatus tendon, and the microvascular structure of the supraspinatus tendon suggests this region has a tenuous blood supply and an associated limited capacity for intrinsic repair.13 This is a common location of partial-thickness and full-thickness degenerative rotator cuff tears.

Pathologic changes in the subacromial space can be both a cause and an effect of rotator cuff disease. For example, a hooked type III acromion, a thickened calcified coracoacromial ligament, or an excrescence on the anterolateral corner of the acromion can cause abrasion of the bursa and supraspinatus tendon, resulting in the inflammation and pain characteristic of early impingement syndrome. Alternatively, a large retracted rotator cuff tear in which the force coupling has failed will permit superior migration of the humeral head, which may articulate with the coracoacromial arch. Over time, this pathologic articulation results in rotator cuff arthropathy. Normal balanced kinematics rely on a functioning rotator cuff to allow for proper scapulohumeral articulation and concentric glenohumeral articulation against a stable fulcrum.

Pathogenesis of Cuff Disease

The pathogenesis of rotator cuff disease is multifactorial, including static and structural causes. Dynamic events combine with biologic factors to create a pathologic condition. The effect of aging on the rotator cuff tissue, especially at the insertion of the tendons, has been demonstrated by fiber thickening and granulation tissue. Combined with a tenuous blood supply, the local biologic environment may not be conducive to intrinsic repair, but it is more likely that cuff disease begins with a combination of static structural conditions and dynamic events.14 In the end, the most consistent risk factor for the development of a rotator cuff tear is advancing age.

Static and Dynamic Causes

Structural abnormalities of the coracoacromial arch may cause abnormal compression of the cuff, leading to cuff disease, but dynamic events may also contribute to cuff injury in the setting of normal subacromial anatomy. Secondary changes in the sub-acromial morphology may occur as a result of dynamic events and may contribute to the progression of disease. This interrelationship between dynamic and static causes of rotator cuff pathology can be inconsistent. Primary structural abnormalities do not always lead to cuff pathology, and not all structural abnormalities are primary.

Static structural causes of cuff disease are related to the cora-coacromial arch morphology. Changes or abnormalities in the arch can lead to focal regions of increased compression at the point where the rotator cuff articulates with the arch. For example, an acromion with an anterior hook, or a lateral slope, can pinch the cuff tendon. An os acromiale or nonunion of an acromial fracture will compress the underlying cuff by changing the shape of the acromion and by promoting the regional growth of osteophytes. Coracoacromial ligament ossification or hypertrophy changes the flexibility and shape of the anterior scapu-lohumeral articulation, causing abnormal compression of the cuff in provocative positions.

Dynamic events that lead to rotator cuff injury in the setting of normal subacromial anatomy may be due to high-energy traction to the arm causing an acute traumatic tear of the rotator cuff tendon or an avulsion of the tuberosities. Without a clear traumatic event, however, an injury to the rotator cuff is usually caused by either external or internal impingement. External impingement occurs when the bursal side of the rotator cuff is compressed against the coracoacromial arch. Internal impingement exists when the articular side of the cuff is pinched between the posterior superior glenoid and an eccentrically articulating humeral head.

A common cause of external impingement is muscle weakness, which allows for a superior orientation of the humeral head, causing the cuff to abrade on the undersurface of the acromion and coracoacromial ligament. A type II superior labrum anterior to posterior (SLAP) tear can allow excessive humeral head motion toward the coracoacromial arch. Weak scapular stabilizers can aggravate these problems by placing the acromion at an angle that promotes contact with the underlying cuff tendon. A tight posterior capsule will cause the humeral head to ride superior, as is seen in overhead athletes with gleno-humeral internal rotation deficit.15-17

The theory of internal impingement and its role in causing articular-side rotator cuff tears and superior labral lesions is controversial. Internal impingement occurs with the arm in the cocked position of 90 degrees abduction and full external rotation.18 In throwers and overhead athletes, this position brings the articular surface of the rotator cuff insertion against the posterosuperior glenoid rim. Repeated forceful contact between the undersurface of the rotator cuff and the postero-superior glenoid and labrum is said to cause posterior superior labral lesions. With time, undersurface partial-thickness rotator cuff tears follow. Despite contact between these two structures occurring physiologically, the theory holds that repetitive contact with excessive force can produce injury. There are, however, many patients with this constellation of pathologic findings who are not overhead athletes,19 and most throwers do not develop the condition despite achieving the position regularly.20 Burkhart et al15-17 have developed a comprehensive evaluation of arthroscopic findings, patient outcomes, and biomechanical experimental data to indicate that the so-called internal impingement found in throwers is caused by a complex syndrome related to scapular dyskinesis and kinetic chain abnormalities, which result in scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyski-nesis of scapular movement (i.e., the SICK scapula). This combination of pathomechanics initiates a cascade leading to type II SLAP tears and partial thickness rotator cuff tears.

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