Advanced Clinical Pathology: The Shoulder (Page 2)

Hill-Sachs lesion
A Hill-Sachs posterolateral compression fracture can be seen in patients with subluxation and single or multiple episodes of dislocation.  This compression defect is identified on the posterolateral humeral head.  There is a normal bare area of bone where the capsule attaches laterally to the anatomic neck of the humerus posteriorly.  This bare area or normal flattening of the posterior aspect of the humeral head in its inferior portion should not be mistaken for a Hill-Sachs defect.

SLAP tears
Snyder has described SLAP (superior labrum from anterior-to-posterior) relative to the biceps tendon anchor lesions, which vary from simple fraying and fragmentation of the biceps labral complex, to a bucket-handle tear, to a tricorn bucket-handle tear in which one rim of the tear actually extends up into the biceps tendon, splitting it as the tear goes up toward the bicipital groove.  A fall on the outstretched abducted arm with associated superior joint compression and a proximal subluxation force is one proposed mechanism of injury.  A sudden contraction of the biceps tendon which avulses the superior labrum is another mechanism of injury.  Less severe, repetitive stress acting through the biceps tendon may also produce SLAP lesions.

SLAP tears are actually four distinct but related lesions.

In type I lesions, there is a frayed and degenerative superior labrum with a normal (stable) biceps tendon anchor.

Type II lesions have similar labral fraying, but have detachment of the superior labrum and biceps anchor, making them unstable.  A type II lesion may appear similar to the normal free edge of the meniscoid-like superior labrum.  In the latter, the articular cartilage of the superior glenoid extends to the attachment of the labrum.  In a type II SLAP lesion however, there is usually a space or gap between the glenoid articular cartilage and attachment of the superior labrum and biceps anchor.  Displacement of the labrum from the superior glenoid of more than 3 to 4 mm is usually associated with an abnormal superior labrum and biceps anchor attachment.  A type II SLAP lesion may also be associated with anterior glenohumeral joint dislocation.  Tearing of the superior labrum biceps anchor may contribute to anteroinferior capsule and labral stress in the development of anterior instability.

Type III lesions involve a bucket-handle tear of the superior labrum (a vertical tear through a meniscoid-like superior labrum) without extension into the biceps tendon.  The biceps anchor is stable and the remaining labrum is intact.

Type IV lesions also involve a bucket-handle tear associated with a meniscoid-type superior labrum, but in this case with extension into the biceps tendon.  The biceps anchor and the superior labrum are well-attached.  A partially-torn biceps tendon may displace the superior labral flap into the joint.

The Rotator Cuff
The rotator cuff is formed by four scapulohumeral muscles, subscapularis, supraspinatus, infraspinatus and teres minor.  Tendons of these four muscles blend closely with each other and the shoulder joint capsule.  Their primary function is to centralize the humeral head, limiting superior translation during abduction.  The supraspinatus, infraspinatus, and teres minor tendons insert on the greater tuberosity, whereas the subscapularis tendon inserts on the lesser tuberosity.  The subscapularis tendon lies on the anterior aspect of the anterior capsule of the glenohumeral joint, and its superior portion is intraarticular.  The subscapularis bursa lies between the subscapularis tendon and the scapula.  As the subscapularis muscle becomes attenuated from repeated episodes of dislocation, it may be the source of recurrent instability.  The rotator cuff interval is located between the superior aspect of the subscapularis tendon and the inferior aspect of the supraspinatus tendon.  This interval contains the coracohumeral ligament and the superior glenohumeral ligament.  The rotator interval lesion has been attributed to a possible deficiency of the superior glenohumeral ligament.  Surgical closure of the interval appears to eliminate excessive inferior translation.

The triangular space through which the scapular circumflex vessels travel is formed by the teres major, the lower border of the teres minor, and the long head of the triceps.  Lateral to the triangular space, the quadrilateral space (through which the axillary nerve and posterior humeral circumflex artery travel) is formed by the lower border of the teres minor, the upper border of the teres major, the lateral border of the long head of the biceps, and the medial border of the humerus.

Pathogenesis of Shoulder Impingement

The pathogenesis of rotator cuff tears includes acute trauma, chronic impingement, or both.  Some controversy exists as to whether chronic mechanical impingement precedes the development of complete rotator cuff lesions or whether primary degeneration of the cuff results in tears leading to chronic impingement syndrome.

There is an important relationship among the rotator cuff, the long head of the biceps, the subacromial bursa, the AC joint, the acromion, and the humeral head in the spectrum of impingement disorders.  The most common location for impingement is between the anterior one-third of the acromion and the underlying tendons.  A decrease in the subacromial space secondary to anatomic or pathologic changes is usually associated with a large tear that has compromised the centralizing ability of the cuff, allowing proximal humeral migration.

Etiology of Shoulder Impingement

A variety of causes of the painful shoulder impingement syndrome has been proposed, including hypovascularity in the supraspinatus tendon, mechanical wear, acute trauma, or repetitive microtrauma from overuse.  Factors that contribute to bony supraspinatus outlet compromise include (1) anterior acromial spurs; (2) the shape of the acromion (e.g., curved or overhanging edge); (3) the slope of the acromion (e.g., flat or decreased angle); and (4) the morphology of the AC joint (e.g., hypertrophic bone, callus formation).  Less frequent mechanisms of impingement (not outlet impingement) include (1) prominence of the greater tuberosity (e.g., fracture malunion or nonunion); (2) loss of humeral head depressors, as seen in rotator cuff tears and biceps tendon rupture; (3) loss of the glenohumeral joint fulcrum function from articular surface destruction or ligamentous laxity; (4) impaired scapular rotation from trapezius paralysis or AC joint disruption; (5) lesions of the acromion including an unfused anterior acromial epiphysis (apophysis); (6) fracture malunion or nonunion; and (7) subacromial bursal thickening (chronic bursitis or cuff thickening in calcific tendinitis).  The shape of the acromion, as seen on sagittal oblique MR images or on the outlet view on plain film radiographs, is also thought to be a factor in the etiology of impingement syndrome.  Acromial morphology has been classified into three different types by Bigliani.  The type 1 acromion has a flat undersurface; the type 2 acromion has a smooth, curved, inferior surface; and the type 3 acromion has an anterior hook or beak.  It is the type 3 acromion which is thought to be associated with a greater predisposition to rotator cuff tears (i.e., tears involving the critical zone immediately proximal to the greater tuberosity insertion of the supraspinatus tendon).

Neer developed a three-stage classification system for impingement in which subacromial impingement is presented as a mechanical process of progressive wear (i.e., a pretear impingement lesion) that causes 95% of rotator cuff tears.  The degeneration, thinning, and full thickness tears of the supraspinatus may extend to involve the long head of the biceps and infraspinatus tendons.  The three stages of Neer’s classification are as follows:

Stage 1: Tendon edema and hemorrhage but no radiographic findings nor irreversible changes

Stage 2: Fibrosis and tendinitis but no radiographic findings nor irreversible changes

Stage 3: Partial or complete rupture or tear of the rotator cuff, often in association with anterior acromial spurs or greater tuberosity excrescence. 

When present, radiographic changes include greater tuberosity sclerosis and hypertrophic bone formation.  Bursal thickening, fibrosis, and partial tears of the superficial rotator cuff may be present.

Rotator cuff tendons examined at surgery display areas appearing gray, dull, edematous, and friable.  Histologic examination reveals degenerative changes such as angiofibroblastic hyperplasia without inflammatory cells.  Because leukocyte infiltration of the rotator cuff tendon is rare, the tendinitis or inflammation of the cuff as described in Neer's classification (especially in the later stages of rotator cuff pathology) has not been adequately documented.

Arthroscopic visualization of the rotator cuff from the articular and bursal surfaces has provided new insight into the progression of this disease process and the progressive stages of impingement might be more accurately described as:

Type 1:  Rotator cuff degeneration or tendinosis without visible tears of either surface

Type 2:  Rotator cuff degeneration or tendinosis with partial thickness tears of either articular or bursal surfaces

Type 3:  Complete thickness rotator cuff tears of varying size, complexity, and functional compromise.

Most rotator cuff tears do not begin at the bursal surface of the tendon, as tears secondary to impingement had originally been described.  In fact, it is more common to find partial tears of the rotator cuff involving the articular surface of the rotator cuff adjacent to the tendon insertion.  Articular cuff lesions may be the result of tensile strength failure from overuse, whereas bursal cuff lesions are more closely associated with impingement.  Frequently, no direct mechanical cause of impingement can be found in patients suspected of having impingement syndrome.  It is not unlikely, therefore, that intrinsic tendon degeneration (degenerative tendinopathy), and not mechanical impingement, may be the primary pathology in the development of most rotator cuff disorders.  Rotator cuff tendinitis has been attributed to repeated eccentric tensile overload of the rotator cuff tendons.  Rotator cuff degeneration has also been observed in the absence of anteroinferior acromial spurs.  Ozaki and colleagues found a correlation between bursal-sided and full-thickness rotator cuff tears and degenerative changes in the coracoacromial ligament and anterior third of the inferior acromion.  Articular surface partial tears, however, were associated with normal acromial morphology and histology.  Most rotator cuff tears, therefore, seem to be attributable to degenerative lesions associated with increasing age, and the acromial changes present are secondary.  Athletes may demonstrate both degenerative rotator cuff tendinitis and primary mechanical impingement.  Relative rotator cuff hypovascularity in the critical zone of the supraspinatus (the distal 1 cm) may be associated with tendon degeneration or may exacerbate changes associated with mechanical impingement.

In the Neer classification of well-defined stages of impingement (edema, hemorrhage, fibrosis, and tendinitis leading to spur formation), cuff tears may be more correctly viewed as part of a progression of tendon degeneration leading to tendinopathy, with the subsequent development of a partial or complete rotator cuff tear and associated secondary changes.

Massage Application in Rotator Cuff Problems
Often supraspinatus muscle impingement and rotator cuff tears have not progressed to the point of surgery. Massage Therapy can be of benefit to increase localized circulation, increase localized scar tissue formation and return the muscles to more balanced function. Gentle, yet deep, digital gliding applied to the supraspinatus muscle (medially to laterally) will help to increase localized circulation. Gentle, yet deep, cross-fiber friction applied to the supraspinatus muscle tendon will increase localized scar tissue formation to help heal the tendon. Digital glides and cross-fiber friction to the other rotator cuff muscles will help to reduce imbalances caused by tightness. Specific exercises may be necessary to restore functional strength to the rotator cuff muscles involved.

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