Shoulder Dislocation

Background

Shoulder dislocations may occur from a traumatic injury or from loose capsular ligaments. Different conditions may affect the stabilizing structures of the shoulder and, thus, negatively affect patients with shoulder dislocations.[1]

Note the images below.

Normal shoulder. Anterior dislocation.

This article focuses on glenohumeral joint dislocation. Although acromioclavicular (AC) joint separations are sometimes called shoulder dislocations by nonmedical persons, these are not true shoulder dislocations. Shoulder dislocations occur when the head of the humerus comes out of its socket, the glenoid.

For patient education resources, see the Breaks, Fractures, and Dislocations Center and Sports Injury Center, as well as Shoulder Dislocation and Shoulder Separation.

Related Medscape Reference topics include the following:

Acromioclavicular InjuryAcromioclavicular Joint SeparationsDislocation, ShoulderSuperior Labrum LesionsNextEpidemiologyFrequencyUnited States

The shoulder is the most commonly dislocated joint in the body.[1, 2, 3]

Although most shoulder dislocations occur anteriorly, they may also occur posteriorly, inferiorly, or anterior-superiorly.

Patients with a previous shoulder dislocation are more prone to redislocation.

Other factors that show a clear correlation to redislocation are the age of the patient and concomitant rotator cuff tears and fractures of the glenoid.

Younger patients (teenagers and those aged 20 years) have a much higher frequency of redislocation than patients in their 50s and 60s.[4] Many physicians believe that age is less of a predisposing risk factor for redislocation than activity level.

Patients who tear their rotator cuffs or fracture the glenoid during their shoulder dislocation have a higher incidence of redislocation than patients without these problems.

PreviousNextFunctional Anatomy

Shoulder stability is maintained by the glenohumeral ligaments, the joint capsule, the rotator cuff muscles, the negative intra-articular pressure, and the bony/cartilaginous anatomy.

The main stabilizers of the shoulder joint are the ligaments and the capsule complex. Multiple ligaments are present, but the inferior glenohumeral ligament is the most important and the one most commonly injured during an anterior shoulder dislocation. The injury may be a tear of the ligament/capsule off one of its bony attachments, and/or it may cause a stretch injury to these structures.

Tears in the rotator cuff muscles may also lead to shoulder instability. Four rotator cuff muscles are present in the shoulder. They are found superficial to the glenohumeral ligaments and the bones. Large tears may lead to shoulder instability, even with intact glenohumeral ligaments. Instability of the shoulder can also occur from injury to the nerves that control the shoulder muscles, specifically the axillary nerve.

PreviousNextSport-Specific Biomechanics

The shoulder is a very mobile joint; therefore, it is often placed in awkward positions during sports. Thus, the force from a fall or a blow may be sufficient to cause shoulder damage. If the force is strong enough, the athlete tears the ligaments/tendons, fractures the glenoid or humerus, and dislocates the shoulder.

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Swimmer's Shoulder

Background

Swimmer's shoulder is the term used to describe the problem of shoulder pain in the competitive swimmer. Swimming is an unusual sport in that the shoulders and upper extremities are used for locomotion, while at the same time requiring above average shoulder flexibility and range of motion (ROM) for maximal efficiency. This is often associated with an undesirable increase in joint laxity. Furthermore, it is performed in a fluid medium, which offers more resistance to movement than air. This combination of unnatural demands can lead to a spectrum of overuse injuries seen in the swimmer's shoulder, the most common of which is rotator cuff tendinitis.

NextEpidemiologyFrequencyUnited States

The incidence of swimmer's shoulder has been reported to be as low as 3% and as high as 67%. When specifically defined as "significant shoulder pain that interferes with training or progress in training," an incidence of 35% has been reported in elite and senior level swimmers.

PreviousNextFunctional Anatomy

The shoulder girdle is made up of 3 bones (the scapula, clavicle, and proximal humerus), 2 joints (the glenohumeral and acromioclavicular joints), and numerous ligaments, muscles, and tendons. The subacromial bursa overlies the rotator cuff and can provide it with some mechanical protection from the bony acromion above in the face of impingement.

The key ligaments are the glenohumeral ligaments (inferior, middle, superior), which are thickened regions of the joint capsule, of which the inferior glenohumeral ligament is most important. Their role is to help stabilize the glenohumeral joint, in support of the rotator cuff muscles.

The key muscle group of the shoulder is the rotator cuff, made up of (from anterior to posterior) the subscapularis, supraspinatus, infraspinatus, and teres minor. The primary role of the rotator cuff is to function as the dynamic and functional stabilizer of the glenohumeral joint. The long head of the biceps tendon, located between the subscapularis and supraspinatus, also assists the rotator cuff in stabilizing the glenohumeral joint. These muscles and their tendons can be overused and injured in shoulder dominant activities such as swimming, with the most commonly injured portion of the cuff being the supraspinatus. On the other hand, the "power muscles" of the shoulders, including the latissimus dorsi, pectoralis, and deltoid, are responsible for moving the arm through space or water, but only infrequently sustain significant injury.

Finally, the trapezius, levator scapulae, rhomboids, and serratus anterior muscles stabilize and position the scapula and shoulder girdle, and are therefore very important to the swimming stroke. Without a stable platform from which to work, the shoulder and arm cannot function efficiently. Fortunately, they also are only occasionally the source of significant injury in the swimmer.

PreviousNextSport-Specific Biomechanics

The 4 basic strokes used in competitive swimming are the freestyle, backstroke, breaststroke, and butterfly. Biomechanically, each stroke can be divided into as many as 5 different phases; however, for the purpose of this article, each stroke is divided into two main phases: propulsion and recovery.

Strength and power are required for maximal propulsion, while flexibility is required for an efficient and faster recovery. Increased shoulder flexibility and ROM are beneficial to all strokes but can result in increased laxity of the glenohumeral joint capsule and ligaments, the static stabilizers of the shoulder. This laxity must then be compensated for by a stronger rotator cuff, to keep the humeral head centered in the glenoid socket during stroke activity, a requirement for efficient stroke work as well as to avoid injury to the labrum and cuff.

To better understand how the shoulder works in swimming, it may be helpful to think of the upper extremity as a lever or "canoe paddle" mechanism. The swimmer's hand functions as the flat end of the paddle. The rotator cuff functions as a fulcrum stabilizing the glenohumeral joint so that the power muscles of the shoulder are able to pull the arm through the water. This would be analogous to the way in which a canoeist uses one hand to stabilize the upper end of a paddle as a fulcrum, so that the lower hand can pull the paddle through the water more efficiently.

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Shoulder Impingement Syndrome

Background

In 1972, Neer first introduced the concept of rotator cuff impingement to the literature, stating that it results from mechanical impingement of the rotator cuff tendon beneath the anteroinferior portion of the acromion, especially when the shoulder is placed in the forward-flexed and internally rotated position.[1]

Neer describes the following 3 stages in the spectrum of rotator cuff impingement:

Stage 1, commonly affecting patients younger than 25 years, is depicted by acute inflammation, edema, and hemorrhage in the rotator cuff. This stage usually is reversible with nonoperative treatment. Stage 2 usually affects patients aged 25-40 years, resulting as a continuum of stage 1. The rotator cuff tendon progresses to fibrosis and tendonitis, which commonly does not respond to conservative treatment and requires operative intervention. Stage 3 commonly affects patients older than 40 years. As this condition progresses, it may lead to mechanical disruption of the rotator cuff tendon and to changes in the coracoacromial arch with osteophytosis along the anterior acromion. Surgical l anterior acromioplasty and rotator cuff repair is commonly required.

In all Neer stages, etiology is impingement of the rotator cuff tendons under the acromion and a rigid coracoacromial arch, eventually leading to degeneration and tearing of the rotator cuff tendon.

Although rotator cuff tears are more common in the older population, impingement and rotator cuff disease are frequently seen in the repetitive overhead athlete. The increased forces and repetitive overhead motions can cause attritional changes in the distal part of the rotator cuff tendon, which is at risk due to poor blood supply. Impingement syndrome and rotator cuff disease affect athletes at a younger age compared with the general population.

NextEpidemiologyFrequencyUnited States

No documented information on the occurrence of shoulder impingement syndrome exists.

PreviousNextFunctional Anatomy

The shoulder consists of 2 bones (humerus, scapula), 2 joints (glenohumeral, acromioclavicular), and 2 articulations (scapulothoracic, acromiohumeral) that are joined by several interconnecting ligaments and layers of muscles. Minimal bony stability in the shoulder permits a wide range of motion (ROM). Soft tissue structures are the major glenohumeral stabilizers. Static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. Dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles (eg, pectoralis major, latissimus dorsi, serratus anterior).

The rotator cuff consists of 4 muscles that control 3 basic motions, abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor muscles control external rotation, and the subscapularis muscle controls internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head on the glenoid fossa, forming a force couple with the deltoid to allow elevation of the arm. This force couple is responsible for 45% of abduction strength and 90% of external rotation strength.

The supraspinatus outlet is a space formed on the upper rim, humeral head, and glenoid by the acromion, coracoacromial arch, and acromioclavicular joint. This outlet accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been attributed as a cause of impingement syndrome and rotator cuff disease, though other causes have been discovered. Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described how variations in acromial size and shape can contribute to impingement.[2]

Cadaveric studies show 3 variations in acromion morphology, as follows: type 1 is flat, type 2 is curved, and type 3 is hooked anteriorly. Although the curved configuration was the most common (43% prevalence, compared to 17% flat and 40% hooked), the hooked configuration most strongly was associated with full-thickness rotator cuff tears. Other sites of impingement in the supraspinatus outlet space include the coracoacromial ligament (where thickening can occur) and the undersurface of the acromioclavicular joint (where osteophytes can form). The medial coracoid rarely is involved. These impingement sites in the supraspinatus outlet are compressed further when the humerus is placed in the forward-flexed and internally rotated position, forcing the greater tuberosity of the humerus into the undersurface of the acromion and coracoacromial arch.

Nonoutlet impingement also can occur. Causes may be loss of normal humeral head depression from either a large rotator cuff tear or weakness in the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. This condition also may occur because of thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.

PreviousNextSport-Specific Biomechanics

Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff pathology. Shoulder pain and rotator cuff disease are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, volleyball, tennis).

Secondary impingement often is attributed to impingement, which seldom is mechanical in nature in young athletes. Rotator cuff disease in this population may be related to subtle instability, and, therefore, may be secondary to such factors as eccentric overload, muscle imbalance, glenohumeral instability, or labral lesions. This has led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint.

Secondary impingement may be the most common cause in young athletes who frequently place large, repetitive overhead stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures, which leads to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendons.

These increased demands may lead to rotator cuff pathology (eg, partial tearing, tendonitis). Furthermore, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging upon the coracoacromial arch. This leads to rotator cuff inflammation. In these patients, treatment should address underlying instability.

The concept of glenoid impingement has been advanced as an explanation for partial-thickness tears in throwing athletes, particularly those involving the articular surface of the rotator cuff tendon. Such tears may occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon from abnormal motion of the glenohumeral joint or increased forces on the rotator cuff necessary to stabilize the shoulder.

Arthroscopic studies of these patients note impingement between the posterior superior edge of the glenoid and the insertion of the rotator cuff tendon with the arm placed in the throwing position (abducted and externally rotated). Lesions were noted along the area of impingement at the posterior aspect of the glenoid labrum and articular surface of the rotator cuff. This concept is believed to occur most commonly in throwing athletes and must be considered when assessing for impingement.

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