Treating patients with chronic shoulder dislocations can be extremely challenging. An orthopedic surgeon needs to recognize his or her limitations and refer the patient requiring complex surgical intervention to a specialist. Alterations in the normal shoulder anatomy contribute to the difficulty in treating these patients. The longer the glenohumeral joint is dislocated, the more contracted and adherent the surrounding soft-tissue structures become, including the rotator cuff and capsule. Operating in this situation places neurovascular structures at increased risk of injury. Additionally, the initial impaction fractures of the humeral head and glenoid rim increase in size over time. As the patient attempts to increase the range of motion, this results in progressive bone erosion in these lesions over time. When these defects occupy a significant portion of the humeral head, usually 40% or more, arthroplasty is the usual surgical treatment. Reconstruction of the glenoid with bone grafting may be necessary at the time of surgery. Often patients develop significant osteopenia in the humerus as a result of decreased use of the extremity. As one might expect, the weakened bone is at increased risk of fracture with any intervention. Finally, fractures associated with the dislocation may not have healed or may be malunited. All of these factors influence the treatment plan and may account for the mixed results with surgical management reported in the literature.

In this chapter, chronic dislocations of the glenohumeral joint will be discussed in detail. The normal and pathologic surgical anatomy will be highlighted. The pathophysiology will be discussed including associated conditions predisposing to its development. Evaluation will focus on ways to diagnosis the dislocation as early as possible. A treatment algorithm will be described addressing both nonsurgical and surgical options. Because this textbook focuses specifically on arthroplasty, it will be discussed at length with only cursory mention of other options. Finally, the results of shoulder arthroplasty for this condition will be reviewed.

The normal anatomy of the shoulder consists of a complex arrangement of bone and soft-tissue structures that together allow for a large range of motion at a cost of some stability. The humeral head articulates with the glenoid of the scapula. This articulation is not inherently stable because only 25% of the head contacts the glenoid at any given time. The presence of the labrum, a dense collagenous structure, deepens the glenoid by approximately 50%.

The static stabilizers of the shoulder include the joint capsule and three glenohumeral ligaments. The superior glenohumeral ligament originates from the superior portion of the labrum and runs inferiorly and laterally before inserting near the lesser tuberosity. This ligament functions to prevent inferior subluxation of the humerus. The middle glenohumeral ligament travels laterally from the superior aspect of the glenoid and the anterior aspect of the labrum before it blends with the subscapularis tendon. The ligament functions as an accessory stabilizer to anterior translation of the humerus with the arm abducted and externally rotated. The inferior glenohumeral ligament originates from the anterior glenoid labrum, courses laterally
and inferiorly, and inserts about the anatomic neck of the humerus. This ligament is the most important restraint to anterior and inferior translation of the humerus.

The dynamic stabilizers of the glenohumeral joint are the four muscles of the rotator cuff. These muscles surround the joint, and their tendons blend with the capsule as they insert onto the tuberosities of the humerus. The cuff muscles function to stabilize the glenohumeral joint by acting as a functional unit keeping the humeral head centered within the glenoid during movement of the arm. Additionally, the cuff confers a cavity-compression mechanism of the joint surfaces during motion (1).

Pathologic changes occur in the soft tissues about the shoulder in the presence of a longstanding dislocation. The dislocated humeral head does not lie directly anteriorly or posteriorly; there is a resultant medialization that occurs as a result of the pull of the surrounding musculature. Thus, the capsule is generally abnormal on both the side of dislocation and the opposite side. In some cases, the head does not become significantly displaced medially. The prominent head causes attenuation of the capsule over the head with adherence to the glenoid on the opposite side. When the head is eventually reduced, whether definitively or in preparation for replacement, the redundant capsule causes laxity on the side of dislocation.

As noted earlier, the rotator cuff muscles provide for the dynamic stabilization of the shoulder. The proper functioning of these muscles results in part from maintenance of normal resting length of the muscle. The dislocated humeral head alters the resting length as the rotator cuff contracts. The longer the muscles stay at the shortened length, the more difficult the reconstructive surgery becomes. Alterations in the cuff muscles are addressed at the time of surgery either by extensive releases or lengthening procedures.

The initial dislocation frequently results in bone lesions of the humeral head and occasionally the glenoid. During an anterior dislocation, the posterolateral portion of the humeral head is compressed against the anterior glenoid by contracting of the surrounding muscles. This classic defect was termed the Hill-Sachs lesion after the authors who first described it (2). The analogous injury that occurs with posterior dislocation is called a reverse Hill-Sachs lesion. This impression fracture occurs on the anteromedial aspect of the humeral head as the internal rotators pull the head against the posterior rim of the glenoid. Over time, with dislocation in either direction, the glenoid rim erodes further into the humeral head defect. In missed dislocations, attempts at restoring motion through exercise enlarge the impaction fracture, further securing the head in the dislocated position and making reduction and reconstruction more difficult.

The glenoid may be fractured as well during a dislocation. If the fracture involves 25% of the surface or more, it may contribute to recurrent dislocation. Whereas recurrent anterior instability frequently is attributed to avulsion of the anterior capsule from the anterior glenoid, the so-called Bankart lesion (3,4), fractures of the anterior glenoid rim also may cause this instability pattern. Posterior dislocations have been associated with fractures of the posterior glenoid. The glenoid fracture results either from direct trauma with an anterior force pushing the head out of joint posteriorly or indirectly from force transmitted through the limb as seizure or electrical shock (1). With chronic dislocations, the glenoid rim can wear eccentrically as a result of the humeral head displacement. Because of this wear pattern, a bone-graft reconstruction may be necessary at the time of surgical intervention.

Understanding the location of the neurovascular anatomy helps prevent damage during surgery. The axillary nerve crosses the inferolateral surface of the subscapularis muscle approximately 3 to 5 mm medial to the musculotendinous border. The nerve is located by sweeping a finger from superior to inferior along the anterior surface of the muscle. As the soft tissues contract with persistent anterior dislocation, the axillary nerve and vessels adhere to the subscapularis and inferior capsule. During surgery, these structures are at increased risk for damage if they are not carefully identified and protected.

A lack of consensus makes defining chronic shoulder dislocations difficult. A review of published literature on this topic finds “chronic” defined in several ways. In 1891 Souchon (5) arbitrarily defined dislocations older than 1 month as chronic. Shultz and colleagues (6) reported that dislocations missed for more than 24 hours were chronic. Other authors designated injuries older than several days as chronic (1). Hawkins and colleagues (7) would not attempt closed reduction in a patient whose shoulder had been dislocated for more than 6 weeks. Recognizing that the lack of a standard definition of the problem made comparing results from different authors impossible, Rowe and Zarins (8) tried to remedy the problem. They recommended 3 weeks as the accepted definition of chronic dislocation without providing specific support for this choice. Some authors have suggested using the term “locked dislocation of the shoulder” without using time of dislocation as a defining factor (7). At our institution, the definition of Rowe and Zarins is used to assist in developing a treatment plan.

Most frequently a physician encounters a locked anterior or posterior dislocation. Other rare patterns, including central impaction and superior, have been reported (9). Because treatment choices differ depending on the direction of the dislocation, this is another option for classification. The degree of displacement, from subluxation to full dislocation, further defines the injury.

No matter how the term chronic is defined, careful clinical and radiographic examination at the time of initial
presentation would decrease the number of missed dislocations. In the acute setting, patients frequently present after seizure or major trauma. Contributing to a missed diagnosis may be the patient’s inability to communicate as a result of a postictal state, distracting injuries, or unconsciousness. Treating physicians should carefully examine the shoulders of such patients and have a low threshold to obtain x-rays. In unconscious trauma patients, areas of abrasion, contusion, or swelling should be x-rayed to decrease the potential for a missed injury. Moreover, one must ensure that adequate views are obtained to facilitate an accurate diagnosis. A trauma shoulder series should include orthogonal shoulder x-rays, especially an axillary view and anteroposterior views in internal and external rotation. Frequently emergency room personnel and x-ray technicians fail to obtain the axillary view because of a patient’s pain and restricted motion. In fact, a physician can gently abduct the arm, just enough to place the x-ray tube between the arm and the body, while the technician angles the beam from below into the axilla, centered on the coracoid process. The cassette is placed above the shoulder and gently pressed into the patient’s neck (10). The resulting image provides valuable information. Associated fractures of the humerus and glenoid are readily apparent. The presence of a glenoid rim fracture deserves special attention because this may lead to a subsequent missed dislocation even if properly reduced initially (11).

In chronic situations, patients usually will present with complaints of decreased shoulder motion and pain. A history of alcohol or drug abuse, as well as seizure or previous trauma, deserves close attention. These patients may delay seeking treatment because of their addictions or failure to recall any falls or trauma. In such situations, orthopedic surgeons have misdiagnosed and treated patients for adhesive capsulitis and rotator cuff tendinitis without getting an adequate x-ray series. As a result of misdiagnosis, patients endured painful physical therapy and even manipulation under anesthesia before a dislocation was recognized (24).

Shoulder dislocations comprise almost half of the dislocations involving major joints. The incidence of posterior dislocations is estimated at 2%. Chronic unreduced dislocations are uncommon injuries, but Rowe and Zarins (8) have shown that 50% of orthopedic surgeons in practice for 5 to 10 years had treated at last one such patient. The likelihood increased to 90% for those in practice 20 years or more. Of the missed dislocation, they reported that 65% were anterior and 35% were posterior. Accurate figures on the incidence or number of chronic dislocations are difficult to obtain. Various articles on the topic have defined the injury in different ways, and not all such dislocations are recognized. In our experience, however, missed or locked posterior dislocations are far more common than anterior.

The clinical significance of unreduced dislocations lies in the loss of motion and pain. Patients frequently complain of functional deficits, such as difficulty combing hair, washing the face, and feeding (7). It has been suggested those with a posterior dislocation may tolerate the loss of shoulder motion better than those with an anterior dislocation resulting from the resultant arm position. Although a posterior dislocation causes the arm to be held at the side in internal rotation, the patient is able to maneuver the hand about the head, face, and back. In contrast, with an anterior dislocation, the arm is held away from the body in external rotation. The externally rotated position makes it difficult to reach the head and frequently impossible to reach the back (12). Once again our experience is the direct opposite in that patients with chronic posterior dislocations have more pain and are more functionally impaired than those with anterior dislocations. With attempts to increase motion, the humerus and scapula grind against each other, causing pain.

When treating a patient for any reason, a careful history must be obtained. One should note certain medical conditions, such as seizure disorders and alcoholism, that are associated with missed shoulder dislocations. Even diabetes has been reported as a culprit after a patient fell during a hypoglycemic episode caused by a change in his insulin dose (13). If available, family members can be questioned about any trauma that a patient may not recall.

The next step is a careful physical examination of the patients from above and behind. Start by noting the contour of the shoulder, including the bony landmarks of the coracoid and acromion. These structures appear abnormally prominent with a posterior dislocation as a result of the absence of the humeral head anteriorly (Fig. 11-1). In chronic anterior dislocation there is a loss of deltoid prominence and an accentuation of the posterior acromion. These findings may be subtle and best noted by examining the patient from behind. Also look for evidence of muscle atrophy, especially of the deltoid, supraspinatus, and infraspinatus. The increase in atrophy usually parallels the length of dislocation (7,10).