Shoulder instability can result from traumatic and atraumatic causes and can be classified as anterior, posterior, or inferior. The most commonly dislocated joint is the glenohumeral joint, with rates as high as 24 per 100,000 persons annually. This dislocation results from contact sports, falls, bicycle accidents, and similar high-impact trauma. [1] Atraumatic shoulder pain can be attributed to structures related to the rotator cuff, glenohumeral articulation, joint capsule, biceps tendon, labrum, and bony structures. [2] Patients can be classified into the following 2 clinical categories, which represent the 2 ends of a broad spectrum:
Traumatic anterior glenohumeral instability accounts for 95% of glenohumeral instability seen in clinical practice. Shoulder dislocations can also be classified either as an acute single event or as recurrent episodes (glenohumeral instability). Glenohumeral instability can be classified further by underlying causes: atraumatic (congenital laxity), macrotraumatic (resulting from an event), and microtraumatic (repetitive injury) (see the images below).
Other subdivisions include direction and voluntary/involuntary mechanisms. A first-time acute shoulder dislocation may also represent the initial presentation of recurrent dislocation. Anterior dislocations are usually the result of direct or indirect trauma, with the arm forced into abduction and external rotation (see the image below). This is by far the most frequent type of shoulder dislocation and represents more than 90% of injuries. Of single acute dislocations, 40% become recurrent as a result of associated damage of the surrounding ligamentous and capsular structures that stabilize the joint.
The most important structure stabilizing the shoulder—one that limits gross anterior-inferior subluxations and dislocation—is the inferior glenohumeral ligament (IGHL). This ligament forms a sling with discrete anterior and posterior bands. It is lax when the humerus is in the neutral position, and it allows normal shoulder movement. The ligamentous complex becomes taut in abduction and external rotation and, thus, stabilizes the joint at the end range of shoulder movement in the abduction external rotation (ABER) direction. During a dislocation, forces exceed the threshold that the ligamentous complex can bear, leading to tears or stretching. This may lead to laxity and instability. Failure of the IGHL can occur at the insertion site (40%), in the ligamentous substance (35%), and at the humeral insertion site (25%). Avulsions are seen more frequently in the anterior band and the anterior aspect of the axillary pouch, whereas ligamentous substance tears are more common in the posterior aspect of the axillary pouch. Bankart lesions represent failure of the IGHL at the glenoid insertion. IGHL capsule laxity represents intrasubstance ligamentous failure, whereas humeral avulsions of the GHL (HAGL) represent failure of the IGHL at its humeral insertion. The MGHL is often absent or underdeveloped and plays a minor role. Tears of the GHL can occur without associated labral tears and can also cause shoulder instability. The following lesions may be seen in anterior dislocation:
A subset of these lesions initially were defined using arthroscopy (ie, anterior labroligamentous periosteal sleeve avulsion [ALPSA] lesion, Perthes lesion, glenoid labral articular disruption [GLAD], humeral avulsion of the glenohumeral ligament [HAGL]) but are also well demonstrated by magnetic resonance (MR) arthrography. A Bankart lesion is the most common lesion in anterior instability. The tear is usually large enough to involve not only the labrum, where the anterior band of the IGHL inserts, but also the middle labrum and, sometimes, the superoanterior labrum. Tears of the anteroinferior labrum are the most common subtype. The second most common subtype involves tears of the entire anterior labrum. The following classification system was devised to aid in surgical planning:
Computed tomography (CT) arthrography and magnetic resonance imaging (MRI) can help classify the lesions for surgical planning. In a Bankart lesion, the scapular periosteum ruptures as the labroligamentous ligaments are avulsed from the glenoid. In Bankart variants, the scapular periosteum remains intact relative to the labroligamentous complex. If the labroligamentous complex is displaced medially and shifted inferiorly, rolling up on itself, the lesion is called an ALPSA lesion. An ALPSA lesion is associated with more severe injury. The diagnosis of this lesion in the acute setting is usually a straightforward procedure employing arthrographic findings. In chronic cases, healing and resynovialization occurs. Therefore, the ALPSA lesion may be difficult for surgeons to visualize during arthroscopy. Avulsion of the inferior glenohumeral joint from its attachment at the anatomic neck of the humerus is known as an HAGL lesion. It is often associated with tears of the subscapularis tendon and results from a shoulder dislocation. A bony humeral avulsion of the glenohumeral ligament (BHAGL) can be similar to an HAGL lesion, but it also involves the bone. This lesion occurs significantly less frequently than classic Bankart lesions. HAGL lesions are seen in approximately 9% of anterior shoulder instabilities. HAGL lesions are treated with surgical reattachment of the GHL to its humeral avulsion site. The IGHL complex may also tear at its midportion. The IGHL complex should be examined along its entire course, from its humeral origin to its labral insertion, since defects have been found at the humeral origin and within the substance of the ligament. If the labroligamentous avulsion occurs with an intact scapular periosteum and if the periosteum is stripped medially, becoming redundant, the lesion is called a Perthes lesion. A Perthes lesion is distinguished from an ALPSA lesion via the redundant periosteum versus the rolled-up, medially displaced periosteal labroligamentous mass. The avulsed labrum resumes a normal position at the glenoid margin, in which partial healing takes place. A GLAD lesion is a tear of the anteroinferior labrum (nondisplaced) with avulsion of the adjacent glenoid cartilage. A glenoid chondral defect is therefore visualized. The labrum is not detached, and there is no capsular stripping. This lesion is clinically stable. The mechanism is glenohumeral impaction in the ABER position. Clinically, these patients complain of pain rather than instability. The lesion can be treated with arthroscopic debridement without need for a stabilization procedure. A Bennett lesion is an extra-articular, posterior, capsular avulsive injury associated with a posterior labral injury and posterior undersurface rotator cuff damage. This injury is seen most commonly in baseball pitchers. The diagnosis of this lesion should raise suspicion for associated labral and rotator cuff abnormalities. The mechanism is from traction of the posterior band of the IGHL during the decelerating phase of pitching. Clinically, the throwing athlete presents with posterior shoulder pain during pitching, with posterior point tenderness. If left untreated, patients progress from functional to anatomic instability. Regarding osseous lesions, infractions or fractures of the glenoid rim (osseous Bankart lesions) are diagnostic of anterior instability when they are demonstrated on radiographs. When these lesions are detected, no other imaging is needed. However, not all anterior instabilities or recurrent dislocations are associated with an osseous Bankart lesion. The sole presence of a Hill-Sachs lesion is pathognomonic of anterior instability and is seen in 50% of patients. The need to detect the lesion is reduced if other pathognomonic findings exist (ie, anterior instability found on physical examination or Bankart lesion). The Hill-Sachs lesion describes a characteristic defect of the posterolateral surface of the humeral head and represents a compression fracture. The resultant lesion is influenced by the patient's age at dislocation and the length of time since the initial dislocation. Lesions commonly seen in younger patients include the following:
Bankart lesions are seen less often in older patients. Older patients typically present with supraspinatus tendon (30% of tears in older patients), fracture of the greater tuberosity (one third of older patients), avulsion of the subscapularis and capsule from the lesser tuberosity (one third of older patients), and HAGL lesion. Intra-articular loose bodies are not uncommon and require surgical intervention. Most loose bodies are composed of bone, cartilage, or both. They may also consist of fibrous tissue, fibrin, fat, or blood. [3] Posterior dislocations and posterior glenohumeral joint instabilities are rare (approximately 2-4%) (see the image below). They may result from a fall on an outstretched hand, direct trauma to the shoulder, or violent muscle contractions from electric shocks or seizures. As a result of acute dislocation, instability may occur, and surgical correction of the underlying damage may be indicated. Posterior shoulder pathology may be more difficult to accurately diagnose than its anterior counterpart, and commonly, patients present with complaints of pain rather than instability. Posterior instability can encompass both dislocation where the humeral head is completely displaced from its articulation with the glenoid and subluxation when an incomplete or partial dislocation of the joint occurs. It is also vital to differentiate between physiologic posterior laxity, which may be present in the asymptomatic shoulder, and instability, where excessive glenohumeral translation leads to symptoms. [4]
Posterior instability caused by repeated microtrauma without frank dislocations may result in persistent shoulder pain in young athletes. Abduction, flexion, and internal rotation (eg, swimming, throwing, punching) are the mechanisms involved in these cases. When injuries occur in this position, the capsulolabral structures are taut, and the patterns of injury that occur most often are the reverse of those of anterior dislocation. Most patients with atraumatic posterior instability can be treated with conservative measures involving strengthening of the posterior stabilizing muscles. If this fails, surgery may be required. A fall on an outstretched hand with the arm in abduction is another mechanism of posterior dislocation. Posterior instability may also occur as an operative complication in patients with multidirectional instability after a misdirected anterior capsular procedure. An acute posterior dislocation may remain unrecognized in 50% of patients and subsequently may present as a frozen shoulder. The posterior band of the IGHL complex is primarily responsible for capsuloligamentous restraint to a posterior translation of 90° of abduction. The anterosuperior capsule, or rotator interval capsule, also has been shown to be important in limiting the posterior and inferior translation. Imaging findings of posterior dislocation, which typically are the reverse of those found in anterior instability, are as follows:
The most common finding is a tear or shredding of the posterior labrum. The most likely explanation for a high incidence of teres minor tears is that the underbelly of the teres minor muscle is inseparable from the posterior capsule of the GHL. [5] In contrast to traumatic shoulder dislocation, which is a frequent injury in young active patients, the onset of multidirectional instability is never the result of trauma alone. The etiology here is multifactorial, depending on labral, ligamentous, or collagenous abnormalities and impaired muscular control. The symptoms of multidirectional instability are a heavy feeling in the shoulder girdle, stiffness, mild pain, and a feeling of instability when lifting objects. [6] Imaging is usually not necessary because multidirectional instability is mostly a diagnosis of exclusion. MRI is used principally to exclude conventional causes of instability (ie, Bankart lesion). No visible labroligamentous lesions are seen in patients with true multidirectional instability. The capsular mechanism is redundant, and the labrum is often hypoplastic. Degenerative changes of the glenohumeral joint in association with labral degeneration or tearing may be seen. Physical examination with traction applied on a patient's abducted arm causes inferior subluxation of the humeral head. This results in a visible sulcus (sulcus sign) between the prominence of the acromion and the inferiorly subluxed humeral head. Luxatio erecta (or inferior dislocation) is uncommon. This dislocation usually occurs when a direct axial force is applied to a fully abducted arm or when a hyperabduction force leads to leverage of the humeral head across the acromion, resulting in inferior dislocation of the humerus. In luxatio erecta, the inferior capsule almost always is torn. Associated bony injuries include fractures of the greater tuberosity, acromion, clavicle, coracoid process, and glenoid rim. Brachial plexus and axillary artery injuries are possible serious complications. Long-term complications include adhesive capsulitis and recurrent subluxations or dislocations. The American College of Radiology (ACR) has published appropriateness criteria for imaging of both traumatic and atraumatic shoulder pain. Recommendations for imaging of atraumatic shoulder pain include the following [2] :
Recommendations for imaging of traumatic shoulder pain include the following [7] :
In general, the imaging modality chosen for shoulder dislocation depends on its availability and the treatment plan for a particular patient. [5, 8, 9] Radiography is inexpensive and is readily available. It should be performed as the initial imaging investigation in patients presenting with a clinical problem related to the shoulder. It complements the other advanced techniques and provides an overview of the bony components of the shoulder joint. In some patients, radiography obviates further imaging. (See the radiographic images of shoulder dislocation below.)
Although radiographs are routinely taken before and after the reduction of a shoulder dislocation, radiographs are only indicated for patients with a first-time dislocation or when the mechanism involves blunt force trauma that may have produced a fracture, or when the physician is clinically uncertain of the joint position. A patient with previous dislocations may be spared the time, expense, and radiation associated with routine radiography when the physician is clinically confident of the dislocation or reduction. [10] MR arthrography is considered the gold standard for imaging traumatic shoulder pain. MR arthrography is comparable to noncontrast MRI in assessment of extra-articular soft tissues, and MR arthrography has been shown to be superior to noncontrast MRI in diagnosing intra-articular pathology such as superior labral anterior-to-posterior (SLAP) tears, labroligamentous injuries, and partial rotator cuff tears. However, it is an invasive procedure and is not recommended for the initial evaluation. [7] (See the MR images below displaying shoulder dislocations injuries.)
According to Ng et al, MRI is a useful and objective method to assess capsular laxity in patients with recurrent shoulder dislocation. [11] The sensitivity and specificity to detect capsular laxity were 92% and 100%, respectively, for clinical tests and 85% and 96% for MRI. The authors investigated the usefulness of MRI in assessing capsular laxity in 64 patients with recurrent shoulder dislocation who underwent MR arthrography. The patients were divided into 3 groups: no shoulder dislocation; first dislocation; and recurrent dislocation. In a study by Saupe, the MR appearance of traumatic posterior shoulder dislocation was characterized by reverse Hill-Sachs lesions in 86% of patients and posterocaudal labrocapsular lesions in nearly 60% of patients. Full-thickness rotator cuff tears were seen in approximately 20% of patients. In 31 of the 36 patients, a reverse Hill-Sachs lesion was found; 11 had a reverse osseous Bankart lesion; 12 full-thickness rotator cuff tears were seen in 7 patients; 6 patients had biceps tendon abnormalities; 21 had posterior labrocapsular complex tears; and 27 had a retroverted scaphoglenoid angle. [12] Magee et al reported that MR arthrography showed statistically significant increased sensitivity for detection of partial-thickness articular surface supraspinatus tears, anterior labral tears, and SLAP tears compared with conventional MRI at 3-T. [13] The study included 150 consecutive conventional shoulder MRI and MR arthrography examinations on patients 50 years of age or younger who subsequently underwent arthroscopy. All patients selected for arthroscopy had abnormal findings on clinical examination and MRI or MR arthrography. Three full-thickness and 9 partial-thickness supraspinatus tendon tears, 7 superior labral anterior-to-posterior (SLAP) tears, 6 anterior labral tears, and 2 posterior labral tears were seen on MR arthrography but not on conventional MRI. Conventional MRI provides a good overview of shoulder lesions and anatomy, particularly the soft-tissue structures. However, it is less accurate than MR arthrography for depiction of small labroligamentous lesions associated with shoulder dislocation. [14, 15, 16] CT arthrography largely has been superseded by MR arthrography. CT arthrography usually is used when MRI is not available. It is useful in showing bony lesions and anterior and posterior labral and capsular lesions. CT arthrograms have been shown to be comparable to MR arthrography in diagnosing Bankart, Hill-Sachs, SLAP, and full-thickness rotator cuff tears, but inferior to MR arthrography for diagnosing partial-thickness rotator cuff tears, including bursal-sided tears. [7] (See the CT images below.)
US can evaluate musculoskeletal soft tissues in real time. Consequently, US plays an increasingly important role in shoulder imaging, demonstrating accuracies in the detection of rotator cuff and adjacent soft-tissue abnormalities. [2] However, US has limited usefulness in patients with traumatic shoulder pain that cannot be localized to the rotator cuff or biceps tendon. US is comparable to MRI in evaluating full-thickness rotator cuff tears and rotator cuff atrophy, but inferior to MRI in evaluating partial-thickness rotator cuff tears and other intra-articular pathology. [7] US is well tolerated and, as with MRI, involves no ionizing radiation. Radiography cannot demonstrate labral, ligamentous, or capsular lesions. MRI is more sensitive and specific and has superseded CT arthroscopy for demonstrating intra-articular and periarticular soft-tissue structures. Although conventional MRI and MR arthrography are the modalities of choice, their use is limited by their cost and limited availability. In regions with fewer resources, CT arthrography is a good alternative. Limitations of arthrography include discomfort to patients, risk of septic arthritis, and the need for contrast administration. Use of gadopentetate dimeglumine in intra-articular injections has not been approved by the Food and Drug Administration (FDA). The radiologist needs to be aware of the potential pitfalls (ie, the false-positive and false-negative findings) that can occur with each imaging technique. Familiarity with the limitations of each technique and with normal anatomic variants is therefore important. In this evolving area of imaging, the radiologist should keep up to date on the best modality to use. For example, MRI is more sensitive and specific in the demonstration of intra-articular and periarticular soft-tissue structures and has superseded CT arthrography as the modality used for such imaging. Conventional MRI and MR arthrography are currently the modalities of choice. Potential problems associated with arthrography include patient discomfort, risk of septic arthritis, and the need for contrast administration. Use of gadopentetate dimeglumine for intra-articular injections has not been approved by the FDA. Institutional board approval is required for its use, and obtaining written informed consent from the patient is mandatory. For patient education information, see the Breaks, Fractures, and Dislocations Center, as well Shoulder Dislocation, |
Which of the following projections or positions will best demonstrate Subacromial and Subcoracoid dislocation?
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