William N. Levine
Eric M. Gordon
Sir Astley Cooper's 1839 report from Guy's Hospital on the details of a dislocation in an epileptic is considered the classic on posterior glenohumeral instability and contains a description of the characteristic findings of loss of external rotation, an anterior void with posterior fullness, and a detached subscapularis and reverse Hill-Sachs lesion confirming the diagnosis on postmortem exam. Cooper referred to this injury as “an accident which cannot be mistaken.” Sixteen years later and still 40 years prior to the advent of x-ray studies, Malgaigne published a report of 37 cases of posterior dislocation, illustrating that with a thorough physical exam one can make a proper diagnosis. Despite these early reports of posterior instability, it remains one of the most commonly misdiagnosed and mistreated disorders in all of orthopaedics.
Pathogenesis
Etiology
Posterior instability is complex and multifactorial. It includes both dislocation and subluxation and may result from trauma, repetitive overuse or microtrauma, or without trauma. Traumatic posterior instability may result from direct forces applied to the humeral head or proximal shaft, or indirectly by way of a lever arm and/or muscle imbalances. Repetitive overuse or microtrauma is most often seen in younger athletic patients who participate in contact or overhead sports. Atraumatic instability may result from underlying bony and/or soft tissue abnormalities. Furthermore, it may be unidirectional, bidirectional with a posterior component, or multidirectional with a predominantly posterior component.
The most vulnerable position for traumatic posterior instability occurs with the shoulder in forward flexion, adduction, and internal rotation. This position will also reproduce symptoms in patients with recurrent instability. Axial loading through the humeral shaft acting as a lever arm, as occurs during a motor vehicle accident, drives the humeral head posteriorly. In cases of electrical shock or seizure, violent muscular contraction of the adductors and internal rotators (latissimus dorsi, pectoralis major, subscapularis, and teres major) may overwhelm the opposing external rotators (infraspinatus and teres minor) as well as bony and soft tissue restraints.
Certain anatomic variations predispose patients to atraumatic posterior instability. Bony abnormalities including excessive retroversion of the glenoid and humeral head, and glenoid dysplasia and hypoplasia have been implicated in the development of posterior instability. Ligamentous laxity, posterior or inferior capsular laxity, or labral dysplasia and aplasia further predispose patients to subluxation or frank posterior dislocation. Instability may also occur in the setting of muscular or structural imbalance exacerbated by certain positions. This may be further complicated by the presence of a volitional component of the patient to sublux or dislocate posteriorly.
Epidemiology
Posterior instability has a reported incidence of 2% to 5%. The incidence may in fact be higher owing to undetected and missed cases. Posterior dislocations and subluxations are very commonly missed in the emergency room with a reported incidence as high as 60% to 80%. This is typically owing to inappropriate radiographs—it is critically important to obtain 90-degree orthogonal radiographs to avoid this preventable missed diagnosis.
Approximately 50% of cases occur traumatically, mostly in men between 35 and 55 years old with as many as 15%
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of cases bilaterally. Recurrent posterior shoulder instability primarily affects younger men between ages 20 and 30 years who participate in competitive overhead or contact sports with only about half of patients reporting a previous initiating injury.
More than 97% of posterior dislocations are subacromial in which the main component is internal rotation and the humeral head is fixed posteriorly. The lesser tuberosity is located in glenoid, and the greater tuberosity is no longer seen lateral to humeral head. Although historically, posterior dislocations were associated with shock or electroconvulsive therapy, this is now rarely the case.
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Figure 36-1 Axial computed tomogram of a 28-year-old RHD female with congenital hypoplasia and dislocation of the left shoulder. |
Pathophysiology
Shoulder stability is a function of static and dynamic stabilizers as well as arm position. Contributing factors to static stabilization include bony, labral, ligamentous, and capsular contributing factors. Dynamic stabilizers include the rotator cuff and muscular attachments to the humerus. Variations in the anatomy may predispose patients to developing instability or may be the result of a traumatic event or series of events leading to recurrence of subluxation or dislocation. While a number of specific individual variations have been implicated in the development or recurrence of instability, the cause is multifactorial.
Normal glenoid osseus retroversion is approximately 4 to 7 degrees and varies widely among the population. Although excessive retroversion of the glenoid, as well the humeral head, have been implicated as primary causes of posterior instability, they may be more accurately considered as contributing factors if present. Localized erosion of the posterior glenoid occurring either primarily or as a result of repeated events of instability may further contribute to symptoms of instability. Primary or congenital glenoid dysplasia/hypoplasia is a very rare disorder characterized by incomplete ossification of the lower two thirds of the glenoid and adjacent scapular neck, and may be isolated or associated with other anomalies such as humeral head flattening or hypoplasia (Fig. 36-1). Far more common bony abnormalities include engaging defects of the anterior humeral head and fractures of the posterior rim of the glenoid, which, depending on size, play a critical role in posterior instability and require thorough evaluation to determine effective treatment.
Classification
Numerous systems of classification have been described, subdividing various types of posterior instability to assist in proper treatment and outcome determination. To date, however, no single classification system has been agreed on.
Posterior dislocation may be unidirectional, bidirectional, or multidirectional with primarily posterior instability.
Heller classified posterior instability with the following system:
iii. Voluntary
Diagnosis
History and Physical Examination
Diagnosis begins with a thorough history, which may or may not indicate a traumatic event. Patients may complain more about stiffness or functional disability than pain at the time of evaluation—especially if the evaluation is nonacute (past the first several weeks following the instability event). There is often a history of radiographs that have been interpreted as “normal.” Patients with missed posterior dislocations often are being treated for “frozen shoulder.” Other important components include a history of seizures (a posterior fracture-dislocation occurring without trauma is considered pathognomonic of seizure), diabetes (hypoglycemic seizure), alcohol or drug use, polytrauma, and psychiatric illness. Inquiry should be made regarding diseases or illness associated with ligamentous laxity such as Ehlers-Danlos syndrome. In athletes complaining of shoulder pain, it is important to ascertain details of their activities and which motions or positions elicit or aggravate their symptoms. Activities such as pitching, volleyball, gymnastics, swimming,
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golf, archery, and contact sports place increased physiologic stresses on the glenohumeral joint that may lead to or exacerbate posterior instability. Attempts to reproduce symptoms with specific movements and positions should be made during the exam.
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Figure 36-2 Clinical photo of patient from Figure 36-1 attempting maximal external rotation of both upper extremities. Notice the fixed internally rotated position of the left shoulder. |
Physical examination begins with inspection, which may demonstrate difficulty with removal of coat or movements such as touching one's head. Attention should be paid to the symmetry and contour of the shoulders, muscle size and tone, and the appearance of bony prominences including the acromion, coracoid, and proximal humerus. Active and passive range of motions should be evaluated with the patient seated and in supine positions. The classic finding in fixed posterior dislocation is the inability to externally rotate on the affected side (Fig. 36-2). All patients should be evaluated for generalized ligamentous laxity, which includes the four standard parameters of index finger metacarpophalangeal (MCP) hyperextension, thumb abduction with palmar-flexed wrist, knee hyperextension, and elbow hyperextension.
Specific tests are useful in patients with recurrent instability who are reduced and/or asymptomatic at the time of exam. A positive posterior apprehension test elicits pain (and apprehension) with flexion, adduction, and internal rotation. The anterior and posterior load and shift test is performed with the patient positioned supine at the edge of the exam table, shoulder in neutral rotation, 45-degree abduction, and forward flexion. After gently loading the humeral head with an axial force directed proximally at the elbow, anteriorly and posteriorly translating forces are applied by directly grasping and moving the humeral head. This test is graded in the following manner:
A translation of 2+ in any direction may be normal and therefore requires additional attention to patient responses of pain or apprehension with testing to properly diagnose posterior instability. The sulcus test/sulcus sign is performed by placing downward traction on the neutrally positioned arm and measuring the dimple or sulcus between the lateral acromion and humeral head. Voluntarism should be ascertained during the physical examination as it is a negative prognostic indicator for surgical intervention.
Radiologic Features
The minimum requirement for the proper radiologic evaluation of the shoulder in all cases should include three views: an anteroposterior (AP) (preferably performed perpendicular to the scapular plane), a scapular-Y or outlet view (90 degrees from the true AP), and an axillary view. Because routine AP and lateral x-ray views are often inadequate to establish diagnosis, it is imperative that an axillary view be obtained to confirm diagnosis (Figs. 36-3, Figs. 36-4 36-5).
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Figure 36-3 A 47-year-old RHD male with a missed posterior dislocation. True anteroposterior (AP) read by radiologist as “normal.” |
In the case of posterior dislocation, several findings may be present on AP radiographs. The vacant glenoid or posterior rim sign occurs with the loss of normal humeral overlap on the glenoid. A distance of >6 mm between the anterior glenoid rim and humeral head suggests a posterior dislocation. A trough line or compression fracture of the anteromedial humeral head occurs in approximately 75% of posterior dislocations. This reverse Hill-Sachs lesion, often occurring at the time of the original injury, may enlarge with subsequent dislocations. The cystic head sign or light bulb sign results from the fixed internal rotation of the humerus. On the scapular-Y view with a posterior dislocation, the humeral head may be seen posterior to the glenoid. Up to 50% of traumatic posterior dislocations will have nondisplaced fractures, mostly of the lesser
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tuberosity, owing to avulsion of the subscapularis, and less often of the posteroglenoid rim (reverse Bankart). Computed tomography is useful for further diagnosis and bony evaluation as well as preoperative planning in the case of bony injury or abnormality requiring surgical reconstruction (Fig. 36-6).
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Figure 36-4 Scapular lateral radiograph of patient from Figure 36-3 also read as “normal.” |
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Figure 36-5 Axillary radiograph confirming the posterior dislocation in same patient from Figures 36-3 and 36-4. |
MRI may be necessary in cases that do not have significant bony abnormalities and may show any of the following:
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Figure 36-6 Axial computed tomogram in a 37-year-old RHD male following a seizure. |
Diagnostic Workup Algorithm
From the history:
From the physical exam:
From diagnostic imaging:
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Treatment
Acute Traumatic Posterior Instability
Acute, traumatic posterior dislocations can be managed in much the same way as anterior dislocations, when recognized acutely. Following satisfactory muscular relaxation and pain control, with the patient in the supine position, longitudinal and lateral traction should be applied with gentle internal rotation followed by external rotation to disimpact the head and stretch and then relax the posterior capsule. Another method of disimpaction is to flex the arm to 90 degrees and gently adduct. Pressure is then applied directly to the posterior humeral head anteriorly to complete the reduction.
Care should be taken to perform maneuvers gently and avoid creating fractures if the head is locked. Following reduction, a sling in neutral to external rotation may be used for immobilization; however, if there is concern for recurrent instability, a gunslinger type brace or spica cast should be applied. The recommended position of immobilization to optimize stability and healing of the posterior labrum and capsule is abduction, external rotation, and extension for a period of 4 weeks.
Open reduction is indicated when there is a large impaction defect or the injury is more than 6 weeks old (chronic, “locked”). Other indications for surgery in the acute setting include displaced tuberosity or glenoid fracture requiring reduction, or an open injury. A deltopectoral approach is made and is usually all that is necessary in most patients. A separate posterior incision is rarely required to facilitate reduction.
Following disimpaction, defects smaller than 25% can be repaired using subchondral elevation with bone grafting if the injury is <2 weeks old. Small defects >2 weeks old may be filled using transfer of the subscapularis (McLaughlin) or the lesser tuberosity (Neer); however these are nonanatomic repairs that risk rotator cuff weakness or dysfunction and can complicate future procedures. Larger defects ≤40% to 50% can be filled with structural allograft. Repairs should be assessed intraoperatively for stability, addressing injuries to the labrum, capsule, rotator cuff, or glenoid if necessary. In the case of defects >50% of the humeral head or presence of significant osteoarthritis, a hemiarthroplasty should be performed. Total shoulder arthroplasty is a surgical option for an older patient with significant glenoid articular wear. Postoperatively the patient should be immobilized in neutral rotation for 6 weeks before initiation of therapy except in cases of simple arthroplasty, which can begin gentle passive motion immediately.
A final option is nonoperative treatment leaving the patient with a fixed dislocation. This is recommended in cases of prolonged dislocation, particularly in the elderly or low functional individuals or in cases of only minor disability.
In cases of traumatic posterior dislocation, poorer results are to be expected with increasing duration of dislocation, increasing size of a humeral head defect, increasing degree of deformity or arthritis, and the presence of concomitant injury. Complications include recurrence of dislocation, osteoarthritis secondary to trauma or abnormal joint forces from reconstruction, osteonecrosis, and loss of motion.
Recurrent Posterior Instability
Failure rates as high as 50% have been reported given the complex and multifactorial nature of recurrent posterior instability. In almost all cases, treatment of posterior instability begins with nonoperative measures unless symptoms of pain or dysfunction are present to a degree that warrants more immediate surgery. Surgery must be tailored to address each specific underlying component of instability. Physical therapy should include rotational and scapular strengthening with an emphasis on external rotation strengthening (particularly the infraspinatus) while avoiding impingement, voluntary episodes of instability, or positions that may result in subluxation while restoring normal shoulder motion and strength. Attention should also be given to muscular imbalances, weakness, or disturbances of normal coordinated motion. In general, nonoperative measures should be used for a minimum of 3 to 6 months before considering the patient a candidate for surgery, although in certain cases or causes of instability such as injury where nonoperative treatment has been shown to be less effective, the decision to proceed with surgery sooner is warranted.
Contraindications to surgery include voluntary instability owing to an underlying psychologic problem that is better addressed with psychotherapy, biofeedback, and muscle retraining. Patients with a poorly controlled seizure disorder require strict medical management. Patients with ligamentous hyperlaxity also represent a treatment challenge that is best addressed with extensive nonoperative management.
When operative management is chosen, it is essential to determine the degree and direction of instability and identify all bony and soft tissue abnormalities. Various procedures are available that address bony and soft tissue abnormalities and can be performed with either open or arthroscopic technique. Although more technically demanding, arthroscopic procedures have the advantage of reduced hospital stay, less postoperative pain, and improved cosmesis.
Open Procedures Addressing Bony Abnormalities
Posterior bone blocks are used in patients with congenital posterior dislocation, glenoid hypoplasia, and posterior bony defects. A posterior deltoid-splitting approach obviates the need for any tendon detachment and exposes the interval between the infraspinatus and teres minor, which is itself split, exposing the posterior capsule. A horizontal or T-shaped capsulotomy exposes the posterior glenohumeral
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joint. An allograft bone block is secured with two screws to the posterior scapular neck at midlevel, projecting extracapsularly past the glenoid margin. Bone blocks are more often used in secondary procedures when primary soft tissue procedures have failed (Figs. 36-7, 36-8,36-9).
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Figure 36-7 This is an axial CT scan demonstrating significant posterior glenoid bone deficiency, mild posterior subluxation, and early degenerative joint disease (DJD) in a 23-year-old RHD male who previously underwent an arthroscopic posterior labral repair, which has failed. |
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Figure 36-8 Intraoperative view of a posterior deltoid-splitting approach to the glenohumeral joint in the 23-year-old RHD male who previously underwent an arthroscopic posterior labral repair that had failed (same patient as in Fig. 36-7). |
In the case of excessive glenoid retroversion, an opening wedge osteotomy of the scapular neck or glenoid plasty can be used. This was originally performed using a posteroinferior acromion wedge of bone to fill the defect without the use of hardware for fixation. Results of this procedure have been mixed, partly because of the technically demanding nature and high complication rate, which includes glenoid articular fracture, nonunion, loss of graft position, osteonecrosis, degenerative arthritis, and resultant impingement.
Open Procedures Addressing Soft Tissue Abnormalities
A posterior-inferior capsular shift through a posterior approach has been used in patients with unidirectional, bidirectional (posterior and inferior), and multidirectional instability with a predominantly posterior component with good to excellent results regardless of direction or cause. Using a 60-degree oblique incision, the deltoid is split in a posterolateral raphe extending down no greater than 5 cm (to protect the axillary nerve) from the posterolateral corner of the acromion, and detached medially up to 4 cm for improved exposure. The infraspinatus is separated from the supraspinatus and teres minor and carefully elevated off the underlying capsule from medial to the glenoid rim out laterally to its humeral insertion. The infraspinatus is then incised either obliquely creating two tendon flaps or vertically, if the tendon is attenuated, leaving a 1-cm stump on the greater tuberosity. The capsule is incised 1 cm medial to its humeral insertion, leaving a cuff parallel to the anatomic neck with nonabsorbable mobilizing sutures placed along the free medial edge. With increasing degrees of capsular laxity, a larger extent of inferior dissection, capsular incision, and shifting of inferior tissue superiorly should be performed. This is performed by making a horizontal capsular incision (T-fashion split), creating flaps inferiorly and superiorly. The superior flap is reattached to the cuff on the humerus shifting it inferiorly and then reinforced with attachment of the inferior flap shifting it superiorly and obliterating the inferior pouch. The infraspinatus is repaired placing the lateral portion deep to the medial portion, adding further reinforcement. Postoperatively the patient is immobilized for 4 to 6 weeks in neutral rotation with slight abduction prior to initiating therapy.
Repair of posterior labral injuries/reverse Bankart by open technique may be performed through a posterior deltoid-splitting approach with development of the interval between the infraspinatus and teres minor, and a vertical capsular incision to expose the joint. Suture anchor labral repair is then performed.
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Figure 36-9 Postoperative true anteroposterior (AP) radiograph (A) and axillary (B) showing bone graft fixed with two screws and washers (same patient as in Figs. 36-7 and 36-8). |
Arthroscopic Procedures
Arthroscopic approaches provide excellent visualization and are well suited for addressing the anatomy of the capsulolabral complex of the glenohumeral joint. Arthroscopic procedures are well developed for the repair of pathology specific to posterior instability and include reverse Bankart repair, capsular plication, and rotator interval closure, when indicated. Concurrent pathology such as rotator cuff tears, impingement, and SLAP lesions can be addressed at the same time. Regional or general anesthesia is used with patients in the lateral decubitus position and the arm in lateral traction.
The reverse Bankart lesion can be clearly visualized through a standard anterosuperior portal. Dual posterior portals provide access to the posterior inferior labrum, which can be repaired with suture anchors. The bone beneath the labrum should be decorticated to provide a bleeding bed, and anchors should be placed into the glenoid rim rather than the neck. The size of the lesion dictates the number of anchors necessary to provide secure fixation and restoration of the labral “bumper” (Figs. 36-10 and 36-11).
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Figure 36-10 20 year-old RHD elite hockey player with right shoulder traumatic posterior labral tear. Anterosuperior viewing portal shows a posterior labral tear from 7 to 11 o'clock (probe is in tear at the 9 o'clock position). |
Posteroinferior capsular redundancy can be reduced with capsular plication using curved, corkscrew suture passers or crescent hooks after first abrading the capsule with a nonaggressive shaver. Nonabsorbable braided sutures are used, and capsular tissue is gathered toward the glenoid labrum (Figs. 36-12 and 36-13). Alternatively, if the posterior labrum is deficient or the capsular plication suture is felt to be pulling the labrum away from the glenoid, a suture anchor should be used for the plication.
Widened rotator interval closure begins with preparation of the capsule of that region with a rasp or shaver to elicit a bleeding response. Using a spinal needle, a braided suture is passed 1 cm medial to the humeral insertion of the supraspinatus, anterior to its anterior edge
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(superior portion of the interval). A penetrating suture grasper is passed through the anterior portal, positioned just outside of the joint capsule, through capsule deep to the subscapularis (anterior portion), and grasps the suture pulling it outside of the joint. A suture hook or curved grasper is used to retrieve the superior suture into the portal, and a sliding knot is tied in the cannula closing the interval (Fig. 36-14).
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Figure 36-11 Anterosuperior viewing portal showing completed labral repair from 7 o'clock to 11 o'clock in same patient as in Figure 36-10. |
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Figure 36-12 Anterosuperior viewing portal in a 15-year-old RHD female with multidirectional/posterior instability. The arrows point to a nitinol wire as it passes through the posteroinferior capsule into the intact labrum. |
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Figure 36-13 Anterosuperior viewing portal showing completed posterior capsular plication (same patient as in Fig. 36-12). |
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Figure 36-14 Rotator interval closure viewed from a posterior arthroscopic portal in a 17-year-old RHD female with multidirectional instability with posterior symptoms. |
Postoperative care of patients following posterior arthroscopic repairs and stabilization procedures should begin with sling/brace immobilization with the arm in abduction and neutral to slight external rotation worn for 3 to 6 weeks full time depending on the type of repair and reliability of the patient. Gentle passive range of motion exercises can begin at 3 to 6 weeks followed by gradual strengthening with an emphasis on external rotation.
Outcomes and Conclusion
Factors considered when evaluating outcomes include recurrence of instability, level of function and ability to perform activities of daily living (ADLs), return to previous activity, return to sport, pain, and general patient satisfaction. Scoring systems used to standardize and measure outcomes include the American Society of Shoulder and Elbow Surgeons (ASES) score, the simple shoulder test (SST), Rowe score, UCLA score, L'Insalata score, visual analog score, and SF-36 score.
With increased understanding of the anatomy and mechanics of shoulder instability, improved diagnostic imaging, and arthroscopic techniques tailored toward specific pathology, tremendous strides have been made in the management of posterior instability.
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Suggested Readings
Heller KD, Forst J, Forst R, et al. Posterior dislocation of the shoulder: recommendation for a classification. Arch Orthop Trauma Surg. 1994;113:228–231.
Matsen FA 3rd, Titelman RM, Lippitt SB, et al. Glenohumeral instability. In: Rockwood CA Jr, Matsen FA 3rd, Wirth MA, et al., eds. The Shoulder. Vol 2. 3rd ed. Philadelphia: WB Saunders; 2004:655–794.
Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am. 2005;87:639–650.
Robinson CM, Aderinto J. Recurrent posterior shoulder instability. J Bone Joint Surg Am. 2005;87:883–892.