Shoulder Dislocation

Introduction

Introduction to Shoulder Dislocation

The shoulder (glenohumeral) joint is the most mobile joint in the body, a feature that comes at the cost of inherent instability. It is the most commonly dislocated major joint, with anterior dislocation accounting for over 95% of cases. The injury typically occurs when the arm is forced into abduction and external rotation, overcoming the static and dynamic stabilisers of the joint. A thorough understanding of the anatomical structures that maintain shoulder stability—the glenoid labrum, glenohumeral ligaments, rotator cuff, and surrounding muscles—is essential for accurate diagnosis, safe reduction, recognition of associated neurovascular injuries, and successful surgical management of recurrent instability.

This module examines the applied anatomy of shoulder dislocation, including the mechanisms of injury, pathoanatomical lesions, associated neurovascular complications, clinical assessment, imaging findings, and principles of management.

Study

1. Anatomical Basis of Shoulder Stability

Stability of the glenohumeral joint is provided by a combination of static and dynamic stabilisers. The shallow glenoid fossa is deepened by the fibrocartilaginous glenoid labrum, which increases the concavity by about 50%. The glenohumeral ligaments—superior, middle, and inferior—are thickenings of the anterior joint capsule. The inferior glenohumeral ligament (IGHL) is the most important, acting as a sling to prevent anteroinferior displacement when the arm is abducted and externally rotated, the position in which most anterior dislocations occur. The coracohumeral ligament strengthens the superior capsule.

Dynamic stabilisers include the rotator cuff muscles (supraspinatus, infraspinatus, teres minor, subscapularis), which compress the humeral head into the glenoid, and the long head of biceps brachii, which depresses the humeral head. The deltoid, pectoralis major, and latissimus dorsi provide additional muscular support. Failure of the IGHL-labral complex is the key pathological event in anterior dislocation.

2. Anterior Shoulder Dislocation: Mechanism and Pathoanatomy

Anterior dislocation most commonly results from a fall on the outstretched hand with the shoulder in abduction and external rotation, or from a direct blow to the posterior aspect of the shoulder. The humeral head is levered anteriorly, tearing the anteroinferior capsule and labrum from the glenoid rim. This produces a Bankart lesion—an avulsion of the anteroinferior labrum along with its attached periosteum and capsule. A bony Bankart lesion occurs when a fragment of the glenoid rim is also avulsed. The compression of the posterolateral aspect of the humeral head against the anterior glenoid produces a Hill-Sachs lesion, a depression fracture of the humeral head.

The rotator cuff, particularly the subscapularis tendon, may be stretched or torn, especially in older patients. The axillary artery and brachial plexus may be stretched, with the axillary nerve being the most commonly injured nerve.

3. Posterior and Inferior Dislocations

Posterior dislocation accounts for 2–4% of shoulder dislocations and is commonly missed. It occurs from forced internal rotation and adduction, often during seizures, electrocution, or high‑energy trauma. The humeral head displaces posteriorly and may produce a reverse Hill‑Sachs lesion (an impression on the anterior humeral head) and a reverse Bankart lesion (posterior labral detachment). The classic finding on anteroposterior radiographs is the ‘light bulb’ sign, where the humeral head appears symmetrical due to fixed internal rotation.

Inferior dislocation (luxatio erecta) is rare and results from hyperabduction forces that lever the humeral head inferiorly. The arm is locked in an overhead position. Neurovascular injury is common, and associated fractures of the greater tuberosity and rotator cuff tears are frequent.

4. Neurovascular Complications

The axillary nerve (C5, C6) is at greatest risk in anterior dislocation because it winds around the surgical neck of the humerus and is stretched as the humeral head displaces anteriorly. Injury leads to weakness of deltoid (loss of shoulder abduction) and teres minor, with sensory loss over the ‘regimental badge’ area on the lateral aspect of the shoulder. The musculocutaneous nerve, radial nerve, and brachial plexus cords may also be injured. Vascular injury to the axillary artery is more common in older patients with atherosclerotic vessels and can present as a pulsatile haematoma or absent distal pulses. The axillary artery passes anterior to the shoulder joint and can be compressed or torn.

5. Clinical Assessment

A patient with an acute anterior shoulder dislocation typically presents with the arm held in slight abduction and external rotation. The normal rounded contour of the deltoid is lost, giving a flattened ‘square‑shoulder’ appearance. The humeral head may be palpable anteriorly, in the infraclavicular fossa or subcoracoid region. A thorough neurological examination must be performed before and after reduction, specifically testing deltoid function (axillary nerve), biceps function (musculocutaneous nerve), and distal radial, median, and ulnar nerve function. Vascular status is assessed by distal pulses and capillary refill.

6. Imaging Findings

Radiographic evaluation includes an anteroposterior (AP) view, a transscapular Y‑view, and an axillary view. The axillary view is the most reliable for confirming anterior or posterior displacement. On the AP view, the humeral head is seen lying inferior and medial to the glenoid. A Hill‑Sachs lesion is seen as a compression defect on the posterolateral humeral head, best visualised on an AP view in internal rotation. CT and MRI are reserved for complex cases, suspected fractures, or evaluation of labral and rotator cuff pathology in recurrent instability.

7. Management Principles

Prompt closed reduction is the primary treatment, following pre‑reduction neurovascular assessment. Numerous techniques exist (e.g., Kocher, Milch, Stimson), all aiming to overcome muscle spasm and relocate the humeral head without iatrogenic injury. Post‑reduction, radiographs confirm concentric reduction. The arm is immobilised in internal or external rotation (controversial) for 1–4 weeks. Surgical intervention is indicated for irreducible dislocations, displaced greater tuberosity fractures, large bony Bankart lesions, and young athletes with a high risk of recurrence. Surgical options include arthroscopic Bankart repair, remplissage for engaging Hill‑Sachs lesions, and the Latarjet procedure (coracoid transfer) for significant glenoid bone loss.

8. Recurrent Instability

Recurrent dislocation occurs in up to 80% of young patients (under 20 years) after a first‑time anterior dislocation. The primary anatomical lesion is the Bankart lesion, which creates a permanent defect in the labral‑capsular restraint. Repeated dislocations can enlarge the Hill‑Sachs defect and cause progressive glenoid bone loss, leading to chronic instability. Surgical stabilisation aims to restore the labral ring and recreate the concavity‑compression mechanism.

Summary

Summary of Shoulder Dislocation

The glenohumeral joint relies on the labrum, inferior glenohumeral ligament, and rotator cuff for stability. Anterior dislocation, usually in abduction and external rotation, tears the anteroinferior labrum (Bankart lesion) and compresses the humeral head (Hill‑Sachs lesion). The axillary nerve is the most commonly injured structure. Posterior dislocation, though rarer, is often missed and associated with seizures. Prompt reduction, neurovascular assessment, and appropriate imaging are essential. Surgical repair of the Bankart lesion reduces the high risk of recurrent instability in young patients.