Displacement of the humeral head from the glenoid fossa, most commonly in an anterior direction, resulting from trauma or ligamentous laxity.

Exam domain	One-glance essentials
Definition / diagnosis	*The shoulder is the most commonly dislocated joint* — large humeral head vs small shallow glenoid ("golf ball on a tee") sacrifices stability for mobility ^[1]^[2] *Anterior dislocation = 95%* of cases; posterior ~4% (seizures/electrocution); inferior (luxatio erecta) is rare but carries the highest neurovascular injury risk ^[1]^[2] TUBS = Traumatic, Unilateral, Bankart, Surgery vs AMBRI = Atraumatic, Multidirectional, Bilateral, Rehabilitation, Inferior capsular shift — key classification framework ^[1]^[3]
Epidemiology / risks	*Young males (<25) in contact sports* have the highest incidence and recurrence (65–95%); first dislocation typically from sporting trauma ^[1]^[2] Elderly patients with atherosclerosis → higher risk of axillary artery injury; patients >40 → dominant pathology shifts to rotator cuff tear rather than labral injury ^[1]^[3] Epilepsy and electrocution are classic risk factors for posterior dislocation — exam favourite association ^[1]^[2]
Core mechanism	*Anterior dislocation: ABER (Abduction + External Rotation)* → anterior capsule/labrum fails → humeral head displaces anteroinferiorly → Bankart lesion ("essential lesion") ± Hill-Sachs impaction ^[1]^[2] *Posterior dislocation: seizure/electrocution* → massive internal rotator contraction overwhelms external rotators → posterior capsule fails → reverse Hill-Sachs (anteromedial impaction) ^[1]^[3] *Young patient → labral tear (Bankart) → high recurrence; old patient (>40) → rotator cuff tear → low recurrence but poor function* — age-dependent pathological response ^[1]^[2]
Clinical picture	Anterior: arm held in slight abduction and external rotation, loss of normal deltoid contour ("squared-off shoulder"), palpable humeral head anteriorly, patient resists internal rotation ^[1]^[2] *Posterior dislocation: arm locked in internal rotation and adduction* + flattened anterior shoulder + inability to externally rotate — classically missed ^[1]^[3] *ALWAYS check axillary nerve* (regimental badge area sensation + deltoid power) and distal pulses before AND after any reduction attempt ^[1]^[2] Inferior (luxatio erecta): arm locked overhead in full abduction — highest rate of neurovascular compromise ^[1]^[2]
Investigations	*Minimum imaging: AP + Axillary lateral (or Scapular Y-view)* — a single AP view is NEVER sufficient; posterior dislocations will be missed ^[1]^[2] *Posterior dislocation X-ray signs: "lightbulb sign" (rounded humeral head on AP), "rim sign" (>6 mm gap), loss of half-moon overlap, vacant glenoid sign ^[1]^[3] CT: fracture-dislocation assessment, glenoid bone loss quantification (>20–25% → Latarjet), Hill-Sachs engagement; MRI/MRA: gold standard for labral tears (young) and rotator cuff tears (>40) ^[1]^[2] EMG/NCS* only if persistent axillary nerve deficit at 3–6 weeks — denervation changes take time to develop; not useful acutely ^[2]^[3]
Management	*Adequate analgesia/sedation BEFORE reduction; intra-articular lidocaine is an effective alternative to IV sedation; pre-reduction X-rays are mandatory* (unless vascular emergency) ^[1]^[2] *Closed reduction: Hippocratic (traction-countertraction), Stimson (gravity), External Rotation method; Kocher's method carries higher fracture risk* — use with caution ^[1]^[3] *Surgical indications: recurrent instability, young (<25) active patient (early stabilisation), glenoid bone loss >20–25% (Latarjet), engaging Hill-Sachs (remplissage), failed rehab in MDI ^[1]^[2] Arthroscopic Bankart repair: standard for anterior instability without significant bone loss; patients >40* → prioritise rotator cuff assessment and repair over labral surgery ^[1]^[2]
Complications	*Axillary nerve injury* is the most common neurological complication (~5–35%); most are neurapraxia → recover within 6–12 weeks; always document before AND after reduction ^[1]^[2] *Recurrence is strongly age-dependent: <20 years: ~70–90% (without surgical stabilisation); 20–30 years: ~50–70%; >40 years: ~15–25%; >60 years: <10% — younger age at first dislocation = higher recurrence risk ^[1]^[2] Rotator cuff tear* dominates in patients >40 (up to 40–80%); recurrence risk is low but functional loss is significant; USS post-reduction for screening ^[1]^[3] Axillary artery injury → absent pulses → vascular surgery emergency; more common in elderly; secondary OA develops with recurrent dislocations over time ^[1]^[2]
Prevention / follow-up	*Early surgical stabilisation in young (<25) active patients* increasingly supported to prevent the high recurrence rate rather than "wait and see" approach ^[1]^[2] Rotator cuff and scapular stabiliser strengthening is the cornerstone of both non-operative management and post-operative rehabilitation to prevent recurrence ^[1]^[3] *Prevent adhesive capsulitis* → early mobilisation + adequate pain relief; shorter immobilisation in elderly (1–2 weeks) vs longer in young if non-operative (up to 3 weeks) ^[1]^[2]
Exam traps	*Posterior dislocation is the most commonly missed diagnosis in shoulder trauma* — AP X-ray may look near-normal; always obtain axillary/Y-view; classic triad: seizure + IR contracture + lightbulb sign ^[1]^[2] *Greater tuberosity fracture paradoxically reduces recurrence* (healing response tightens anterior structures) — do not assume fracture-dislocation = worse prognosis for instability ^[1]^[3] Rotator cuff tear in elderly mimics dislocation (cannot lift arm) — distinguish by normal deltoid contour and preserved passive ROM; always assess cuff in patients >40 post-reduction ^[1]^[2] *Never operate on voluntary dislocators* — psychological component; AMBRI → rehabilitation first, not surgery; misclassifying AMBRI as TUBS leads to surgical failure ^[1]^[2]

References

^[1] Lecture slides: GC 236. Common Shoulder Problems [Updated in 2025].pdf ^[2] Senior notes: Maksim Surgery Notes.pdf (pp. 231–234) ^[3] Senior notes: Maksim Surgery Notes.pdf (pp. 231–232)

Shoulder Dislocation

Shoulder dislocation refers to the complete displacement of the humeral head from the glenoid fossa of the scapula, such that the articular surfaces completely lose contact. This is distinct from subluxation, where only partial displacement occurs with some residual contact between the articular surfaces.

"Dislocation" → from Latin dis- (apart) + locare (to place) — literally "placed apart."

The shoulder (glenohumeral joint) is the most commonly dislocated major joint in the body ^[1]^[2]. This is a direct consequence of its anatomy: it sacrifices bony stability for an extraordinary range of motion.

High Yield – GC Lecture Point

The shoulder joint is the most commonly dislocated joint in the body — this is a recurring exam point. The reason is the inherent mismatch between the large humeral head and the shallow, small glenoid fossa (often likened to a "golf ball on a tee"). ^[1]^[2]

2. Epidemiology and Risk Factors

Incidence: Approximately 15–17 per 100,000 person-years globally. In Hong Kong, incidence mirrors international figures, with higher rates in young active populations.
Bimodal age distribution:
- Young males (15–30 years): Predominantly from sports and trauma — this is the peak group.
- Elderly (> 60 years): Falls on outstretched hand; often associated with rotator cuff tears due to degenerative tissue.
Sex: Male-to-female ratio ~2–3:1 in young adults. In the elderly, the sex difference narrows.
Anterior dislocation accounts for ~95% of all glenohumeral dislocations; posterior ~2–4%; inferior (luxatio erecta) and superior are rare. ^[1]^[2]

Risk Factor	Mechanism / Explanation
Young age (< 25 years)	Higher activity levels, sports participation; also the strongest predictor of recurrence — younger the first dislocation, higher the recurrence rate (up to 90% in < 20 years old).
Male sex	More contact sports, higher-energy trauma.
Contact/collision sports	Rugby, football, basketball, martial arts — mechanisms involving forced abduction and external rotation.
Overhead sports	Swimming, volleyball, throwing — repetitive microtrauma to capsuloligamentous restraints.
Previous dislocation	Each episode further damages the labrum, capsule, and bony structures → lowers the threshold for redislocation.
Hyperlaxity / connective tissue disorders	Marfan syndrome, Ehlers-Danlos syndrome — inherently lax ligaments → multidirectional instability (MDI). ^[1]
Bony abnormalities	Glenoid hypoplasia, large Hill-Sachs defect, glenoid bone loss — reduce the bony "bumper" effect.
Epilepsy / Electrocution	Posterior dislocation classically associated with seizures (violent internal rotation from tonic muscle contraction) and electric shock. ^[1]^[2]

Exam Pearl – Posterior Dislocation

The classic triad for posterior shoulder dislocation is: seizure, electrocution, and extreme trauma. Always think posterior dislocation when a patient presents post-ictal with a "locked" shoulder in internal rotation. ^[1]^[2]

3. Anatomy and Function of the Glenohumeral Joint

Understanding shoulder dislocation from first principles requires a solid grasp of the anatomy. The glenohumeral joint is a ball-and-socket synovial joint designed for maximum mobility at the expense of inherent stability.

Humeral head: Large, spherical, approximately one-third of a sphere. The articular surface area is approximately 3–4 times that of the glenoid.
Glenoid fossa (of scapula): Small, shallow, pear-shaped — only covers about 25–30% of the humeral head at any given time. Often described as a "golf ball sitting on a tee" — this immediately tells you why dislocation is so common. ^[1]^[2]
Glenoid version: The glenoid has a slight retroversion (~7°). Excessive retroversion predisposes to posterior instability.
The bony architecture alone provides minimal stability — hence, soft tissue restraints (labrum, capsule, ligaments, rotator cuff) are critically important. ^[1]

A fibrocartilaginous rim attached circumferentially to the glenoid margin.
Functions: Deepens the glenoid socket by ~50%, increases concavity compression, and serves as the attachment point for the glenohumeral ligaments and long head of biceps (superiorly). ^[1]^[2]
Bankart lesion: Detachment of the anteroinferior labrum from the glenoid rim — this is the "essential lesion" of anterior shoulder dislocation and the primary reason for recurrent instability.

These are the primary restraints against dislocation in different arm positions:

Structure	Function / Restraint
Superior glenohumeral ligament (SGHL)	Resists inferior translation in adduction; prevents inferior subluxation when arm at side.
Middle glenohumeral ligament (MGHL)	Resists anterior translation in mid-range abduction (45°). Variable — absent in ~30% of people.
Inferior glenohumeral ligament complex (IGHL)	Most important stabiliser against anterior dislocation. Has anterior band, posterior band, and axillary pouch. The anterior band of the IGHL is the primary restraint against anterior-inferior translation when the arm is in 90° abduction and external rotation (the position of apprehension). ^[1]
Coracohumeral ligament	Resists inferior translation and external rotation in adduction.
Joint capsule	Provides overall containment; negative intra-articular pressure contributes to stability (suction cup effect).

Why Does Anterior Dislocation Happen in ABER Position?

When the arm is in Abduction and External Rotation (ABER), the anterior band of the IGHL is maximally taut and is the sole restraint. If a posteriorly directed force is applied to the hand/arm in this position (e.g., blocking in basketball, overhead tackle), the IGHL fails → the humeral head is pushed anteriorly and inferiorly over the glenoid rim → anterior dislocation. This is the biomechanical basis of the apprehension test.

The rotator cuff muscles are the primary dynamic stabilisers of the shoulder. ^[1]^[2]

Muscle	Origin	Insertion	Innervation	Action	Role in Stability
Supraspinatus	Supraspinous fossa	Greater tuberosity (superior facet)	Suprascapular nerve (C5,6)	Initiates abduction (first 15–30°)	Compresses humeral head into glenoid; resists inferior translation. ^[1]
Infraspinatus	Infraspinous fossa	Greater tuberosity (middle facet)	Suprascapular nerve (C5,6)	External rotation	Major posterior restraint; resists anterior translation. ^[1]
Teres minor	Lateral border of scapula	Greater tuberosity (inferior facet)	Axillary nerve (C5,6)	External rotation	Assists infraspinatus.
Subscapularis	Subscapular fossa	Lesser tuberosity	Upper & lower subscapular nerves (C5,6)	Internal rotation	Anterior restraint; holds humeral head against glenoid anteriorly. ^[1]

These muscles form a force couple system that centres the humeral head within the glenoid during dynamic movements — the "concavity-compression" mechanism. The deltoid provides the main power, but without the cuff compressing the head into the socket, the deltoid's upward pull would simply sublux the head superiorly.

Long head of biceps: Runs from the supraglenoid tubercle through the bicipital groove — acts as an anterior-superior restraint (depresses humeral head). ^[1]
Scapulothoracic musculature: Serratus anterior, trapezius, rhomboids — maintain scapular positioning and provide a stable platform for the glenoid. Scapular dyskinesis (abnormal scapular movement) can predispose to instability.
Negative intra-articular pressure: The sealed joint capsule maintains a slight vacuum, contributing to the "suction cup" effect on the humeral head.

This is critical for understanding associated injuries:

Axillary nerve (C5, C6): Wraps around the surgical neck of the humerus posteriorly, courses through the quadrilateral space. It is the most commonly injured nerve in anterior shoulder dislocation (~5–35% of cases). Supplies the deltoid and teres minor, and provides sensation over the "regimental badge area" (lateral deltoid). ^[1]^[2]
Musculocutaneous nerve: May be stretched with anterior displacement.
Axillary artery: Vulnerable especially in elderly patients with atherosclerotic, less elastic vessels. Runs anterior to the subscapularis. Disruption → vascular emergency.
Brachial plexus: Particularly the posterior cord (gives rise to axillary nerve and radial nerve) — may be stretched.

Clinical Pearl – Always Check Axillary Nerve

After any shoulder dislocation (and especially after reduction), you MUST document axillary nerve function — test sensation over the "regimental badge area" (lateral aspect of the deltoid) and test deltoid contraction (ask the patient to abduct against resistance). Failure to document this is a medicolegal pitfall. ^[1]^[2]

4. Etiology and Pathophysiology

4.1 Mechanism of Injury

Most common mechanism: Indirect force with the arm in abduction, external rotation, and extension (ABER position) — e.g., falling on an outstretched hand, blocking in sports, overhead tackle. ^[1]^[2]
The humeral head is levered anteriorly over the glenoid rim, tearing the anterior capsule and labrum.
Direct blow to the posterior shoulder can also push the head forward (less common).

Pathological sequence of anterior dislocation (understanding this is key):

Classic mechanisms: seizures, electrocution, or high-energy trauma. ^[1]^[2]
Why seizures? During a generalised tonic-clonic seizure, there is simultaneous violent contraction of all shoulder muscles. The internal rotators (subscapularis, pectoralis major, latissimus dorsi) are more powerful than the external rotators (infraspinatus, teres minor) → net effect is forceful internal rotation → the humeral head is driven posteriorly.
Why electrocution? Same mechanism — massive uncoordinated muscle contraction.
Direct blow to the anterior shoulder (less common).
The humeral head displaces posteriorly and impacts on the posterior glenoid rim → reverse Hill-Sachs lesion (McLaughlin lesion) = anteromedial humeral head impaction fracture.

The arm is locked in full abduction — the patient presents with the arm above the head and cannot bring it down (looks like they are "raising their hand"). ^[1]
Mechanism: Hyperabduction force drives the humeral head inferiorly below the glenoid.
High association with neurovascular injury (axillary artery, brachial plexus), rotator cuff tears, and greater tuberosity fractures.

Extreme forward/upward force on an adducted arm.
Associated with fractures of the acromion, clavicle, and rotator cuff disruption.

Understanding these lesions is essential for grasping why recurrence occurs and what surgery aims to fix:

Lesion	Description	Pathophysiology	Clinical Significance
Bankart lesion	Detachment of the anteroinferior labrum from the glenoid rim	The labrum tears as the humeral head levers over it; the IGHL (which inserts on the labrum) loses its anchor point	The "essential lesion" of traumatic anterior instability — the primary reason for recurrent dislocation. Surgical repair (Bankart repair) is the definitive treatment. ^[1]^[2]
Bony Bankart	Fracture of the anteroinferior glenoid rim with the labrum	The humeral head chips off a piece of bone as it dislocates	Reduces the glenoid arc → loss of bony buttress → higher recurrence even after soft-tissue repair. May require bone augmentation (e.g., Latarjet procedure).
Hill-Sachs lesion	Posterolateral compression fracture of the humeral head	When the humeral head dislocates anteriorly, the posterolateral aspect impacts against the hard anteroinferior glenoid rim, denting the softer cancellous bone of the humeral head	A large "engaging" Hill-Sachs lesion can catch on the glenoid rim during abduction/external rotation → causes re-dislocation. ^[1]^[2]
Reverse Hill-Sachs (McLaughlin lesion)	Anteromedial humeral head impaction fracture	Occurs in posterior dislocation — the head impacts on the posterior glenoid rim
ALPSA lesion	Anterior Labroligamentous Periosteal Sleeve Avulsion — the labrum and periosteum strip off the glenoid neck but remain in continuity	Heals in a medialised, non-anatomic position → functionally incompetent labrum	Leads to recurrent instability despite apparent "healing."
HAGL lesion	Humeral Avulsion of the Glenohumeral Ligament — the IGHL tears from its humeral insertion	Instead of the labrum tearing, the ligament itself avulses from the humeral side	Important surgical consideration — if you only repair the labrum and miss the HAGL, instability persists.
SLAP lesion	Superior Labrum Anterior to Posterior tear	May occur concurrently, especially with traction injuries or falls on outstretched hand	Affects the biceps anchor → may cause biceps dysfunction and instability. ^[1]
Rotator cuff tear	Tear of one or more cuff tendons (especially supraspinatus)	More common in patients > 40 years with dislocation — the cuff is degenerative and tears as the head displaces	In patients > 40 years old, first-time dislocations have up to 40–80% associated rotator cuff tear — this is a critical teaching point. ^[1]
Greater tuberosity fracture	Avulsion fracture of the greater tuberosity	The supraspinatus/infraspinatus insertions are avulsed as the head displaces	Often reduces anatomically when the shoulder is reduced. If it remains displaced > 5mm (some say > 3mm), requires ORIF. Interestingly, the recurrence rate of dislocation is LOW when associated with a GT fracture — because the inflammatory healing response "tightens" the anterior structures.

Age-Dependent Pathology – Key Concept

Young patient (< 25) → Bankart lesion (labral tear) is the predominant pathology → high recurrence rate → often needs surgical repair.
Older patient (> 40) → Rotator cuff tear is the predominant pathology → lower recurrence rate but significant functional deficit → may need cuff repair rather than (or in addition to) labral repair. ^[1]
Any age with greater tuberosity fracture → Lower recurrence rate.

Not all shoulder instability is traumatic. The distinction between traumatic and atraumatic instability is fundamental ^[1]:

Feature	Traumatic (TUBS)	Atraumatic (AMBRI)
Mnemonic	TUBS	AMBRI
Full form	Traumatic, Unilateral, Bankart lesion, Surgery	Atraumatic, Multidirectional, Bilateral, Rehabilitation, Inferior capsular shift (if surgery needed)
Mechanism	Definite traumatic event	No definite trauma; may be from repetitive microtrauma or inherent laxity
Direction	Usually unidirectional (anterior)	Multidirectional
Pathology	Bankart lesion, Hill-Sachs	Capsular redundancy, ligamentous laxity
Treatment	Often surgical (Bankart repair)	Rehabilitation first (rotator cuff and scapular stabiliser strengthening); surgery (inferior capsular shift) if fails
Bilateral?	Usually unilateral	Often bilateral

5. Classification

Type	Percentage	Key Associations
Anterior	~95%	ABER mechanism, Bankart lesion, Hill-Sachs, axillary nerve injury
Posterior	~2–4%	Seizures, electrocution, internal rotation contracture, reverse Hill-Sachs, commonly MISSED on AP X-ray
Inferior (Luxatio Erecta)	< 1%	Arm locked in abduction, high neurovascular injury risk
Superior	Very rare	Acromion fracture

Traumatic vs. Atraumatic (as above — TUBS vs. AMBRI) ^[1]
Voluntary: Patient can deliberately sublux/dislocate their shoulder — often a habitual or psychiatric component. Do not operate — surgery in voluntary dislocators has poor outcomes.

Acute: Dislocation presenting within < 2 weeks of injury.
Chronic (unreduced): Dislocation that has been present for > 2–3 weeks — the longer it remains unreduced, the harder it is to reduce closed and the greater the associated damage (muscle contracture, bony erosion).
Recurrent: Repeated episodes of dislocation after the initial episode.

Dislocation: Complete loss of contact between articular surfaces.
Subluxation: Partial displacement with some residual contact — the patient feels the shoulder "slipping" and then returning.

A more nuanced, modern classification:

Polar Type I: Traumatic structural (≈ TUBS)
Polar Type II: Atraumatic structural (e.g., repetitive microtrauma in swimmers → labral damage without a single big event)
Polar Type III: Habitual/non-structural (muscle patterning abnormalities, voluntary instability)

Patients often fall on a spectrum within the triangle rather than fitting neatly into one category.

6. Clinical Features

Symptom	Pathophysiological Basis
Severe pain	Capsular and labral tearing, muscle spasm, periosteal stretching, and possible fracture (Hill-Sachs, greater tuberosity). Pain is worst at the moment of dislocation and remains severe until reduction.
Feeling of the shoulder "popping out"	The patient often describes a distinct sensation of the humeral head displacing from the socket — corresponds to the humeral head translating over the glenoid rim.
Inability to move the arm	Muscle spasm (protective reflex) locks the arm in place. In anterior dislocation, the arm is held in slight abduction and external rotation (because the humeral head is sitting anteroinferiorly and the patient cannot internally rotate). In posterior dislocation, the arm is held in adduction and internal rotation.
"Dead arm" sensation / numbness	Axillary nerve neurapraxia → loss of sensation over the "regimental badge area" (lateral deltoid). May also involve musculocutaneous nerve → lateral forearm numbness.
Weakness	Axillary nerve injury → deltoid weakness; rotator cuff tear → inability to initiate abduction (supraspinatus) or externally rotate (infraspinatus).
History of arm position at time of injury	Anterior: ABER position. Posterior: forward flexion with internal rotation, or seizure. Inferior: hyperabduction.
Recurrent episodes (in recurrent instability)	Each dislocation further damages the labrum and stretches the capsule → lower force threshold needed → episodes may occur with minimal provocation (e.g., rolling over in bed, reaching for an object). ^[1]^[2]
Apprehension (in recurrent instability)	The patient dreads putting the arm in the provocative position (ABER for anterior instability) because they feel the shoulder is about to dislocate again — this is the basis of the apprehension test.

6.2 Signs

Sign	Pathophysiological Basis
Loss of normal rounded deltoid contour (squared-off shoulder)	The humeral head is no longer sitting under the acromion — the deltoid drapes over the empty glenoid, creating a step/flattening laterally. ^[1]^[2]
Prominent acromion	With the humeral head displaced anteriorly, the acromion becomes the most lateral bony prominence — visually more prominent.
Palpable humeral head anteriorly (in the subcoracoid area)	In ~95% of anterior dislocations, the head sits in the subcoracoid position — you can palpate the hard, round mass just below and medial to the coracoid process.
Arm held in slight abduction and external rotation	The anteriorly displaced humeral head mechanically prevents internal rotation and adduction. The infraglenoid position of the head forces slight abduction.
Loss of external rotation (posterior dislocation) / Loss of internal rotation (anterior dislocation, less obvious)	In posterior dislocation: the head is locked behind the glenoid → external rotation is blocked. The arm is held in adduction and internal rotation. This is a critical distinguishing feature. ^[1]
Fullness in the anterior axillary fold	The displaced humeral head pushes into the anterior structures.
Empty glenoid posteriorly (in anterior dislocation)	You may feel a hollow where the humeral head should be posteriorly.
Loss of sensation over "regimental badge area"	Axillary nerve injury (neurapraxia from stretching over the displaced humeral head or surgical neck). ^[1]^[2]
Weak or absent deltoid contraction	Motor component of axillary nerve injury.
Absent/weak distal pulses (rare but critical)	Axillary artery injury, especially in elderly or with significant displacement.
Bruising	Capsular and soft tissue disruption → haematoma formation. May track inferiorly (gravitational).

Why Is Posterior Dislocation Commonly Missed?

Posterior shoulder dislocation is one of the most commonly missed diagnoses in emergency medicine (reported miss rate historically up to 50%). ^[1]^[2]

Reasons:

The standard AP X-ray may look deceptively normal — the humeral head overlaps with the glenoid and may appear in a normal position. The "lightbulb sign" (internally rotated humeral head looks symmetrically rounded like a lightbulb) may be the only clue on AP view.
The shoulder may not look obviously deformed — the posterior fullness is less dramatic than the anterior void/squared shoulder.
If the patient is post-ictal or intoxicated, they may not give a clear history.

Solution: Always obtain axillary lateral or "Y" (scapular lateral) view in addition to the AP view. On the axillary view, you will clearly see the humeral head posterior to the glenoid. ^[1]^[2]

Sign (Posterior Dislocation)	Pathophysiological Basis
Arm held in adduction and internal rotation	The humeral head is locked behind the glenoid — external rotation is mechanically blocked.
Loss/limitation of external rotation and abduction	The posterior glenoid rim prevents the humeral head from rotating externally.
Posterior shoulder fullness	The humeral head is palpable posteriorly.
Flattened anterior shoulder	The humeral head is no longer sitting anteriorly → anterior hollow.
Coracoid process more prominent anteriorly	Similar to how acromion becomes prominent in anterior dislocation.

Sign	Pathophysiological Basis
Arm locked in full abduction (above the head)	The humeral head is trapped below the glenoid, preventing adduction. The arm appears "raised" — the patient physically cannot bring it down. ^[1]
Humeral head palpable in the axilla	The head has displaced inferiorly into the inferior axillary space.
High rate of neurovascular injury	The axillary nerve and artery are directly compressed by the inferiorly displaced humeral head.

These are assessed by provocative tests rather than acute signs:

Test	Technique	What It Tests	Positive Finding
Apprehension test	Patient supine, arm at 90° abduction and maximally externally rotated. Examiner applies gentle anterior force on the posterior humeral head.	Tests for anterior instability	Patient becomes anxious/apprehensive and resists further movement — they feel the shoulder is about to dislocate. (Note: the test is positive for apprehension, NOT pain alone). ^[1]^[2]
Jobe relocation test	With the patient still in the apprehensive position, the examiner applies a posteriorly directed force on the anterior humeral head.	Confirms anterior instability if apprehension test positive	The apprehension/anxiety resolves because the posteriorly directed force prevents the humeral head from translating anteriorly. ^[1]
Release test (Surprise test)	After relocation, suddenly remove the posteriorly directed hand.	Confirms anterior instability	Sudden return of apprehension/pain confirms the diagnosis.
Sulcus sign	With the arm at the side, apply downward traction to the arm.	Tests for inferior instability / multidirectional instability	A visible sulcus (dimple/groove) appears between the acromion and the humeral head — indicates inferior capsular laxity. Graded 1+ (< 1cm), 2+ (1–2cm), 3+ (> 2cm). ^[1]^[2]
Load-and-shift test	Examiner loads the humeral head into the glenoid (push medially), then shifts anteriorly or posteriorly.	Quantifies the degree of translation in any direction	Graded: 0 = minimal; 1+ = head to glenoid rim; 2+ = head over rim but spontaneously reduces; 3+ = head locks over rim (dislocated).
Posterior apprehension / Jerk test	Arm in 90° forward flexion, adducted, internally rotated. Axial load through the elbow while adducting across the body.	Tests for posterior instability	Clunk or jerk as the humeral head subluxes posteriorly over the glenoid rim, then reduces as the arm is returned.
Hyperabduction test (Gagey test)	Stabilise the scapula and passively abduct the arm.	Tests IGHL laxity	Abduction > 105° (compared to contralateral side) indicates IGHL laxity.

GC Lecture – Key Examination Points

From the GC lecture, the key clinical examination steps emphasised are: ^[1]^[2]^[3]

Look: Squared-off shoulder, flattened deltoid, arm position (abduction/external rotation in anterior; adduction/internal rotation in posterior).
Feel: Palpate humeral head position (anteriorly in subcoracoid space for anterior dislocation), check sensation over regimental badge area (axillary nerve).
Move: Active and passive ROM — severely restricted acutely. Apprehension test for chronic instability.
Neurovascular examination — mandatory, document pre- and post-reduction.

Always systematically assess for associated injuries ^[1]^[2]:

Associated Injury	Details	Why?
Axillary nerve injury	Most common nerve injury (5–35%). Test regimental badge sensation + deltoid power.	Nerve wraps around surgical neck in the quadrilateral space — stretched by anteriorly displaced humeral head.
Bankart lesion	Anteroinferior labral tear — present in up to 97% of traumatic anterior dislocations.	The "essential lesion" — determines recurrence.
Hill-Sachs lesion	Posterolateral humeral head impaction fracture — present in up to 65–70% of first dislocations, up to 90% in recurrent.	Impact of head on glenoid rim during dislocation.
Greater tuberosity fracture	Up to 15–35% of anterior dislocations.	Avulsion by rotator cuff tendons. If it reduces anatomically with reduction of the joint, it can be managed conservatively.
Rotator cuff tear	> 40 years: up to 40–80% incidence	Degenerative cuff is vulnerable. If the patient cannot actively abduct after reduction, suspect cuff tear. ^[1]
Brachial plexus injury	Less common than axillary nerve alone.	Traction on the plexus.
Axillary artery injury	Rare but limb/life-threatening; more common in elderly with atherosclerosis.	Vessel is relatively fixed and inelastic; stretching → intimal tear or rupture.
Fracture-dislocation	Combination of proximal humeral fracture with dislocation.	Must be identified on X-ray before attempting reduction — blind reduction of a fracture-dislocation can cause further damage.
Bony Bankart (glenoid fracture)	Fracture of the anteroinferior glenoid rim.	Important for surgical planning — significant bone loss (> 20–25% of glenoid) → Latarjet procedure rather than Bankart repair.

High Yield Summary

Key Takeaways for Shoulder Dislocation (Definition → Clinical Features):

The shoulder is the most commonly dislocated joint due to the large humeral head vs. small, shallow glenoid ("golf ball on a tee"). ^[1]^[2]
Anterior dislocation = 95% of cases; mechanism = ABER (Abduction, External Rotation); pathology = Bankart lesion + Hill-Sachs.
Posterior dislocation = seizures/electrocution → classically MISSED on AP X-ray ("lightbulb sign"). Always get axillary/Y-view. ^[1]^[2]
Young patient → labral tear (Bankart) → high recurrence. Old patient → rotator cuff tear → low recurrence but poor function. ^[1]
ALWAYS check axillary nerve (regimental badge area sensation + deltoid power) and distal pulses before AND after reduction.
TUBS = Traumatic, Unilateral, Bankart, Surgery. AMBRI = Atraumatic, Multidirectional, Bilateral, Rehabilitation, Inferior capsular shift.
Bankart lesion is the "essential lesion" of anterior traumatic instability. ^[1]^[2]
Hill-Sachs lesion = posterolateral humeral head impaction (anterior dislocation); Reverse Hill-Sachs = anteromedial impaction (posterior dislocation).
Associated greater tuberosity fracture paradoxically reduces the recurrence rate.
Inferior dislocation (luxatio erecta) → arm locked above head, highest neurovascular injury risk.

Active Recall - Shoulder Dislocation (Definition to Clinical Features)

^[1] Lecture slides: GC 236. Common Shoulder Problems [Updated in 2025].pdf ^[2] Lecture slides: CFB (OT01) Introduction to Orthopaedic Surgery.pdf; Injuries to bone and joint WCS.pdf ^[3] Lecture slides: CFB Clinical skills Upper Limb RY 2025.pdf ^[4] Senior notes: Ryan Ho Rheumatology.pdf ^[5] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf ^[6] Senior notes: Maksim Surgery Notes.pdf

Differential Diagnosis of Shoulder Dislocation

The differential diagnosis of an acutely painful, immobile shoulder — or a shoulder presenting with instability, deformity, and limited range of motion — is broad. The key clinical challenge is to distinguish true glenohumeral dislocation from conditions that mimic it, and, once dislocation is confirmed or strongly suspected, to identify the direction and associated pathology. Let's work through this systematically from first principles.

A patient presenting with an acute shoulder injury typically has some combination of:

Pain
Deformity / altered contour
Reduced or absent range of motion
+/- Neurovascular compromise

The question becomes: Is this a dislocation, a fracture, a soft tissue injury, or something else entirely? And if it IS a dislocation — which direction, and what else has been damaged?

2. Differential Diagnosis — Organised by Category

These present with pain, deformity, or loss of movement and can be confused with a true dislocation, especially before imaging:

Differential Diagnosis	Key Distinguishing Features	Why It Mimics Dislocation
Proximal humeral fracture (surgical neck, anatomical neck, greater/lesser tuberosity)	Swelling, bruising, crepitus on palpation. Humeral head still in glenoid on X-ray. Mechanism may be the same (fall on outstretched hand). Neer classification used for proximal humeral fractures. ^[1]^[2]	Pain and inability to move the shoulder — arm may be splinted by the patient. Deformity may be present with significantly displaced fractures.
Fracture-dislocation	Combination of proximal humeral fracture AND dislocation. Must be identified on X-ray before any attempt at closed reduction — blind reduction can displace fracture fragments, damage neurovascular structures, or convert a closed fracture to an open one. ^[1]^[2]	Looks like a dislocation clinically but the fracture component means management is entirely different (often requires surgical ORIF rather than closed reduction).
Acromioclavicular (AC) joint injury / dislocation	Localised tenderness directly over the AC joint (superior shoulder, not anteroinferior). Step deformity at AC joint. Cross-body adduction test positive. Mechanism: direct fall onto the point of the shoulder. Piano key sign in Grade III+. ^[1]^[7]	Pain and deformity at the shoulder. However, the glenohumeral joint itself is intact — the humeral head is in the glenoid.
Rotator cuff tear (acute, massive)	Painful arc sign, drop arm test positive, weakness in abduction/external rotation. Patient over 40 years. Active ROM reduced but passive ROM often preserved (unlike dislocation where both are severely limited). ^[1]^[7]	Acute massive cuff tear after a fall → patient cannot lift the arm → looks "dislocated." But on inspection, the deltoid contour is normal (the head is still in the socket).
Adhesive capsulitis (frozen shoulder)	Global restriction of both active and passive ROM — especially external rotation. Insidious onset over weeks-months, NOT acute. Often follows a period of immobilisation. Risk factors: diabetes mellitus, thyroid disease, previous shoulder injury/surgery. ^[1]^[7]	Limited ROM in all directions can be confused with an unreduced chronic dislocation. But there is no acute trauma, and the X-ray shows the head in the glenoid.
Subacromial impingement / Rotator cuff tendinopathy	Painful arc (60–120° abduction). Pain during activity, passive ROM > active ROM. External rotation often spared (infraspinatus + teres minor are intact). ^[7]	Shoulder pain with difficulty moving arm overhead. But not a true loss of motion — just painful motion through a specific arc.
Biceps tendon rupture (long head)	Popeye sign (bulging biceps muscle belly). Sudden onset pain with a "pop." Elbow flexion and supination still possible (brachialis and supinator compensate). ^[7]	Acute pain and deformity. But the deformity is in the anterior arm (muscle belly), not at the shoulder contour.

GC Lecture High Yield – Shoulder Pain DDx

From the GC lecture on Common Shoulder Problems ^[1], the key differential diagnoses for shoulder pain to consider are:

Rotator cuff syndrome (most common cause of shoulder pain overall)
Frozen shoulder (adhesive capsulitis)
AC joint arthritis / injury
Biceps tendonitis
Cervical radiculopathy (referred pain)
Glenohumeral dislocation / instability
Fracture

These are directly examinable in in-house papers. ^[1]^[7]

Pain perceived at the shoulder may not originate from the shoulder at all. The principle here is referred pain — pain felt at a site distant from its origin, because of shared segmental innervation (dermatomes/sclerotomes).

Differential	Mechanism of Referral	Key Distinguishing Features
Cervical radiculopathy (C5/C6)	C5 nerve root supplies the deltoid and shoulder capsule; C6 supplies biceps and lateral forearm. Disc herniation or foraminal stenosis compresses these roots → pain referred to the shoulder. ^[1]^[8]	Neck pain, radiating pain down the arm following a dermatomal pattern, weakness/numbness in the arm. Spurling's test positive. Shoulder ROM itself is full (the shoulder is structurally normal).
Cervical myelopathy	Spinal cord compression in the cervical spine can cause upper limb symptoms including shoulder pain. ^[8]	Symptoms may overlap with shoulder pathology — patients can have myeloradiculopathy. Look for long tract signs (hyperreflexia, Babinski, gait disturbance, bladder dysfunction).
Myocardial ischaemia / infarction	Cardiac pain referred to the left shoulder/arm via viscerosomatic convergence of T1–T4 sensory afferents.	Left shoulder/arm pain with chest tightness, exertional component, risk factors for IHD. No shoulder deformity, ROM is normal.
Diaphragmatic irritation (e.g., subphrenic abscess, splenic injury, ruptured ectopic pregnancy)	The diaphragm is innervated by the phrenic nerve (C3-C5) — the same segments that supply the shoulder (suprascapular nerve, axillary nerve). Irritation of the diaphragm → pain referred to the shoulder tip (Kehr's sign for splenic injury).	Shoulder tip pain without trauma, with abdominal symptoms.
Pancoast tumour (lung apex tumour)	Direct invasion of the brachial plexus (lower trunk) and sympathetic chain by a tumour at the lung apex.	Horner's syndrome (miosis, ptosis, anhidrosis) + shoulder/arm pain + hand wasting (T1). Weight loss, smoking history.

Once glenohumeral dislocation is established (clinically + radiographically), you must determine the direction — because the associated pathology, management, and complications differ:

Feature	Anterior Dislocation (95%)	Posterior Dislocation (2–4%)	Inferior / Luxatio Erecta (< 1%)
Mechanism	ABER (abduction, external rotation)	Seizure, electrocution, high-energy trauma ^[1]^[2]	Hyperabduction force
Arm position	Slight abduction + external rotation	Adduction + internal rotation (arm "locked") ^[1]^[2]	Arm locked above head (full abduction) ^[1]^[7]
Shoulder contour	Squared-off, loss of deltoid rounding, prominent acromion	Posterior fullness, flattened anterior shoulder	Humeral head in axilla
Humeral head palpable	Anteriorly (subcoracoid)	Posteriorly	In axilla / inferiorly
ROM restriction	Cannot internally rotate	Cannot externally rotate (hallmark finding) ^[1]^[2]	Cannot adduct
X-ray (AP)	Head clearly anterior to glenoid	May look deceptively normal ("lightbulb sign") → commonly MISSED ^[1]^[2]	Head below glenoid
Key associated lesion	Bankart + Hill-Sachs	Reverse Hill-Sachs (McLaughlin)	Highest neurovascular injury risk

Posterior Dislocation – The Most Commonly Missed Diagnosis

Posterior shoulder dislocation is one of the most commonly missed diagnoses in emergency medicine. The AP X-ray can look nearly normal — the humeral head overlaps with the glenoid. The "lightbulb sign" (internally rotated humeral head appears symmetrically rounded) is the only clue on AP view. Always obtain an axillary lateral or scapular Y-view to confirm. ^[1]^[2]

If the clinical picture is seizure + shoulder pain + internal rotation contracture → think posterior dislocation FIRST.

This distinction is crucial because it determines the entire management pathway:

Feature	Traumatic (TUBS)	Atraumatic (AMBRI)
History	Definite traumatic event (fall, tackle, collision)	No single event; may be insidious or from repetitive microtrauma
Direction	Unidirectional (usually anterior)	Multidirectional ^[1]
Laterality	Usually unilateral	Often bilateral
Laxity	Normal baseline laxity	Generalised hyperlaxity (Beighton score elevated; think connective tissue disorders such as Ehlers-Danlos, Marfan) ^[1]
Pathology	Bankart lesion (structural labral tear)	Capsular redundancy, no distinct labral tear
Sulcus sign	Usually negative or 1+	Often 2+ or 3+
Primary treatment	Surgery (Bankart repair)	Rehabilitation first (rotator cuff + scapular stabiliser strengthening) ^[1]
If surgery needed	Bankart repair / Latarjet	Inferior capsular shift

2.5 Important Specific Differentials to Not Miss

Presents with acute severe shoulder pain, warmth, effusion, restricted ROM, and systemic features (fever, raised inflammatory markers).
The shoulder is red, hot, swollen — held immobile by the patient.
Must aspirate for synovial fluid analysis (cell count, Gram stain, crystal analysis, culture) — this is an orthopaedic emergency because untreated septic arthritis destroys articular cartilage within hours. ^[9]
Risk factors: immunosuppression, RA (pre-existing joint damage), recent joint procedure, IV drug use.
Why it mimics dislocation: the patient holds the arm rigidly, resists all movement → looks similar to an unreduced dislocation.
Key difference: Systemic features (fever, rigors), joint effusion palpable, inflammatory markers markedly elevated. X-ray shows the head in the glenoid.

An older patient or patient with known malignancy who sustains a proximal humeral fracture with minimal trauma.
Lytic lesions visible on X-ray.
Important not to attempt forceful reduction without reviewing imaging — fragile bone may shatter.

Axillary artery injury: Particularly in elderly patients. Presents with absent distal pulses, expanding haematoma, cold pale hand. This is a vascular emergency.
Brachial plexus injury: Extensive neurological deficit beyond just the axillary nerve territory → consider plexus injury (especially posterior cord or whole plexus).

The systematic approach taught in the GC lectures ^[1]^[2]^[3] can be summarised as:

Step 1: History

Mechanism: ABER → anterior; seizure/electrocution → posterior; hyperabduction → inferior; fall on point of shoulder → AC joint; fall on outstretched hand → fracture or dislocation.
First episode vs. recurrent: Recurrent episodes with minimal provocation → structural instability (Bankart lesion). First episode in young → think traumatic; in old → think cuff tear.
Pre-existing conditions: DM → frozen shoulder; RA → septic arthritis risk; epilepsy → posterior dislocation; malignancy → pathological fracture.
Symptoms elsewhere: Neck pain/radiculopathy → cervical spine; chest pain → cardiac; abdominal pain → diaphragmatic referral.

Step 2: Examination

Look: Shoulder contour (squared = dislocation; step at AC joint = AC injury; swelling = effusion/fracture; arm position = direction clue).
Feel: Humeral head position; localised tenderness (AC joint = AC injury; greater tuberosity = fracture; bicipital groove = biceps tendinopathy); regimental badge area sensation.
Move: Active vs. passive ROM. Both severely restricted → dislocation or frozen shoulder. Passive > active → cuff tear or impingement.
Neurovascular exam: Axillary nerve, distal pulses — mandatory in ALL cases. ^[1]^[2]

Step 3: Imaging

Minimum: AP + axillary lateral (or scapular Y-view) X-ray — this is the standard trauma shoulder series. ^[1]^[2]
Why both views? The AP view alone can miss posterior dislocation. The axillary/Y-view definitively shows the relationship between the humeral head and glenoid in the axial plane.

Exam Rule: Three-View Shoulder Series

For any suspected shoulder dislocation, always request at minimum an AP view and an axillary lateral (or scapular Y-view). A single AP view is NOT sufficient — this is how posterior dislocations are missed. ^[1]^[2]

Diagnosis	Key Feature That Distinguishes from Dislocation
Proximal humeral fracture	Head in glenoid on X-ray; crepitus; may have similar mechanism
Fracture-dislocation	Fracture + dislocation together on X-ray; DO NOT attempt blind reduction
AC joint injury	Tenderness over AC joint (not glenohumeral); step deformity at AC joint; piano key sign
Rotator cuff tear	Passive ROM preserved; active ROM lost; drop arm test; typically > 40 years
Frozen shoulder	Insidious onset; global restriction (active + passive); no acute trauma; DM association
Impingement / tendinopathy	Painful arc (60–120°); pain, not block, limits motion; external rotation spared
Biceps rupture	Popeye sign; deformity in arm not shoulder; elbow flexion/supination intact
Cervical radiculopathy	Neck pain; dermatomal radiation; Spurling's positive; shoulder ROM full
Septic arthritis	Fever; hot swollen joint; raised WCC/CRP; aspirate diagnostic
Referred pain (cardiac, diaphragmatic)	No shoulder deformity; ROM full; systemic symptoms (chest pain, abdominal pain)

High Yield Summary

Differential Diagnosis of Shoulder Dislocation — Key Points:

Always consider fracture and fracture-dislocation before attempting reduction — review X-rays (minimum 2 views: AP + axillary/Y-view) first. ^[1]^[2]
Posterior dislocation is the most commonly missed — classic triad: seizure/electrocution + internal rotation contracture + "lightbulb sign" on AP X-ray. ^[1]^[2]
Rotator cuff tear mimics dislocation in older patients (cannot lift arm) — distinguish by passive ROM being preserved and deltoid contour being normal.
Frozen shoulder mimics chronic unreduced dislocation — but onset is insidious, bilateral sometimes, and associated with diabetes. ^[1]^[7]
AC joint injury is localised superiorly (over the AC joint) — glenohumeral joint is intact.
Cervical radiculopathy can present as shoulder pain — always check for neck symptoms, dermatomal pattern, and Spurling's test. ^[8]
Septic arthritis is an emergency — if the joint is hot, swollen, and the patient is febrile, aspirate first.
TUBS vs. AMBRI differentiates traumatic unidirectional instability (surgical) from atraumatic multidirectional instability (rehabilitation first). ^[1]
Don't forget non-musculoskeletal referral: cardiac ischaemia (left shoulder), diaphragmatic irritation (shoulder tip — Kehr's sign), Pancoast tumour.

Active Recall - Differential Diagnosis of Shoulder Dislocation

References

^[1] Lecture slides: GC 236. Common Shoulder Problems [Updated in 2025].pdf ^[2] Lecture slides: CFB (OT01) Introduction to Orthopaedic Surgery.pdf; Injuries to bone and joint WCS.pdf ^[3] Lecture slides: CFB Clinical skills Upper Limb RY 2025.pdf ^[7] Senior notes: Maksim Surgery Notes.pdf (pp. 231–234) ^[8] Lecture slides: GC 227. Cervical Spine Pathology.pdf (p. 44) ^[9] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p. 1683)

Diagnostic Criteria, Diagnostic Algorithm, and Investigations for Shoulder Dislocation

1. Diagnostic Criteria — The Clinical-Radiological Diagnosis

Shoulder dislocation does not have a formal "diagnostic criteria" in the way that rheumatological or metabolic conditions do (e.g., ACR criteria for RA, IMWG criteria for myeloma). Instead, the diagnosis is made by a combination of:

Compatible clinical history (mechanism, arm position, symptoms)
Physical examination findings (deformity, arm position, loss of ROM, neurovascular status)
Confirmatory radiographic imaging — this is the definitive step

Key Principle: Always Image Before Reduction

You must obtain radiographs BEFORE attempting reduction (unless in extremis with vascular compromise). The reason is that you need to:

Confirm the diagnosis — is it truly a dislocation, or a fracture mimicking one?
Determine the direction — anterior, posterior, or inferior.
Identify associated fractures — fracture-dislocations require a completely different management pathway (often surgical). Blind reduction of a fracture-dislocation can displace fragments, damage neurovascular structures, or worsen the injury. ^[1]^[2]

The clinical diagnosis can be made with high confidence when the following are present:

Criterion	Anterior (~95%)	Posterior (~2–4%)	Inferior (< 1%)
History	Forced ABER; fall/tackle	Seizure, electrocution, trauma	Hyperabduction force
Arm position	Slight abduction + external rotation	Adduction + internal rotation	Full abduction, arm above head
Shoulder contour	Squared-off; loss of deltoid rounding	Posterior fullness; flattened anteriorly	Humeral head in axilla
ROM	Cannot internally rotate	Cannot externally rotate (hallmark)	Cannot adduct
Palpable humeral head	Anteriorly (subcoracoid)	Posteriorly	Inferiorly (axilla)

The definitive diagnosis of shoulder dislocation is radiographic. ^[1]^[2]

A dislocation is confirmed when the humeral head is completely displaced from the glenoid fossa on appropriate X-ray views. The specific radiographic criteria by direction:

Direction	AP X-ray Finding	Axillary / Y-view Finding
Anterior	Humeral head overlapping or medial to the glenoid; head sitting in subcoracoid position; loss of normal glenohumeral overlap	Head clearly anterior to glenoid centre
Posterior	May appear deceptively normal. Look for: "Lightbulb sign" (head internally rotated → symmetric round contour); loss of normal half-moon overlap between humeral head and glenoid ("rim sign" — widened gap > 6mm between medial humeral head and anterior glenoid rim); vacant glenoid sign ^[1]^[2]	Head clearly posterior to glenoid centre — this view is DIAGNOSTIC
Inferior	Humeral head below glenoid; shaft pointing superiorly (luxatio erecta)	Head inferior to glenoid

GC Lecture High Yield – Posterior Dislocation X-ray Signs

The GC lecture emphasises that posterior dislocation is commonly missed on standard AP X-ray. The key radiographic signs to look for are: ^[1]^[2]

"Lightbulb sign" — the internally rotated humeral head appears symmetrically rounded (like a lightbulb), because you lose the normal asymmetric profile of the greater tuberosity.
"Rim sign" — widened space ( > 6mm) between the anterior glenoid rim and the medial border of the humeral head.
Loss of the normal "half-moon" overlap between the humeral head and glenoid on AP view.
Always obtain a second view (axillary lateral or scapular Y-view) to definitively exclude posterior dislocation.

The following algorithm represents the standard clinical approach from presentation to confirmed diagnosis:

GC Lecture – Algorithmic Approach

The key algorithmic steps emphasised in the GC and CFB lectures are: ^[1]^[2]^[3]

Clinical assessment first (history + examination + neurovascular status).
Pre-reduction imaging — minimum 2 views.
Closed reduction (if no fracture-dislocation).
Post-reduction neurovascular check + imaging.
Further imaging (MRI/USS) based on age and clinical suspicion for associated pathology.

3. Investigation Modalities — Detailed Analysis

3.1 Plain Radiography (X-ray) — First-Line, Mandatory

This is the cornerstone investigation. It is quick, cheap, widely available, and provides the essential information needed to make management decisions.

Minimum requirement: AP view + Axillary lateral view (or Scapular Y-view) ^[1]^[2]

View	Technique	What It Shows	Key Findings in Dislocation
AP (anteroposterior) view	Standard shoulder X-ray; beam directed anteriorly to posteriorly	Glenohumeral relationship in the coronal plane; bony anatomy (acromion, clavicle, proximal humerus, glenoid)	Anterior: head clearly medial/inferior to glenoid. Posterior: may look deceptively normal — look for lightbulb sign, rim sign. Inferior: head below glenoid. Also identifies: Hill-Sachs lesion (posterolateral head defect); Bankart fracture (glenoid rim fragment); Greater tuberosity fracture. ^[1]^[2]
Axillary lateral view	Beam directed superiorly through the axilla with arm slightly abducted; cassette above the shoulder	Cross-sectional relationship between humeral head and glenoid — definitively shows anterior vs. posterior displacement	The single most important view for confirming direction of dislocation. Shows humeral head anterior (anterior dislocation), posterior (posterior dislocation), or inferior to the glenoid. Also shows: reverse Hill-Sachs (anteromedial defect in posterior dislocation). ^[1]^[2]
Scapular Y-view ("Y-view")	True lateral of the scapula; the scapular body, spine, and coracoid form a "Y" shape	Humeral head position relative to the glenoid (centre of the "Y")	Normal: humeral head sits centrally at the intersection of the Y. Anterior dislocation: head is anterior to the Y centre. Posterior: head is posterior. Useful alternative when the patient cannot abduct for an axillary view (too much pain). ^[1]^[2]

Why Two Views Are Non-Negotiable

A single AP view can be misleading because:

Posterior dislocation: The head overlaps with the glenoid on AP, and the dislocation occurs in the plane perpendicular to the AP beam — you are looking "straight through" the displacement and can miss it entirely.
Fractures: Some fracture lines (e.g., non-displaced greater tuberosity fractures) may only be visible on the second view.
The axillary/Y-view resolves the humeral head position in the second plane (axial/transverse), turning a 2D image into a 3D understanding. ^[1]^[2]

View	Purpose	When to Use
West Point view	Tangential view of the anteroinferior glenoid rim	To assess bony Bankart lesion (glenoid rim fracture) — useful for surgical planning in recurrent instability
Stryker notch view	Profiles the posterolateral humeral head	To assess Hill-Sachs lesion size — the patient lies supine with hand behind head; beam angled 10° cephalad
AP with internal rotation	Shows the posterolateral humeral head en face	Better visualisation of Hill-Sachs defect
Zanca view	AP with 15° cephalic tilt	For AC joint assessment if AC injury is in the differential ^[7]

Finding	Description	Clinical Significance
Bankart fracture (bony Bankart)	Fragment of the anteroinferior glenoid rim avulsed with the labrum	Indicates significant glenoid bone loss. If > 20–25% of glenoid surface, soft tissue Bankart repair alone will fail → need bony procedure (e.g., Latarjet). ^[1]
Hill-Sachs lesion	Posterolateral compression fracture/indentation of the humeral head	Present in up to 65% of first-time and 90% of recurrent anterior dislocations. A large, "engaging" Hill-Sachs lesion catches on the glenoid rim during abduction/ER → drives re-dislocation. Assessed by "glenoid track" concept. ^[1]
Greater tuberosity fracture	Avulsion fracture of the greater tuberosity	Often reduces anatomically with joint reduction. If displaced > 5mm after reduction → requires ORIF. Paradoxically associated with lower recurrence rate. ^[1]
Reverse Hill-Sachs (McLaughlin lesion)	Anteromedial humeral head impaction fracture	Pathognomonic for posterior dislocation.
"Lightbulb sign"	Symmetrically rounded humeral head on AP view	Sign of posterior dislocation — head is internally rotated, so the normal asymmetric greater tuberosity profile is lost. ^[1]^[2]
"Rim sign"	> 6mm gap between anterior glenoid rim and medial humeral head	Sign of posterior dislocation on AP view.

CT is NOT first-line for routine shoulder dislocation, but becomes essential in specific situations.

Indications for CT in shoulder dislocation:

Fracture-dislocation identified on plain films — CT provides detailed 3D bony anatomy for surgical planning ^[1]^[2]
Assessment of glenoid bone loss — critical for deciding between Bankart repair vs. Latarjet procedure
- CT with 3D reconstruction allows quantification of glenoid bone loss (the "en face" glenoid view)
- > 20–25% glenoid bone loss → Latarjet procedure preferred over soft tissue Bankart repair
Assessment of Hill-Sachs lesion size and engagement ("glenoid track" analysis)
Chronic/unreduced dislocation — to plan surgical approach
Failed reduction — to identify interposed bone fragments or soft tissue blocking reduction

CT Finding	Interpretation
Glenoid bone loss (percentage of inferior glenoid diameter)	Quantifies structural deficiency; guides surgical decision (Bankart vs. Latarjet)
Hill-Sachs size and engagement	"Glenoid track" concept: if the Hill-Sachs extends medial to the glenoid track → "off-track" → engaging → higher recurrence → may need remplissage or bone procedure
Fracture fragment position and comminution	Guides ORIF approach
3D reconstruction	Provides a "bird's eye" view of the glenoid and humeral head — invaluable for preoperative planning

3.3 Magnetic Resonance Imaging (MRI) — Gold Standard for Soft Tissue Assessment

MRI is the investigation of choice for assessing soft tissue injuries associated with shoulder dislocation. It provides exquisite detail of the labrum, capsule, rotator cuff, and cartilage.

Indications for MRI after shoulder dislocation:

Young patient (< 25–30 years) with first-time anterior dislocation being considered for early surgical stabilisation — MRI confirms the Bankart lesion and guides surgical planning ^[1]
Recurrent instability — to assess labral, capsular, and bony pathology before surgery
Suspected rotator cuff tear — especially in patients > 40 years old who cannot actively abduct or externally rotate post-reduction ^[1]
Suspected SLAP lesion, HAGL lesion, ALPSA lesion — MRI (especially MR arthrogram) is the only reliable way to identify these
Chronic instability with normal X-rays — to identify soft tissue cause

Modality	Technique	Best For
Standard MRI	No contrast injection	Rotator cuff tears, effusion, bone marrow oedema (Hill-Sachs), large labral tears
MR arthrogram (MRA)	Intra-articular gadolinium injection followed by MRI	Gold standard for labral pathology — the contrast distends the joint capsule and outlines labral tears, capsular stripping, HAGL lesions, and ALPSA lesions with far greater sensitivity than standard MRI ^[1]

Finding	MRI Appearance	Significance
Bankart lesion	Detached anteroinferior labrum; labrum may be displaced medially or absent; contrast (in MRA) extends between labrum and glenoid rim	Essential lesion of anterior instability; target of Bankart repair
ALPSA lesion	Labrum is displaced medially and healed in a non-anatomic medialized position along the glenoid neck; the periosteal sleeve is intact	"Healed but incompetent" labrum → functionally equivalent to a Bankart → recurrent instability
HAGL lesion	Detachment of the IGHL from its humeral insertion; seen as a J-shaped pouch of contrast at the humeral neck	If missed, a labral repair alone will NOT address the instability
SLAP lesion	Superior labral tear extending anterior-to-posterior, involving the biceps anchor	May coexist with anterior instability; affects the long head of biceps
Rotator cuff tear	Discontinuity of tendon fibres, retraction, muscle atrophy (in chronic cases); supraspinatus most commonly affected	Critical in patients > 40 — determines whether cuff repair is needed in addition to, or instead of, labral repair ^[1]
Hill-Sachs lesion	Bone marrow oedema and cortical depression at posterolateral humeral head	Helps assess size and engagement potential
Capsular redundancy	Patulous, lax capsule — especially the axillary pouch	Seen in multidirectional instability (AMBRI)
Bone marrow oedema (glenoid or humeral head)	High signal on T2/STIR sequences	Indicates recent bony impaction (acute Hill-Sachs or bony Bankart)

GC Lecture – When to Order MRI

From the GC/CFB lectures: MRI is NOT needed for every shoulder dislocation. It is indicated when the clinical question is about soft tissue pathology that will change management — primarily labral tears in young patients being considered for surgery, and rotator cuff tears in older patients. In a straightforward elderly patient with a first-time dislocation and good functional recovery, MRI may not be necessary. ^[1]^[3]

Feature	Details
Role	Quick, non-invasive, no radiation; operator-dependent
Best for	Rotator cuff tears — excellent sensitivity and specificity in experienced hands (comparable to MRI for full-thickness tears) ^[1]
Also useful for	Shoulder effusion (haemarthrosis), dynamic assessment (subluxation during provocation), biceps tendon pathology
Limitations	Cannot assess labrum, cannot assess deep bony pathology, operator-dependent, limited for posterior structures
When to use	Post-reduction in patients > 40 who cannot actively abduct — rapid assessment for cuff tear before deciding on MRI

3.5 Other Investigations

This is not an "imaging investigation" but is an essential component of the diagnostic workup that must be performed and documented. ^[1]^[2]^[3]

Test	Target	Technique	Abnormal Finding
Sensation: regimental badge area	Axillary nerve (C5,6)	Light touch over lateral deltoid	Absent/reduced → axillary nerve neurapraxia
Motor: deltoid contraction	Axillary nerve motor branch	Resisted abduction (may not be possible acutely due to pain — re-test after reduction)	Unable to contract deltoid
Distal pulses	Axillary/brachial artery	Palpate radial and ulnar pulses; compare with contralateral side	Absent/weak → vascular injury (especially in elderly)
Capillary refill, hand colour and temperature	Peripheral perfusion	Inspect and feel the hand	Cold, pale hand with delayed cap refill → vascular emergency

Medicolegal point: Failure to document neurovascular status before and after reduction is indefensible in court. Always write: "Pre-reduction: axillary nerve sensation intact / deficit over regimental badge area; distal pulses present / absent. Post-reduction: [repeat assessment]." ^[1]^[2]

Indication	When to order
Suspected axillary artery injury	Absent distal pulses, expanding haematoma, cold pale hand, significant bruising, especially in elderly patients with displaced fracture-dislocations

Indication	When to order
Suspected axillary nerve or brachial plexus injury that has not recovered	NOT done acutely (denervation changes take 2–3 weeks to develop). Performed at 3–6 weeks post-injury if there is persistent neurological deficit, to assess extent of nerve damage and guide prognosis.

Not routinely required for uncomplicated shoulder dislocation. However:

Scenario	Blood Tests
Post-seizure dislocation	CK (rhabdomyolysis risk from prolonged seizure), glucose (hypoglycaemia as seizure trigger), electrolytes (hyponatraemia, hypocalcaemia), anticonvulsant levels
Suspected septic arthritis	FBC, CRP, ESR, blood cultures
Elderly with significant bruising	FBC (anaemia from occult haemorrhage), coagulation screen (if on anticoagulants)
Pre-operative workup	Standard pre-op bloods if surgery planned

After closed reduction, post-reduction radiographs are mandatory ^[1]^[2]:

Purpose	What to Look For
Confirm concentric reduction	Humeral head centred in the glenoid on both AP and axillary/Y-views
Identify newly visible fractures	Fractures may become apparent after reduction (e.g., a greater tuberosity fragment that was obscured by the dislocated head)
Assess greater tuberosity position	If there was a GT fracture, check if it reduced anatomically. If displaced > 5mm → needs fixation
Joint congruence	Any widened joint space suggesting interposed soft tissue (e.g., subscapularis, biceps tendon — prevents full reduction)

Stage	Investigation	Purpose
1. Pre-reduction	AP + Axillary/Y-view X-ray	Confirm dislocation, determine direction, identify fractures
	Neurovascular exam	Document baseline nerve/vascular status
2. Post-reduction	Repeat AP + Axillary/Y-view X-ray	Confirm reduction, identify new fractures
	Repeat neurovascular exam	Document post-reduction status
3. Further imaging	CT	Fracture-dislocation detail, glenoid bone loss quantification, surgical planning
	MRI / MR arthrogram	Labral tears (young), rotator cuff tears (> 40), HAGL/ALPSA/SLAP
	USS	Quick cuff assessment post-reduction (> 40), bedside
4. Special	CTA	Suspected vascular injury
	EMG/NCS	Persistent nerve deficit at 3–6 weeks

High Yield Summary

Diagnostic Criteria, Algorithm, and Investigations — Key Points:

Diagnosis = Clinical + Radiographic. There are no formal "diagnostic criteria" — the diagnosis is confirmed when X-ray shows complete displacement of the humeral head from the glenoid. ^[1]^[2]
Minimum imaging: AP + Axillary lateral (or Scapular Y-view). A single AP view is NEVER sufficient — posterior dislocations will be missed. ^[1]^[2]
Pre-reduction imaging is mandatory to identify fracture-dislocations. Post-reduction imaging is mandatory to confirm reduction.
Posterior dislocation X-ray signs: lightbulb sign, rim sign (> 6mm gap), loss of half-moon overlap, vacant glenoid sign. ^[1]^[2]
Neurovascular documentation before AND after reduction is non-negotiable (axillary nerve sensation at regimental badge, deltoid power, distal pulses). ^[1]^[2]^[3]
CT: For fracture-dislocations, glenoid bone loss quantification (> 20–25% → Latarjet), Hill-Sachs engagement (glenoid track), and surgical planning.
MRI/MRA: Gold standard for soft tissue — labral tears (young patients), rotator cuff tears (> 40 years), HAGL, ALPSA, SLAP lesions. MRA (with intra-articular gadolinium) is superior for labral pathology.
USS: Quick bedside rotator cuff assessment in patients > 40 post-reduction.
EMG/NCS: Only if persistent nerve deficit at 3–6 weeks (not acutely — denervation changes take time to develop).

Active Recall - Diagnosis and Investigations of Shoulder Dislocation

References

Management of Shoulder Dislocation

The management of shoulder dislocation follows a logical sequence: resuscitate → reduce → reassess → rehabilitate → consider surgery. Every step has a clear rationale rooted in the underlying pathoanatomy. Let's work through this systematically.

2. Acute Management — The First Hour

Before focusing on the shoulder, ensure the patient is haemodynamically stable. In high-energy trauma (e.g., motorcycle accident, fall from height), shoulder dislocation may be one component of polytrauma.

ATLS principles apply in high-energy mechanisms ^[1]^[2]
Assess for other injuries: chest, abdomen, pelvis, spine
Only after the patient is stable should you focus on the shoulder

A dislocated shoulder is extremely painful. Muscle spasm (protective reflex of the deltoid, pectoralis, and rotator cuff) makes the patient guard the arm and resist any attempt at examination or reduction.

Why is analgesia the first priority?

Pain drives muscle spasm → spasm locks the humeral head in the dislocated position → makes reduction impossible or traumatic.
Adequate analgesia and/or sedation relaxes the muscles, allowing atraumatic reduction. The less force used, the lower the risk of iatrogenic fracture or further soft tissue damage.

Analgesic Strategy	Details	When to Use
Intra-articular local anaesthetic	10–20 mL of 1% lidocaine injected directly into the glenohumeral joint (via posterior or lateral approach into the palpable sulcus between acromion and humeral head)	Effective, quick, avoids systemic sedation — particularly useful in the ED when sedation resources are limited or the patient is a poor candidate for IV sedation (e.g., elderly with comorbidities). Studies show comparable success rates to procedural sedation. ^[1]
Procedural sedation (IV)	Combination of a short-acting benzodiazepine (e.g., midazolam) + short-acting opioid (e.g., fentanyl) or propofol	Standard approach when resources and monitoring are available. Requires pulse oximetry, ECG, and resuscitation equipment. Provides both analgesia AND muscle relaxation.
Entonox (50% N₂O / 50% O₂)	Inhaled analgesic	Quick onset, self-administered, good for initial pain relief while setting up for reduction
General anaesthesia	Full GA with muscle relaxation	Reserved for failed closed reduction under sedation, or fracture-dislocations requiring open surgical management

Practical Tip – Intra-articular Injection

Intra-articular lidocaine injection is an underappreciated technique. It works because the joint capsule has been torn during the dislocation → the anaesthetic bathes the exposed nerve endings, periosteum, and muscle attachments directly. It avoids the risks of IV sedation (respiratory depression, aspiration, need for monitoring), and is ideal for the ED setting. Many experienced emergency physicians use this as their first-line approach.

Document before reduction ^[1]^[2]^[3]:

Assessment	What to Record
Axillary nerve	Sensation over regimental badge area (lateral deltoid); deltoid contraction if patient can cooperate
Distal pulses	Radial and ulnar pulses; compare with contralateral
Hand perfusion	Colour, temperature, capillary refill
Other nerves	Musculocutaneous (lateral forearm sensation); radial nerve (wrist/finger extension); median/ulnar if clinically indicated

3. Closed Reduction Techniques

Closed reduction is the definitive acute treatment for uncomplicated shoulder dislocation ^[1]^[2]. The goal is to return the humeral head to the glenoid fossa atraumatically, using the principle of overcoming muscle spasm through gentle traction, leverage, or manipulation — NOT brute force.

GC Lecture – Reduction Principles

The GC and CFB lectures emphasise that reduction should be performed with minimal force after adequate analgesia/sedation. Forced reduction risks iatrogenic fracture (especially of the proximal humerus in osteoporotic patients), further neurovascular damage, and conversion of a simple dislocation to a fracture-dislocation. ^[1]^[2]

3.1 Techniques for Anterior Dislocation

There are many described techniques. No single technique is universally superior — the key is operator familiarity and adequate muscle relaxation. The most commonly taught and examined techniques are:

Step	What You Do	Biomechanical Rationale
1	Patient supine. Steady longitudinal traction applied to the arm (held at ~30° abduction) via the wrist/forearm.	Traction overcomes the muscle spasm that holds the humeral head locked in the dislocated position.
2	Countertraction applied to the thorax using a folded sheet wrapped around the chest under the axilla, pulled by an assistant in the opposite direction.	Without countertraction, the traction would just pull the whole patient off the bed.
3	While maintaining traction, gentle internal and external rotation of the arm.	Rotational movements disengage the humeral head from the glenoid rim and guide it back into the fossa.
Note	The classical Hippocratic method used the surgeon's foot in the axilla as the fulcrum — this is no longer recommended as it risks axillary nerve/vessel damage. Use a sheet instead. ^[1]

Step	What You Do	Biomechanical Rationale
1	Patient prone on a raised bed/trolley with the affected arm dangling over the edge, hanging freely.	Gravity provides continuous gentle traction on the arm — the weight of the arm itself (~4–5 kg) is the reducing force.
2	Apply 2–5 kg of weight to the wrist (or simply let gravity act for 15–30 minutes).	Sustained low-force traction fatigues the spasming muscles, allowing them to relax.
3	Gentle internal and external rotation of the arm once muscle spasm subsides.	Guides the head back into the glenoid.
Advantages	Gentle, low-force, minimal risk of iatrogenic injury. Good for first-time operators.	No forceful manipulation required.
Disadvantages	Slow (can take 15–30 minutes). Patient must be able to lie prone (not suitable if intoxicated, cervical spine not cleared, or obese).

Step	What You Do	Biomechanical Rationale
1	Patient seated or supine. Elbow flexed to 90°. Arm adducted to the side.	Starting position that minimises muscle tension.
2	Slow, steady external rotation of the arm (rotating the forearm outward), taking 5–10 minutes.	External rotation unwinds the subscapularis muscle spasm and disengages the humeral head from the anterior glenoid rim. The slow pace allows muscle fibres to relax gradually rather than triggering a reflex contraction.
3	Often the shoulder reduces with a palpable clunk during external rotation.	The head glides posteriorly over the glenoid rim and drops back into the fossa.
Advantages	No traction needed; very gentle; can be done with just one operator.	Excellent first-line technique.
Contraindication	Should NOT be used if there is an associated fracture involving the surgical neck — external rotation force could displace the fracture.

Step	What You Do
1	Elbow flexed to 90°, arm adducted.
2	Longitudinal traction on the arm.
3	External rotation (slow).
4	Adduction across the chest (bringing elbow towards midline).
5	Internal rotation (hand towards opposite shoulder).
Note	This is a leverage technique and carries a higher risk of fracture (especially in osteoporotic bone). It applies significant torque to the proximal humerus. Many centres now discourage this technique in favour of gentler traction methods. ^[1]

Kocher's Method – A Word of Caution

Kocher's method is a leverage-based technique that generates high forces at the proximal humerus. It has a documented risk of causing iatrogenic fracture (surgical neck, greater tuberosity) — especially in elderly patients with osteoporotic bone. While it is a classic technique that still appears in textbooks and exams, many orthopaedic surgeons and emergency physicians now prefer traction-based methods (Hippocratic, Stimson, external rotation) which are gentler and have lower complication rates. ^[1]

Step	What You Do	Biomechanical Rationale
1	Patient seated upright. No traction applied.	Seated position uses gravity to help.
2	Patient places hand of affected arm on the examiner's shoulder (elbow bent).	Mild abduction/flexion of the shoulder.
3	Gentle massage of the biceps, deltoid, and trapezius to relax the muscle spasm.	Direct relaxation of the spasming muscles that are holding the humeral head locked.
4	Ask the patient to shrug the shoulders back, sit up straight, and bring the elbows together.	These postural adjustments guide the humeral head posteriorly and inferiorly back into the glenoid.
Advantages	No force, no traction, no sedation often needed. Very gentle.	Works by muscle relaxation alone.

Posterior dislocations are rarer and more difficult to reduce. The humeral head is locked behind the posterior glenoid rim, and the reverse Hill-Sachs (McLaughlin) lesion may be engaging on the rim.

Technique	Steps
Traction + External Rotation	Longitudinal traction on the arm (in line with the shaft), with gentle external rotation to disengage the reverse Hill-Sachs from the posterior glenoid rim, and gentle anterior pressure on the humeral head from posteriorly. ^[1]
Lateral traction	Traction applied laterally (abduction) while simultaneously applying a direct anteriorly directed force on the posteriorly displaced humeral head.
GA may be required	Posterior dislocations are often more difficult to reduce closed due to the muscular lock (internal rotators are stronger than external rotators) and the engaging reverse Hill-Sachs.

Technique	Steps
Traction in line with the arm (superior direction) + gradual adduction	The arm is overhead. Apply traction superiorly (in line with the abducted arm), then gradually arc the arm down into adduction. A "two-step" reduction may occur: inferior → anterior → reduced.
High risk	Always done under sedation/GA. High risk of neurovascular injury — be prepared for vascular surgery consultation.

You know reduction has been achieved when:

A palpable "clunk" is felt as the humeral head slides back into the glenoid
Immediate relief of pain — the patient's pain dramatically improves
Restoration of normal shoulder contour — the squared-off appearance resolves
Improvement in ROM — the patient can now gently move the arm
Post-reduction X-ray confirms concentric reduction (humeral head centred in glenoid on AP + axillary/Y-view)

4. Post-Reduction Management

After successful reduction, the shoulder needs to be immobilised to allow soft tissue healing (capsule, labrum, subscapularis).

Parameter	Anterior Dislocation	Posterior Dislocation
Position	Arm in a sling (internal rotation, arm at side). Some evidence suggests immobilisation in external rotation may improve outcomes in young patients by pressing the torn labrum back against the glenoid (like closing a book onto the torn page). ^[1]	Arm in a brace in external rotation and slight abduction (to prevent the internally rotating forces from re-dislocating posteriorly).
Duration	1–3 weeks for most patients; shorter in elderly (risk of frozen shoulder with prolonged immobilisation); longer in young patients if non-operative management chosen. ^[1]^[7]	4–6 weeks (posterior dislocations are less common and have higher re-dislocation risk if not adequately immobilised).
Type of sling	Standard arm sling or shoulder immobiliser.	Gunslinger brace or similar external rotation brace.

GC Lecture – Immobilisation Duration

The GC lecture emphasises that prolonged immobilisation ( > 3 weeks) in elderly patients should be avoided — it increases the risk of adhesive capsulitis (frozen shoulder), which can be more debilitating than the original dislocation. Early gentle pendulum exercises should begin within 1–2 weeks in older patients. ^[1]

Rehabilitation is the cornerstone of non-operative management. ^[1] The goal is to compensate for the damaged static stabilisers (labrum, capsule) by strengthening the dynamic stabilisers (rotator cuff and scapular muscles).

Phase	Timing	Goals	Exercises
Phase 1: Protection	0–2 (elderly) to 0–4 weeks (young)	Pain control, protect healing tissues, prevent stiffness	Pendulum exercises (gentle, gravity-assisted shoulder movement while leaning forward); elbow/wrist/hand ROM; isometric cuff contractions
Phase 2: Early motion	2–6 weeks	Restore passive → active ROM	Assisted active ROM exercises; gentle stretching; begin active ROM as pain allows
Phase 3: Strengthening	6–12 weeks	Rotator cuff strengthening — especially external rotators (infraspinatus, teres minor) and subscapularis; Scapular stabiliser strengthening (serratus anterior, lower trapezius, rhomboids)	Resistance band exercises; proprioceptive training; closed-chain exercises
Phase 4: Return to activity	3–6 months	Sport-specific training; return to contact sports only when strength is > 90% of contralateral side and there is no apprehension	Dynamic stability drills; plyometrics; sport-specific movements

Why external rotator strengthening is paramount: In anterior dislocation, the anterior capsule/labrum is torn — the structural "check-rein" against anterior translation is compromised. By strengthening the infraspinatus and teres minor (external rotators that pull the humeral head posteriorly), you create a dynamic restraint that compensates for the lost static restraint. Similarly, strengthening the subscapularis (anterior dynamic stabiliser) increases concavity compression.

This is the central management decision and is heavily influenced by patient age, activity level, and associated pathology:

Factor	Favours Non-Operative	Favours Operative
Age	> 40 years (lower recurrence ~15–25%; cuff tear is the dominant pathology, not labral)	< 25 years (recurrence rate up to 70–90% with non-operative management alone) ^[1]^[7]
Activity level	Sedentary, low-demand	Active, contact sports, military, overhead athletes
Episode	First dislocation (in selected older patients)	Recurrent dislocation ^[1]
Bone loss	Minimal	Significant glenoid bone loss ( > 20–25%) or engaging Hill-Sachs
Associated pathology	Isolated soft tissue Bankart with no bone loss	Bony Bankart, large Hill-Sachs, HAGL, cuff tear (in older patients needing repair)
Instability type	AMBRI (atraumatic, multidirectional) → rehabilitation first	TUBS (traumatic, unilateral) → surgery more often needed ^[1]
Patient preference	Prefers conservative	Unwilling to accept recurrence risk

GC Lecture High Yield – Operative Indications

From the GC lecture, the main indications for surgical stabilisation are: ^[1]

Recurrent anterior dislocation
First-time dislocation in a young ( < 25), active patient (especially contact sports) — evidence increasingly supports early surgical stabilisation to prevent recurrence
Significant glenoid bone loss ( > 20–25%)
Large engaging Hill-Sachs lesion
Failed rehabilitation in atraumatic instability

5. Surgical Management

Aspect	Details
Principle	Reattach the torn anteroinferior labrum back onto the glenoid rim using suture anchors. This restores the labral "bumper" and re-tensions the IGHL, recreating the static anterior restraint. ^[1]^[7]
Technique	Arthroscopic (keyhole) surgery — 2–3 small portals. The labrum is mobilised, the glenoid neck is prepared (abraded to create a bleeding surface for healing), and suture anchors are inserted into the glenoid rim. Sutures are passed through the labrum and tied, pulling the labrum back onto the bone.
Indications	First-time dislocation in young active patients; recurrent anterior dislocation; glenoid bone loss < 20–25%; non-engaging Hill-Sachs ^[1]
Contraindications	Significant glenoid bone loss ( > 20–25%) — the repair will fail because there is insufficient bone to anchor the labrum onto. Engaging Hill-Sachs — the repair alone will not prevent the Hill-Sachs from catching on the glenoid rim. Voluntary instability — poor outcomes.
Outcomes	Recurrence rate 5–15% in appropriately selected patients (vs. 70–90% with non-operative management in young patients).
Rehabilitation post-op	Sling immobilisation 4–6 weeks → progressive ROM → strengthening from 6 weeks → return to contact sports at 4–6 months.

Aspect	Details
Principle	Transfer the coracoid process (with its attached conjoint tendon — short head of biceps + coracobrachialis) to the anteroinferior glenoid rim, where it is fixed with screws. This provides a "triple block" effect. ^[1]
"Triple block" mechanism	1. Bony block: The coracoid bone graft extends the glenoid arc → compensates for the missing bone. 2. Dynamic sling effect: The conjoint tendon crosses anteroinferior to the joint → when the arm is in ABER (the position of dislocation), the conjoint tendon tightens and acts as a dynamic hammock preventing anterior translation. 3. Capsular repair: The capsule is repaired over the top of the graft, further reinforcing the anterior wall.
Indications	Glenoid bone loss > 20–25%; engaging "off-track" Hill-Sachs lesion; failed Bankart repair; contact athletes with recurrent instability ^[1]
Contraindications	Voluntary instability; atraumatic MDI (relative); significant posterior instability (wrong direction to address)
Outcomes	Recurrence rate 0–5% — very low. However, it is a more invasive operation with potential complications (non-union of coracoid, hardware failure, subscapularis dysfunction, axillary nerve injury).
Approach	Open (traditional) or arthroscopic (technically demanding).

Aspect	Details
Name origin	French for "filling" — you are "filling" the Hill-Sachs defect
Principle	The infraspinatus tendon and posterior capsule are sutured (capsulotenodesis) into the Hill-Sachs defect, converting it from an intra-articular defect to an extra-articular one. The defect can no longer engage on the glenoid rim. ^[1]
Indications	Engaging Hill-Sachs lesion, usually combined with a Bankart repair. Used when the Hill-Sachs is "off-track" but glenoid bone loss is not severe enough to warrant a Latarjet.
Limitation	Slight reduction in external rotation (~10°) — the posterior capsule is tethered into the Hill-Sachs.

Aspect	Details
Principle	Same as arthroscopic Bankart repair but performed through an open deltopectoral approach
Indications	Revision surgery after failed arthroscopic repair; complex labral/capsular pathology; surgeon preference
Advantage	Allows direct visualisation and more robust capsular shift; historically lower recurrence than early arthroscopic techniques (though modern arthroscopic outcomes have largely caught up)

Aspect	Details
Principle	Tighten the redundant, patulous capsule by excising a portion or shifting (imbrication) the capsule, reducing its volume. This eliminates the excess capsular "bagginess" that allows multidirectional translation. ^[1]
Indications	Atraumatic multidirectional instability (AMBRI) that has FAILED rehabilitation (minimum 3–6 months of dedicated physiotherapy before considering surgery) ^[1]
Technique	Can be arthroscopic (capsular plication — suture the capsule to itself to reduce volume) or open (T-capsulotomy and shift)

Aspect	Details
Principle	Reattach the torn rotator cuff tendon to its footprint on the greater tuberosity using suture anchors
Indications	Patients > 40 years with first-time dislocation and confirmed rotator cuff tear (MRI or USS) who cannot actively abduct or externally rotate post-reduction ^[1]
Technique	Arthroscopic or mini-open cuff repair
Note	In this age group, the cuff tear is the main pathology, not the labral tear. Recurrence of dislocation is uncommon. Management priority shifts from preventing re-dislocation to restoring cuff function.

Aspect	Details
Indications	Greater tuberosity fracture that remains displaced > 5mm after reduction of the joint ^[1]
Technique	Screw fixation or suture anchor fixation
Rationale	A displaced GT fracture pulls the supraspinatus/infraspinatus insertion away from its anatomical position → impairs cuff function and may block abduction by impinging under the acromion

Scenario	Management Approach
Fracture-dislocation	DO NOT attempt blind closed reduction. Orthopaedic consultation. Often requires open reduction + internal fixation (ORIF) or hemiarthroplasty / reverse total shoulder replacement (if severely comminuted in elderly). ^[1]^[2]
Chronic unreduced dislocation ( > 2–3 weeks)	Closed reduction usually fails due to contracture and fibrosis. Requires open reduction ± reconstruction. In elderly with significant arthritis, may proceed directly to shoulder arthroplasty.
Posterior dislocation with large reverse Hill-Sachs	If reverse Hill-Sachs involves < 25% of the articular surface → closed reduction + immobilisation in external rotation. If 25–40% → McLaughlin procedure (transfer subscapularis into defect) or modified McLaughlin (lesser tuberosity transfer). If > 40% → hemiarthroplasty or reverse shoulder replacement.
Voluntary instability	DO NOT operate. Surgery has very poor outcomes in voluntary dislocators (high failure rate). Management is psychological/behavioural ± rehabilitation. ^[1]
AMBRI (atraumatic, multidirectional)	Rehabilitation first — minimum 3–6 months of focused rotator cuff and scapular stabiliser strengthening. Surgery (inferior capsular shift) only if rehabilitation fails. ^[1]

Patient Profile	First-Line Management	If Fails/Recurs
Young ( < 25), active, first anterior dislocation	Increasingly: early arthroscopic Bankart repair (evidence shows lower recurrence than rehab alone). Alternatively: immobilisation + rehabilitation	If recurrence → definite surgical stabilisation
Age 25–40, first anterior dislocation, moderate activity	Immobilisation + rehabilitation	If recurrence → arthroscopic Bankart repair (± remplissage if engaging Hill-Sachs)
Elderly ( > 40), first anterior dislocation	Assess for rotator cuff tear (MRI/USS). If cuff intact: immobilisation (short duration) + early rehabilitation. If cuff torn: cuff repair.	Recurrence uncommon in this group
Recurrent anterior instability	Surgical stabilisation	Bankart repair (if < 20–25% bone loss) or Latarjet (if > 20–25% bone loss or failed Bankart)
Multidirectional instability	Rehabilitation (3–6 months minimum)	Capsular plication / inferior capsular shift
Posterior dislocation	Closed reduction → immobilisation in external rotation	Surgery if engaging reverse Hill-Sachs (McLaughlin / arthroplasty depending on size)
Inferior dislocation (luxatio erecta)	Urgent closed reduction under sedation/GA → neurovascular assessment → immobilisation	High rate of associated pathology; surgical intervention often needed

High Yield Summary

Management of Shoulder Dislocation — Key Points:

Adequate analgesia/sedation BEFORE reduction — intra-articular lidocaine is an effective alternative to IV sedation. ^[1]
Pre-reduction X-rays are mandatory (unless vascular emergency). Post-reduction X-rays confirm concentric reduction. ^[1]^[2]
Neurovascular documentation before AND after reduction — axillary nerve (regimental badge + deltoid) and distal pulses. ^[1]^[2]^[3]
Closed reduction techniques: Hippocratic (traction-countertraction), Stimson (gravity/dangling arm), External Rotation method, Cunningham. Kocher's method has higher fracture risk — use with caution. ^[1]
Immobilisation: Sling for 1–3 weeks; shorter in elderly (prevent frozen shoulder), longer in young if non-operative.
Rehabilitation: Rotator cuff and scapular stabiliser strengthening is the cornerstone of non-operative management and is essential post-operatively too.
Surgical indications: Recurrent instability; young ( < 25) active patient with first dislocation (increasingly early surgery); significant glenoid bone loss ( > 20–25%); engaging Hill-Sachs; failed rehabilitation in MDI. ^[1]
Arthroscopic Bankart repair: Standard for anterior instability without significant bone loss.
Latarjet procedure: For glenoid bone loss > 20–25% — provides "triple block" (bony block + dynamic sling + capsular repair). ^[1]
Remplissage: "Fills" the Hill-Sachs defect with infraspinatus/posterior capsule → prevents engagement.
Patients > 40: Priority is rotator cuff assessment and repair, not labral repair.
AMBRI → rehabilitation first; TUBS → surgery more likely. ^[1]
Never operate on voluntary dislocators. ^[1]

Active Recall - Management of Shoulder Dislocation

References

Complications of Shoulder Dislocation

Complications of shoulder dislocation can be categorised into acute (occurring at the time of or shortly after the dislocation/reduction) and chronic (developing over weeks to years). Understanding each complication requires tracing it back to the underlying pathoanatomy — every complication has a "why."

1. Acute Complications

1.1 Neurovascular Injury

This is the most common neurological complication of anterior shoulder dislocation (incidence ~5–35%). ^[1]^[2]^[7]

Aspect	Details
Why it happens	The axillary nerve (C5, C6) courses through the quadrilateral space and wraps around the surgical neck of the humerus posteriorly. When the humeral head displaces anteriorly and inferiorly, the nerve is stretched over the displaced head or compressed against the inferior glenoid rim. The nerve has very little slack and cannot accommodate sudden displacement.
Type of injury	Most commonly a neurapraxia (temporary conduction block from stretching, without structural disruption of the nerve fibres). Axonotmesis (structural damage to axons but intact nerve sheath) and neurotmesis (complete disruption) are rare but more serious.
Clinical features	Loss of sensation over the "regimental badge area" (lateral deltoid skin — supplied by the superior lateral cutaneous nerve of the arm, a branch of the axillary nerve). Weakness or paralysis of the deltoid (cannot abduct against resistance) and teres minor (weak external rotation). ^[1]^[2]
Prognosis	Neurapraxia recovers spontaneously in the vast majority of cases, usually within 6–12 weeks (nerve regrowth rate ~1 mm/day once the conduction block resolves). More severe injuries (axonotmesis) may take 3–6 months. Neurotmesis requires surgical exploration/repair.
Assessment	Clinical: test sensation + deltoid power pre- and post-reduction. If persistent deficit at 3–6 weeks → EMG/NCS to characterise the injury. If no recovery by 3–6 months and EMG shows no reinnervation → consider surgical exploration (nerve grafting or neurotisation).

Why Axillary Nerve and Not Other Nerves?

The axillary nerve is the most vulnerable because:

It is tethered at two points — its origin from the posterior cord of the brachial plexus and its passage through the quadrilateral space — so it cannot "slide" away from the displacing humeral head.
It lies in direct contact with the inferior glenohumeral capsule and surgical neck — exactly the structures that are stretched and displaced during dislocation.
Other nerves (musculocutaneous, radial, median, ulnar) are further from the joint and have more excursion (slack) in their course.

Nerve	Incidence	Mechanism	Clinical Features
Suprascapular nerve	Less common but increasingly recognised ^[7]	Traction on the nerve as it passes through the suprascapular notch, or compression by labral cysts (especially with SLAP/labral pathology)	Weakness of supraspinatus (abduction initiation) and infraspinatus (external rotation); wasting in the supraspinous and infraspinous fossae
Musculocutaneous nerve	Rare	Stretching as it passes through coracobrachialis	Weakness of biceps (elbow flexion + supination); loss of sensation over the lateral forearm
Brachial plexus injury (whole or partial)	Rare; more common in high-energy injuries and inferior dislocation (luxatio erecta)	Massive traction on the entire plexus	Multiple nerve territory deficits; may involve any combination of upper limb motor/sensory loss

Aspect	Details
Incidence	Rare (~1–2%) but limb- and life-threatening. More common in elderly patients (atherosclerotic vessels are rigid and inelastic → cannot stretch → tear or rupture). ^[1]^[2]
Why it happens	The axillary artery is relatively fixed as it crosses anterior to the shoulder joint (between the lateral border of the first rib and the inferior border of teres major). In dislocation, the anteriorly displaced humeral head can directly compress, stretch, or tear the artery. In atherosclerotic vessels, even modest stretching causes intimal tear → thrombosis or rupture.
Clinical features	Absent or diminished radial/ulnar pulses; cold, pale, pulseless hand; expanding axillary haematoma; difference in blood pressure between the two arms. If unrecognised → acute limb ischaemia → compartment syndrome → limb loss.
Management	Vascular surgery emergency. CT angiography to delineate the injury. Surgical repair (primary repair, interposition graft, or bypass). Must be managed before or simultaneously with the dislocation reduction — sometimes the reduction itself restores vascular flow by removing the compressive effect of the humeral head.

1.2 Fractures

Aspect	Details
Incidence	15–35% of anterior dislocations
Why it happens	The supraspinatus and infraspinatus tendons insert on the greater tuberosity. During anterior dislocation, these tendons are put under extreme tension → the bone avulses at the tendon-bone junction (the bone is weaker than the tendon in older patients).
Clinical significance	Often reduces anatomically when the joint is reduced (the cuff tendons pull the fragment back). If displaced > 5mm after reduction → ORIF required (the fragment blocks abduction by impinging under the acromion, and cuff function is impaired). ^[1]
Paradoxical benefit	Lower recurrence rate when associated with a GT fracture — the healing response from the fracture and periosteal stripping creates scar tissue that "tightens" the anterior capsule.

Aspect	Details
Incidence	65–70% of first-time anterior dislocations; up to 90% in recurrent dislocations
Why it happens	When the humeral head dislocates anteriorly, the posterolateral aspect of the soft cancellous humeral head impacts against the hard cortical bone of the anteroinferior glenoid rim — like pressing a tennis ball against the edge of a table, creating a dent.
Clinical significance	Small, non-engaging Hill-Sachs lesions are often clinically insignificant. Large, "engaging" lesions are critical — during abduction and external rotation, the defect catches on the anterior glenoid rim like a groove catching on a rail, mechanically driving re-dislocation. The "glenoid track" concept helps determine engagement. ^[1]

Aspect	Details
Why it happens	The humeral head levers over the anteroinferior glenoid rim, chipping off a fragment of bone with the attached labrum
Clinical significance	Loss of glenoid bone reduces the bony arc → the humeral head has less "track" to remain contained → higher recurrence. If > 20–25% glenoid bone loss → Bankart repair alone will fail → Latarjet procedure required ^[1]

2. Chronic Complications

This is the most important and common chronic complication. ^[1]^[7]

Aspect

Details

Why it happens

The Bankart lesion (labral tear) is the "essential lesion." Once the labrum is detached, the glenoid loses ~50% of its effective depth, the IGHL loses its anchor, and the anterior capsule is stretched. Even after the acute dislocation heals, the labrum often heals in a medialised, incompetent position (ALPSA lesion) rather than anatomically on the glenoid rim. Each subsequent dislocation further damages the labrum, stretches the capsule, and enlarges both the Hill-Sachs and any bony Bankart → progressive lowering of the threshold for re-dislocation.

Recurrence rates by age

This is directly from the GC lecture and is HIGH YIELD ^[1]:

GC Lecture – Recurrence Rates (High Yield)

Recurrence rates for anterior shoulder dislocation with non-operative treatment are strongly age-dependent: ^[1]

Age < 20 years: > 80% recurrence (some studies cite up to 90–95%)
Age < 35 years: 55.7% within 2 years, 66.8% at 5-year follow-up (Robinson CM et al., JBJS 2006) ^[1]
Young male patients in competitive and contact sports: 65–95% recurrence ^[1]
Age 40–60 years: ~15–25% recurrence
Age > 60 years: < 10% recurrence

Key message: the younger the patient at first dislocation, the higher the recurrence rate. This is why there is increasing evidence supporting early surgical stabilisation in young active patients rather than a "wait and see" approach. ^[1]

Risk Factors for Recurrence	Mechanism
Young age ( < 25)	More active lifestyle; more elastic tissues that are prone to re-stretching; incomplete labral healing
Contact sports	Repeated exposure to ABER forces that challenge the repaired/healed anterior structures
Significant glenoid bone loss	Reduced bony arc → less "track" for the humeral head to stay contained
Large engaging Hill-Sachs	Defect catches on glenoid rim during functional movements → drives re-dislocation
Hyperlaxity	Inherently lax capsule and ligaments → less resistance to translation even after healing
Non-compliance with rehabilitation	Weak dynamic stabilisers (rotator cuff, scapular muscles) cannot compensate for damaged static stabilisers

Aspect	Details
Incidence	More common in patients > 40 years and those with prolonged immobilisation ^[1]^[7]
Why it happens	The inflammation from the dislocation and associated capsular/labral tear triggers a fibrotic healing response in the joint capsule. If the shoulder is immobilised for too long, the inflamed capsule contracts and forms dense adhesions — the capsular volume shrinks from the normal ~20–30 mL to as little as 5–10 mL. The normally loose, redundant axillary pouch becomes obliterated by fibrosis. The result is global loss of both active and passive ROM — particularly external rotation (the axillary pouch and anterior capsule tighten first).
Prevention	Early mobilisation is the best treatment for post-traumatic shoulder stiffness — this is explicitly stated in the GC lecture ^[1]. Adequate pain relief facilitates early movement. Immobilisation should be kept to the minimum necessary (1–2 weeks in elderly, 2–4 weeks in younger patients).
Risk factors	Diabetes mellitus (the single strongest risk factor — microangiopathy impairs capsular healing), thyroid disease, prolonged immobilisation, age > 40, female sex
Natural history	Classically described as three phases: freezing (painful) → frozen (stiff) → thawing (recovery), over 12–36 months. Many patients do NOT fully recover ROM spontaneously.
Management	Physiotherapy (stretching, ROM exercises); corticosteroid injection (intra-articular); hydrodilatation (distension arthrography — inject saline + steroid to stretch the capsule); arthroscopic capsular release if conservative measures fail at ~3 months ^[1]

GC Lecture – Adhesive Capsulitis Key Points

From the GC lecture ^[1]:

PREVENTION is the best treatment for post-traumatic shoulder stiffness → early mobilisation + adequate pain relief
There is NO CONSENSUS on management of adhesive capsulitis
Arthroscopic capsular release is one option — consider when conservative treatments fail at 3 months
AVOID releasing too much during surgery (risk of iatrogenic instability/dislocation)
Beware surgical complications: dislocation, axillary nerve injury (0.6%), superficial wound infection ^[1]

Aspect	Details
Incidence	Up to 40–80% in patients > 40 years with first-time dislocation ^[1]^[7]
Why it happens	In older patients, the rotator cuff tendons are degenerative — they have undergone years of wear, microtears, and tendinopathic change. The tendons become the "weakest link" in the chain. When the humeral head dislocates, instead of the labrum/capsule tearing (as in young patients), the degenerative cuff tendons give way. The supraspinatus is most commonly affected (it is the most vulnerable due to its position in the subacromial space and its relatively poor blood supply near the "critical zone" — the area ~1 cm from the insertion where the tendon is most avascular).
Clinical features	Inability to actively abduct or externally rotate the arm after reduction (passive ROM is intact — the examiner can move the arm, but the patient cannot). Positive drop arm test (patient cannot hold the arm in abduction when released). Weakness out of proportion to pain.
Significance	In this age group, the cuff tear is more functionally disabling than the instability. Recurrence rates are actually low (the stiffening from the healing process stabilises the joint), but the cuff tear causes significant functional loss if untreated.
Management	MRI or USS to confirm. If significant full-thickness tear → arthroscopic or mini-open rotator cuff repair (reattach tendon to greater tuberosity footprint using suture anchors). If partial thickness or minimal functional deficit → rehabilitation.

Aspect	Details
Why it happens	Residual capsular inflammation, labral damage, articular cartilage injury, and altered shoulder biomechanics all contribute to persistent pain. Hill-Sachs and Bankart lesions create incongruent articular surfaces → abnormal load distribution → cartilage wear. Muscle deconditioning from immobilisation and guarding compounds the problem. ^[7]
Management	Rehabilitation (progressive strengthening, ROM exercises); analgesics; address underlying pathology (e.g., repair Bankart if causing catching/locking symptoms)

Aspect	Details
Incidence	Develops in 10–20% of patients over 10–20 years, higher with recurrent dislocations ^[7]
Why it happens	Each dislocation causes articular cartilage damage — the humeral head impacts on the glenoid rim (creating the Hill-Sachs), and the glenoid cartilage is abraded by the translating head. Recurrent episodes compound this damage. Additionally, an incongruent joint (from bony defects, malreduced fractures, or malaligned labrum) distributes load unevenly → accelerated cartilage wear → secondary OA. This is the same principle as post-traumatic OA in any joint — damage the articular surface, and degenerative change follows.
Clinical features	Progressive pain with activity, morning stiffness (< 30 min, unlike RA), crepitus, reduced ROM, X-ray shows joint space narrowing, osteophytes, subchondral sclerosis, and subchondral cysts (the classic OA features)
Management	Conservative initially (analgesics, physiotherapy, activity modification). If end-stage → shoulder arthroplasty (anatomical total shoulder replacement if cuff is intact; reverse total shoulder replacement if cuff is deficient — the reverse design relies on the deltoid rather than the cuff for function).

Complication	Details
Missed diagnosis	The single most important "complication" of posterior dislocation is failing to diagnose it in the first place — with historical miss rates up to 50%. A missed posterior dislocation becomes a chronic unreduced dislocation → progressive articular cartilage erosion → secondary OA → may ultimately require arthroplasty. ^[1]^[2]
Reverse Hill-Sachs enlargement	If left unreduced, the anteromedial humeral head impaction defect enlarges as the head continues to abrade against the posterior glenoid rim → engaging reverse Hill-Sachs → locked dislocation.
Avascular necrosis (AVN) of humeral head	More common with fracture-dislocations (especially those involving the anatomical neck) — disruption of the blood supply (ascending branch of the anterior circumflex humeral artery) → humeral head necrosis → collapse → end-stage arthropathy.

Complication	Surgery	Mechanism
Recurrence after Bankart repair	Arthroscopic Bankart	5–15% recurrence; higher if inadequate number of anchors, subcritical bone loss that was underestimated, or non-compliance with rehabilitation
Subscapularis dysfunction	Latarjet (requires subscapularis split)	The coracoid graft is passed through a split in the subscapularis → if the tendon heals poorly or is over-stretched, anterior dynamic stability is compromised
Coracoid non-union / hardware failure	Latarjet	The transferred coracoid may not unite with the glenoid, or the screws may loosen/break → loss of the bony block effect
Axillary nerve injury	Any shoulder surgery (especially open approaches, capsular release)	The nerve is at risk during inferior dissection. Reported incidence ~0.6% for arthroscopic capsular release ^[1]
Over-tightening (loss of ROM)	Bankart repair, capsular shift	If the capsule is over-tensioned or too many anchors are placed, external rotation is restricted → functional deficit; may also contribute to secondary arthritis from abnormal joint mechanics
Infection	Any surgical procedure	Superficial wound infection; rarely deep joint infection (septic arthritis)
Dislocation after capsular release	Arthroscopic capsular release for adhesive capsulitis	If too much capsule is released, the joint becomes unstable → iatrogenic dislocation. This is why the GC lecture warns to "avoid releasing too much" ^[1]

Complication	Acute / Chronic	Key Pathophysiology	Most Affected Group
Axillary nerve injury	Acute	Nerve stretched over displaced humeral head	All ages, highest in inferior dislocation ^[7]
Axillary artery injury	Acute	Inelastic vessel torn by displacing head	Elderly (atherosclerotic)
Greater tuberosity fracture	Acute	Cuff tendon avulsion	All ages
Hill-Sachs lesion	Acute	Head impacts on glenoid rim	All ages; larger with recurrence
Bankart lesion (bony Bankart)	Acute	Head levers over glenoid rim	All ages
Rotator cuff tear	Acute	Degenerative tendon tears during dislocation	Age > 40 ^[1]^[7]
Recurrent instability	Chronic	Incompetent labrum + stretched capsule	Age < 25, contact sports ^[1]
Adhesive capsulitis	Chronic	Capsular fibrosis from inflammation + immobilisation	Age > 40, DM, prolonged immobilisation ^[1]^[7]
Chronic pain / stiffness	Chronic	Residual structural damage + deconditioning	All ages ^[7]
Secondary OA (dislocation arthropathy)	Chronic	Articular cartilage damage from repeated dislocation	Recurrent dislocators ^[7]
Missed posterior dislocation	Acute → Chronic	Failure to recognise on AP X-ray	Post-seizure, post-electrocution ^[1]^[2]

High Yield Summary

Complications of Shoulder Dislocation — Key Exam Points:

Axillary nerve injury is the most common neurological complication (~5–35%). Most are neurapraxia → recover within 6–12 weeks. Always test regimental badge sensation + deltoid power before AND after reduction. ^[1]^[2]
Axillary artery injury is rare but life-threatening; more common in elderly with atherosclerosis. Absent pulses → vascular surgery emergency.
Recurrence is the most important chronic complication and is strongly age-dependent: < 20 years: > 80%; < 35 years: ~67% at 5 years. Young males in contact sports: 65–95%. ^[1]
Rotator cuff tear is the dominant pathology in patients > 40 (up to 40–80%); recurrence risk is low but functional loss from the cuff tear is significant. ^[1]^[7]
Adhesive capsulitis — prevention is the best treatment → early mobilisation + adequate pain relief. Risk factors: DM, age > 40, prolonged immobilisation. ^[1]
Secondary OA develops over years from cumulative articular cartilage damage; worse with recurrent dislocations.
Hill-Sachs (65–70% of first-time) and Bankart lesion (97% of traumatic anterior) are the key structural complications driving recurrence. ^[1]
Missed posterior dislocation — the most commonly missed diagnosis in shoulder trauma. Always get axillary/Y-view. ^[1]^[2]
Greater tuberosity fracture paradoxically reduces recurrence rate (healing response tightens anterior structures).
Surgical complications: recurrence after Bankart repair (5–15%), subscapularis dysfunction after Latarjet, axillary nerve injury (~0.6% in capsular release), over-tightening → ROM loss. ^[1]

Active Recall - Complications of Shoulder Dislocation

References

High Yield Summary

Key Takeaways for Shoulder Dislocation (Definition → Clinical Features):

The shoulder is the most commonly dislocated joint due to the large humeral head vs. small, shallow glenoid ("golf ball on a tee"). ^[1]^[2]
Anterior dislocation = 95% of cases; mechanism = ABER (Abduction, External Rotation); pathology = Bankart lesion + Hill-Sachs.
Posterior dislocation = seizures/electrocution → classically MISSED on AP X-ray ("lightbulb sign"). Always get axillary/Y-view. ^[1]^[2]
Young patient → labral tear (Bankart) → high recurrence. Old patient → rotator cuff tear → low recurrence but poor function. ^[1]
ALWAYS check axillary nerve (regimental badge area sensation + deltoid power) and distal pulses before AND after reduction.
TUBS = Traumatic, Unilateral, Bankart, Surgery. AMBRI = Atraumatic, Multidirectional, Bilateral, Rehabilitation, Inferior capsular shift.
Bankart lesion is the "essential lesion" of anterior traumatic instability. ^[1]^[2]
Hill-Sachs lesion = posterolateral humeral head impaction (anterior dislocation); Reverse Hill-Sachs = anteromedial impaction (posterior dislocation).
Associated greater tuberosity fracture paradoxically reduces the recurrence rate.
Inferior dislocation (luxatio erecta) → arm locked above head, highest neurovascular injury risk.

High Yield Summary

Differential Diagnosis of Shoulder Dislocation — Key Points:

Always consider fracture and fracture-dislocation before attempting reduction — review X-rays (minimum 2 views: AP + axillary/Y-view) first. ^[1]^[2]
Posterior dislocation is the most commonly missed — classic triad: seizure/electrocution + internal rotation contracture + "lightbulb sign" on AP X-ray. ^[1]^[2]
Rotator cuff tear mimics dislocation in older patients (cannot lift arm) — distinguish by passive ROM being preserved and deltoid contour being normal.
Frozen shoulder mimics chronic unreduced dislocation — but onset is insidious, bilateral sometimes, and associated with diabetes. ^[1]^[7]
AC joint injury is localised superiorly (over the AC joint) — glenohumeral joint is intact.
Cervical radiculopathy can present as shoulder pain — always check for neck symptoms, dermatomal pattern, and Spurling's test. ^[8]
Septic arthritis is an emergency — if the joint is hot, swollen, and the patient is febrile, aspirate first.
TUBS vs. AMBRI differentiates traumatic unidirectional instability (surgical) from atraumatic multidirectional instability (rehabilitation first). ^[1]
Don't forget non-musculoskeletal referral: cardiac ischaemia (left shoulder), diaphragmatic irritation (shoulder tip — Kehr's sign), Pancoast tumour.

High Yield Summary

Diagnostic Criteria, Algorithm, and Investigations — Key Points:

Diagnosis = Clinical + Radiographic. There are no formal "diagnostic criteria" — the diagnosis is confirmed when X-ray shows complete displacement of the humeral head from the glenoid. ^[1]^[2]
Minimum imaging: AP + Axillary lateral (or Scapular Y-view). A single AP view is NEVER sufficient — posterior dislocations will be missed. ^[1]^[2]
Pre-reduction imaging is mandatory to identify fracture-dislocations. Post-reduction imaging is mandatory to confirm reduction.
Posterior dislocation X-ray signs: lightbulb sign, rim sign (> 6mm gap), loss of half-moon overlap, vacant glenoid sign. ^[1]^[2]
Neurovascular documentation before AND after reduction is non-negotiable (axillary nerve sensation at regimental badge, deltoid power, distal pulses). ^[1]^[2]^[3]
CT: For fracture-dislocations, glenoid bone loss quantification (> 20–25% → Latarjet), Hill-Sachs engagement (glenoid track), and surgical planning.
MRI/MRA: Gold standard for soft tissue — labral tears (young patients), rotator cuff tears (> 40 years), HAGL, ALPSA, SLAP lesions. MRA (with intra-articular gadolinium) is superior for labral pathology.
USS: Quick bedside rotator cuff assessment in patients > 40 post-reduction.
EMG/NCS: Only if persistent nerve deficit at 3–6 weeks (not acutely — denervation changes take time to develop).

High Yield Summary

Management of Shoulder Dislocation — Key Points:

Adequate analgesia/sedation BEFORE reduction — intra-articular lidocaine is an effective alternative to IV sedation. ^[1]
Pre-reduction X-rays are mandatory (unless vascular emergency). Post-reduction X-rays confirm concentric reduction. ^[1]^[2]
Neurovascular documentation before AND after reduction — axillary nerve (regimental badge + deltoid) and distal pulses. ^[1]^[2]^[3]
Closed reduction techniques: Hippocratic (traction-countertraction), Stimson (gravity/dangling arm), External Rotation method, Cunningham. Kocher's method has higher fracture risk — use with caution. ^[1]
Immobilisation: Sling for 1–3 weeks; shorter in elderly (prevent frozen shoulder), longer in young if non-operative.
Rehabilitation: Rotator cuff and scapular stabiliser strengthening is the cornerstone of non-operative management and is essential post-operatively too.
Surgical indications: Recurrent instability; young ( < 25) active patient with first dislocation (increasingly early surgery); significant glenoid bone loss ( > 20–25%); engaging Hill-Sachs; failed rehabilitation in MDI. ^[1]
Arthroscopic Bankart repair: Standard for anterior instability without significant bone loss.
Latarjet procedure: For glenoid bone loss > 20–25% — provides "triple block" (bony block + dynamic sling + capsular repair). ^[1]
Remplissage: "Fills" the Hill-Sachs defect with infraspinatus/posterior capsule → prevents engagement.
Patients > 40: Priority is rotator cuff assessment and repair, not labral repair.
AMBRI → rehabilitation first; TUBS → surgery more likely. ^[1]
Never operate on voluntary dislocators. ^[1]

High Yield Summary

Complications of Shoulder Dislocation — Key Exam Points:

Axillary nerve injury is the most common neurological complication (~5–35%). Most are neurapraxia → recover within 6–12 weeks. Always test regimental badge sensation + deltoid power before AND after reduction. ^[1]^[2]
Axillary artery injury is rare but life-threatening; more common in elderly with atherosclerosis. Absent pulses → vascular surgery emergency.
Recurrence is the most important chronic complication and is strongly age-dependent: < 20 years: > 80%; < 35 years: ~67% at 5 years. Young males in contact sports: 65–95%. ^[1]
Rotator cuff tear is the dominant pathology in patients > 40 (up to 40–80%); recurrence risk is low but functional loss from the cuff tear is significant. ^[1]^[7]
Adhesive capsulitis — prevention is the best treatment → early mobilisation + adequate pain relief. Risk factors: DM, age > 40, prolonged immobilisation. ^[1]
Secondary OA develops over years from cumulative articular cartilage damage; worse with recurrent dislocations.
Hill-Sachs (65–70% of first-time) and Bankart lesion (97% of traumatic anterior) are the key structural complications driving recurrence. ^[1]
Missed posterior dislocation — the most commonly missed diagnosis in shoulder trauma. Always get axillary/Y-view. ^[1]^[2]
Greater tuberosity fracture paradoxically reduces recurrence rate (healing response tightens anterior structures).
Surgical complications: recurrence after Bankart repair (5–15%), subscapularis dysfunction after Latarjet, axillary nerve injury (~0.6% in capsular release), over-tightening → ROM loss. ^[1]

Shoulder Dislocation

1. Definition

2. Epidemiology and Risk Factors

2.1 Epidemiology

2.2 Risk Factors

3. Anatomy and Function of the Glenohumeral Joint

3.1 Bony Anatomy

3.2 Glenoid Labrum

3.3 Capsuloligamentous Structures (Static Stabilisers)

3.4 Rotator Cuff (Dynamic Stabilisers)

3.5 Other Stabilisers

3.6 Neurovascular Structures at Risk

4. Etiology and Pathophysiology

4.1 Mechanism of Injury

4.1.1 Anterior Dislocation (~95%)

4.1.2 Posterior Dislocation (~2–4%)

4.1.3 Inferior Dislocation (Luxatio Erecta) (< 1%)

4.1.4 Superior Dislocation (Extremely Rare)

4.2 Pathological Lesions in Shoulder Dislocation

4.3 Atraumatic Instability

5. Classification

5.1 By Direction of Dislocation

5.2 By Etiology

5.3 By Timing

5.4 By Degree

5.5 Stanmore Classification (Triangle of Instability)

6. Clinical Features

6.1 Symptoms

6.2 Signs

6.2.1 Acute Anterior Dislocation

6.2.2 Acute Posterior Dislocation — The "Missed" Dislocation

6.2.3 Inferior Dislocation (Luxatio Erecta)

6.2.4 Signs of Recurrent Instability (Chronic/Subacute Setting)

6.3 Associated Injuries — A Structured Approach

7. Summary of Clinical Approach (Pre-DDx, Pre-Ix, Pre-Mx)

Active Recall - Shoulder Dislocation (Definition to Clinical Features)

References

1. The Clinical Problem: What Are You Actually Differentiating?

2. Differential Diagnosis — Organised by Category

2.1 Conditions That Mimic Acute Shoulder Dislocation

2.2 Referred Pain and Non-Musculoskeletal Mimics

2.3 Differentiating the Direction of Dislocation

2.4 Differentiating Traumatic vs. Atraumatic Instability

2.5 Important Specific Differentials to Not Miss

Septic Arthritis of the Glenohumeral Joint

Pathological Fracture (Metastatic Disease / Myeloma)

Neurovascular Injury Mimicking or Complicating Dislocation

3. A Clinical Approach to Differentiating Shoulder Dislocation from Mimics

4. Summary Table: Key Differentials at a Glance

Active Recall - Differential Diagnosis of Shoulder Dislocation

1. Diagnostic Criteria — The Clinical-Radiological Diagnosis

1.1 The Clinical Diagnosis

1.2 The Radiographic Diagnosis (Definitive)

2. Diagnostic Algorithm

3. Investigation Modalities — Detailed Analysis

3.1 Plain Radiography (X-ray) — First-Line, Mandatory

3.1.1 Standard Views

3.1.2 Additional / Special X-ray Views

3.1.3 Key Radiographic Findings to Identify on X-ray

3.2 Computed Tomography (CT) — For Fracture-Dislocations and Surgical Planning

3.3 Magnetic Resonance Imaging (MRI) — Gold Standard for Soft Tissue Assessment

3.3.1 Standard MRI vs. MR Arthrogram

3.3.2 Key MRI Findings

3.4 Ultrasound (USS) — Bedside Assessment of Rotator Cuff

3.5 Other Investigations

3.5.1 Neurovascular Assessment (Clinical, Not Imaging)

3.5.2 CT Angiography (CTA)

3.5.3 Electromyography / Nerve Conduction Studies (EMG/NCS)

3.5.4 Blood Tests

4. Post-Reduction Imaging — Confirming Success

5. Summary: Investigation Hierarchy

Active Recall - Diagnosis and Investigations of Shoulder Dislocation

1. Management Algorithm — Overview

2. Acute Management — The First Hour

2.1 Initial Assessment (ABCDE)

2.2 Analgesia

2.3 Neurovascular Documentation — Pre-Reduction

3. Closed Reduction Techniques

3.1 Techniques for Anterior Dislocation

Hippocratic Method (Traction-Countertraction)