Week 8 Lecture Flashcards
Describe the mechanisms by which the glenohumeral joint maintains stability
Involves passive restraints and dynamic stabilisers
Key source of stability=concavity-compression mechanism. A stabilising mechanism in which compression of the convex humeral head into the concaved glenoid stabilises and protects it against translating forces. Its directly related to depth of concavity and magnitude of compressive force.
GHJ depth = glenoid depth + labrum
Depth is greater superior inferiorly and most shallow A-P
There is negative atmospheric pressure within the joint, the greater the depth of the labrum the greater the negative atmospheric pressure t/f greater resistance to translation.
Static stabilisers GHJ motion passively controlled by tightening of GHJ ligs and capsule at EROM Geometry of the GHJ Glenoid labrum
Dynamic stabilisers
Rotator cuff; ideally positioned biomechanically to provide a compressive force throughout the entire ROM of the GHJ.
Scapular stabilising muscles; provide a mobile yet stable BOS for GHJ functi
• Describe the functional anatomy of the glenoid labrum
A torn labrum> decreased neg atmospheric pressure, decreased concavity t/f decreased stability
Torn labrum > break in circle > channeling effect of laxity as compared to opposite side
Leads to SLAP tears, Traumatic dislocations, Atraumatic laxity
GHJ depth = glenoid depth + labrum
Depth is greater superior inferiorly and most shallow A-P
There is negative atmospheric pressure within the joint, the greater the depth of the labrum the greater the negative atmospheric pressure t/f greater resistance to translation.
• Describe the functional anatomy of glenohumeral joint ligaments.
Focal thickenings of the GHJ capsule, can be divided into 4 parts.
-Tendon of longhead of biceps,
-SGHL,Superior glenohumeral ligment
-MGHL,Middle glenohumeral ligament
-IGHL,Inferior glenohumeral ligament:
Anterior band of IGHL,auxillary pouch of IGHLC, Posterior band of IGH
*Coracohumeral ligament (CHL)
posterior band IGHL
-most important restraint to posterior subluxation
at 90° flexion and IR
-tightness leads to internal impingement and increased shear forces on superior labrum (linked to SLAP lesions)
anterior band IGHL
-primary restraint to anterior/inferior translation
90° abduction and maximum ER(late cocking phase of throwing)
-anchors into anterior labrum
forms weak link that predisposes to Bankart lesions
superior band IGHL
most important static stabilizer about the joint
100% increased strain on superior band of IGHL in presence of a SLAP lesion
*-Inferior glenohumeral ligament is like a hammock
Bands reciprocally tighen as the head is rotated in the abducted postion
Stability further enhanced by tightening ligaments increasing joint compression
External rotation winds it up so it acts like a sling
• Describe the functional anatomy of the rotator cuff
Mid-range stability(45/60-120 ) of GHJ is provided by Rotator cuff which provide a muscular compressive force which results in the concavity compression mechanism.
ER
– infraspinatus ER HOH and imparts posterior roll,
additionally holds posterior capsule relatively taut. Creates additional tensioning of passsive stability system
-Passive tension on otherside of joint by subscapularis and anterior capsular ligament when stretched during ER.
If the RC becomes damaged or weakened, the HOH may migrate upwards and forwards with a resultant increased risk of impingement of subacromial structures. (Deltoid may act unopposed)
Rotator cuff has an anti-impingement function. Deltoid pulls the humerus outward and upward towards the acromion.
Balanced action of the RC opposes this and keeps the humeral head centred, preventing upward dislocation. RC also generates ER needed to prevent impingement of the GT against the glenoid.
Describe the 2 kinds of force couples at the shoulder
GHJ force couples
Coronal force couple:
Deltoid and Supraspinatus vs Inferior cuff
Trasverse force couple:
Anterior(Subscap) vs Posterior cuff(Infraspinatus, Teres minor
* critical for providing superior-inferior stability. SA impingement often develops secondary to compromise of the transverse force couple.
Supraspinatus becomes the “victim” not the culprit.
• Describe normal scapulohumeral rhythm
Scapulohumeral rhythm
120 GHJ: 60 Scap 2:1 ratio
Initial phase (Setting phase)
30 GHJ Abduction(20-80)
Scapula mostly stable (0-30 degrees)
Midphase/critical phase 2:1
60 GHJ abduction
30 scap upwards rotation
GHJ externally rotates to clear GT from acromion and depress humeral head
Final phase 3:5:1
60 GHJ abduction
30 scap upwards rotation
Slight extension and lateral flexion of thorax to assist elevation
• Describe possible extrinsic causes of shoulder pain
Cervical spine referral (c5/6) Thoracic spine referral(upper) Heart(angina)L Liver via diaphragm R Cholecystitis (gall bladder) R Spleen L Apical lung tumours Vascular compromise( thoracic outlet syndrome)
• Discuss the difficulties associated with diagnosis in shoulder pain disorders
Diagnosis requires identification of the specific Patho anatomical source of symptoms& related pathology.
Shoulder PE tests not good at identifying structural pathology and structural pathology as seen in imaging is common in those with no pain.
Lack of specificity of common shoulder tests coz:
Morphology of RC means tendons don’t function as separate entities anatomically or functionally. Fuse to form common insertional aponeurosis t/f cant test 1 tendon in isolation.
Position and innervation of subacrominal bursa
Richly innervated and anatomically blends with GHJ capsule and RC insertions. Any test of interity and pain response from any RC tendons would inherently involve bursal tissue. No test can distinguish between them
Weakness on testing- pain inhibition vs structural failures.
Injection studies suggest weakness detected during testing may be better explained by pain inhibition rather than structural pathology.
*2/3 of RC tears are asymptomatic in general population
FTT common & commonly asymptomatic in general population
• Discuss primary and secondary sub-acromial impingement of the shoulder
PRIMARY subacromial impingement:
( true structural narrowing) Impingement leading to impingement of structures in SA space caused by outlet stenosis in Sub acromial space in a stable shoulder.
Due to Encroachment from above: Sub acromial spur/osteophytes, thickened calcified coracoacromial ligament, Acromiocalvicuar joint arthropathy/spur formation, mal-union of acromial or greater tuberosity fracture
SECONDARY subacromial impingement:
(functional narrowing
Pinching/mechanical compression of any structures between HOH ( greater tuberosisty) and acrominon/CAL as a concequency of functional narrowing. An impairment of musculoskeletal function.
Explain classification of Impingement
INTERNAL
- PSI(posterior superior)*more common
- ASI(Anterior superior)
EXTERNAL
- Subacromial (Primary or Secondary) *most common
- Subcoracoid(Primary or Secondary)
Structures potentially impinged in subacromial space:
Suacromial bursa
Superior glenohumeral capsule and superior glenohumeral ligment
Rotatorcuff tendons and most superior fibres of infraspinatus
Long head of biceps tendon
Signs of Subacromial impingement
Pain with overhead activities / activities involiving loaded shoulder IR rotation with shoulder elevation g tennis serve, swimming, throwing.
Painful arc during active shoulder elevation. Point in range where mechanical impingement of sensitised SA structures is occurring. Usually (45/60- 130 abduction) Pain commonly absent or eases in early and late ROM.May be painfull at EOR again
Pain usually worse in abduction compared to flexion
In middle range humerus needs to clear acromioclavicular space, scap needs to upwardly rotate at this point, if it cant they may get functional narrowing. @ end range scap does most of the work. If it cant glenohumeral joint may jam up to try and get more range.
Pain with loading RC ( empty can test, full can test) due to failure of RC to keep HH centred.
Othopaedic specific tests for impingement may reproduce pain: Hawkins kennedy test, Relocation test.
Common pathomechanics associated with secondary SA impingement
- Suboptimal/impaired RC function/GHJ impairment
- GHJ instability or hyperlaxity
- GHJ hypomobility
- Sub optimal scapula kinematics/MC
- Suboptimal spinal postures
- Combination of the above
• Discuss briefly glenoid (internal) impingement of the shoulder
Can be post or posterior-superior impingement(PSI)
Anterio-superior impingement(ASI) less common
PSI
Pinching/mechanical compression of articular(deeper most) fibres of subscapularis and infraspinatus & posterior labrum between greater tuberosity and posterior superior glenoid rim as consequence of FUNTIONAL NARROWING.
(during abd/ER)eg throwing motion,late cocking phase.
>Posterior shoulder pain
ASI
Impingement of under surface subscapularis and biceps pulley against anterosuperior glenoid rim in positions of horizontal adduction and IR in flexion.
Damage to pulley can lead to LHB instability
- biceps pulley is soft tissue sling that encloses LHB to stabilise it at at entrance to bicipital groove
• Discuss briefly sub-coracoid impingement of the shoulder
Structures potentially impinges
Primary or secondary narrowing of space between coracoid process and humerus and lesser tuberosity.
Structures potentially impinged:
-Subscapularis tendon
-LH biceps tendon
-Middle Glenohumeral ligament and capsule.
• Describe the pathology of
Sub-acromial pain syndrome (SAPS)
Chicken or the egg
What are the 3 limiations to the acromial irritational model
Sub-acromial pain syndrome (SAPS)
Associated with symptoms of subacromial impingement
Limitations to the acromial irritational model
1. Most AC pathology is of the deeper structures(articular side) Deeper fibres are relatively weaker and fail earlier than larger acromial side fibres. Intrinsic tendon degeneration without direct mechanical irritation.
- Acromial shape has a poor relationship to pathology and symptoms(Flat, curved, hooked)
- Subacromial spur (osteophyte) may not be primary may be secondary to chronic strain or tension in coracoacromial ligament increasing bone stress @ the acromial insertion > spur formation( seconday ossification of CAL)
Strain/ tension in CAL due to:
-Failure of RC to stop HH superior translation during elevation
-Increased tendon volumes (reactive tendonopathy)
-Increased bursal volume associated with SA bursitis
t/f type 3 acromion may not be morphological variation but a result of increased strain on CAL as a result of a degenerative process.
THEEEN failure to control superior HH migration and eventual spur formation result in irritation of bursal tissue and bursal side of RC patholgoy
Can be one or the other first
-Subacromial pathology then impingement
Injury to RC leads to superior migration of HH t/f impingement signs
-Or subacromial impingement leading to SA injury
Pathomechanics mean functional narrowing of subacromial space then subacromial strucures become sensitised and secondary SA pathology occurs
*Rotator cuff pathology is more likely due to intrinsic tendon degeneration or failure than extrinsic acromial mechanical compression.
Rotator cuff pathology & injury including long head of biceps
• Tendinopathy
(early reactive – disrepair -degenerative)
reveiw this
• Partial / full thickness tears
Clinical presentation:
>60 yrs
Night pain
Abduction weakness
ER weakness
Positive impingement signs
Presence of all above = 98% chance of RC tear
MRI or US, can have large asymptomatic tears
In young trauma> dislocation more likely than RC tear
If older than 40> RC tears associated with traumatic GHJ dislocation + gt tuberosity #
LHB pathology
Frequently associated with other shoulder pathology. (SAPS & RC)
Same spectrum of pathology as RC
SAPS Clinical presentation
Anterolateral shoulder pain
SA structures may refer to deltoid tuberosity
Can refer more distally, C5,6 distribution
Hx variable gradual onset, overuse, traumatic
Pain with movement/loading with OH activities(worse in positions of IR
Signs of SA impingement usually present
Risk factors for RC tears
Risk factors: increasing age Smoking ( tear size and surgical outcomes) Hypercholesterolemia Familiar predisposition Limited healing ability
• Calcific tendinopathy
Pathology
Most likely patient group
Symptoms
Management
Calcium deposits chemically irritates tendon> inflamm resonse > edema> increased intratendon pressure> pain
Cause unknown
May be associated with tendon degenerative process, usually subscap just distal to tendon insertion.
Most common > 30 yrs female, diabetic
Bilateral
Asymptomatic
Site of deposit not strongly associated with pain severity
Management Conservative NSAID’s, deposits usually reabsorbed. Acutely painful at this stage Address impairments secondary to pain and altered function: GHJ mobility RC function
Needle lavage if non responsive to above> aspirate
Surgical removal , bursectomy, acromioplasty
Define joint laxity and joint instability
- Joint laxity – Degree of translation which falls within physiological range & is asymptomatic = not pathological
- Joint instability – Abnormal symptomatic motion – Shoulder instability: “symptomatic abnormal motion of the HH relative to the glenoid during active shoulder motion”
Glenohumeral instability
3 main ways to classify Glenohumeral instability
Thomas and Matsen classification system
Stanmore Classification of GHJ Instability: “Polar” Groups
Classification
Aetiology- traumatic vs atraumatic
Directional-ant, inf, posterior, multi‐directional (MDI)
Severity-subluxation vs dislocation
Position(s) of symptom provocation eg:
– Anterior instab: HBH, abd+ER
– Inferior instab: carrying object
– Posterior instab: pushing something out front
-MDI( multidirectional instability) Instability in at least 2 directions – True MDI should have both anterior & posterior instability with inferior component
Thomas & Matsen Classification over simplification of a complex issue…
T.U.B.S Traumatic Unidirectional/ Unilateral Bankart Surgery to fix
A.M.B.R.I.I Atraumatic/Acquired Multidirectional Bilateral Rehab (1st)– Restore optimum NM control Inferior capsular shift/tightening* Interval (RC) closure/recon* *Surgery only if conservative measures fail
Stanmore Classification of GHJ Instability: “Polar” Groups Concept
Type I: traumatic / structural (=TUBS)
Type II: atraumatic /structural (microtrauma)
Type III: m/s patterning disorders / non-structural (=AMBRII) (ie NM control STJ/GHJ)
Continuum b/w 3 groups with some pts falling b/w groups (iesub-groups)
*Direction of instab NOT as impt to effective Mx as whether instab is structural, non‐structural or both
- Usually atraumatic or repetitive micro‐ traumatic – In sports requiring large GHJ ROM eg swimming
- May be associated with generalised ligament laxity
- Often bilateral & more common in young
Symptoms of shoulder instability required for diagnosis
• Diagnosis:
Symptoms of instability are required:
– Feelings of looseness, slipping, shoulder going out/falling out,
- apprehension, ‘dead arm’,
- lack of power,
- ‘sense of displacement’ (subluxation, dislocation)
+/‐ pain
Traumatic GHJ dislocation
Anterior
Posterior dislocation
% of dislocations
MOI
Key stabilising structures damaged
Types of injuries
Anterior Dislocation
– >90% of dislocations
– MOI: forced abd + ER
Key stabilising structures damaged:
– Capsulo‐ligamentous structures ‐ IGHLC especially
– Tearof Antero‐inf glenoid labrum = Bankart Lesion
– Bony injury:
•BonyBankartLesion/# = #of Antero‐inferior glenoid margin
•Hill‐Sachs Lesion= Compression # posterior(lateral) HH
Impaction of humerus against anterior rim of glenoid
+/‐ tearing of posterior or superior labrum
– Axillary nerve injury – reduced sens lat shoulder & deltoid weakness
– RC damage possible
• More common if > 40 yo
Posterior Dislocation
– <5% of dislocations
– MOI: • >90 flex + add +/ IR eg FOOSH in some IR/add
• Reverse Hill‐Sachs Lesion
Compression fracture antero‐medial HH
• Reverse Bankart Lesion
Postero‐inferior glenoid rim – fracture or labral Lesion
• Bennett Lesion
Calcification of posterior band of inferior GH ligament at postero‐ inferior glenoid secondary to traction / avulsion injury
• RC damage
Instability
Common S/E Features
• AGE
– Atraumatic instability (Polar Type II & III) <25 yo
– Traumatic instability (Polar Type I) any age!
– MDI more common in young
• Symptoms
– Related to instability +/‐ pain
– Typically direction/position specific if uni‐directional
instability
– associated mechanical symptoms (clicking,
catching, clunking) particularly if associated labral
Pathology
History
– Traumatic (note MOI & degree of trauma) OR
– Atraumatic/micro‐traumatic
• Gradual onset of symptoms
• Sports involving repetitive motions at extremes of range eg swimming, throwing
– Symptoms commonly chronic or recurrent
– Recurrent subluxation / dislocation common following 1st traumatic dislocation (especially if young)
P/E findings for Non‐acute Stage
Glenohumeral joint instability
• Generally normal (sometimes excessive) active & passive physiological & accessory motion into the direction of symptom provocation
– May have less firm EF (later in range)
– May have loss of motion in non‐provocative direction
(eg tight posteriorly in presence of anterior instability)
• RC weakness &/or loss of endurance
• Signs of secondary impingement
• Laxity tests: Anterior & Posterior Drawer, Inferior Drawer
– Not diagnostic of instability unless associated with relevant symptom response
• +’ve instability tests: Apprehension‐relocation Test for anterior instability
Positive test is a reduction in apprehension +/- an increase in ER ROM upon addition of AP glide
• Secondary RC injury (tendinopathy) over time – pain on loading RC, signs of impingement
• Impairments of static & dynamic scapula & GHJ Motor control
– Must link to disorder
– Related to Polar Type III in particular
– Examples:
Inadequate upward rotation & posterior tilt of scapula during over head activity / movt
Excessive anterior & superior HH translation during active movt or loading of GHJ
SLAP lesion
Define
Pathology
Cause
SLAP lesions
(Tear of superior labrum anterior & posterior)
In a SLAP injury, the top (superior) part of the labrum is injured. This top area is also where the biceps tendon attaches to the labrum. A SLAP tear occurs both in front (anterior) and back (posterior) of this attachment point. The biceps tendon can be involved in the injury, as well
Injuries to the superior labrum can be caused by acute trauma or by repetitive shoulder motion
May be associated with labral Non-SLAP lesions
Slap lesion:
Repetitive microtrauma
Tractioning & stripping of labrum @ LHB origin
-Throwing: biceps helps decelerate arm at end of cocking phase
-Carrying
-Sudden drop & catch of heavy object
Long head biceps pathology
Pathology
Frequently associated with other shoulder pathology
Esp SAPS & RC pathology(LHB sits in SA space
Same spectrum of pathology as RC
Tendinopathy contiuum:reactive tendinopathy to degenerate tendon to tendon tear/ rupture
Traumatic or atraumatic
Clinical features
Variable-depends if associated with other pathology
Often symptoms difficullt to distinguish from associated pathology especially RC
Associated SLAP lesion(mechanical symptoms if labral pathology
Anterior shoulder pain ( bicipital groove)
More common in older individuals
Trauma may be trivial - underlying tendon degeneration
Immediate sharp pain/tearing sensation
Bunching of muscle in distal upper arm > popeye sign (better observed on active contraction
Often little ongoing pain/ Fx defecit with biceps strength generally maintained
Surgery generally not required unless involved in power sports
Frozen shoulder contracture syndrome
Nomenclature
Epidemiology/patient population
Commonly known as “adhesive capsulitis”
However: not correct name
– Evidence for capsular adhesions limited
– Adhesions of capsule to humeral head do NOT occur
– Uncertainty regarding inflammatory changes
Epidemiology
• Typically reported as F > M no strong evidence in literature
• Onset commonly 40 – 60 years of age (Peak onset 52 (females) & 55 (males) )
• More common in diabetic population
• Association with thyroid disorders & heart disease uncertain
• Family history or genetic predisposition?
– Most commonly idiopathic onset • ?autoimmune association
– Secondary to trauma or surgery e.g. fracture, RC repair
• May become bilateral
– In sequence or simultaneously
Frozen shoulder contracture syndrome
Pathoaetiology
• Reported abnormalities include:
– Thickening & fibrosis of the RC interval
– Obliteration & scaring of sub‐scapular recess (space b/w biceps & subscapularis)
– Neovascularity
– Increased cytokine concentrations
– Contracture of the inferior & anterior capsule
– Reduced joint volume
– Contracture & fibrosis of coraco‐humeral lig
– Proliferation of fibroblasts & myofibroblasts
– Presence of contractile proteins
– Uncertainty regarding inflammatory changes
Diagnosis of Frozen shoulder Contracture syndrome
Symptoms
• Early diagnosis difficult
– Presents similar to other shoulder disorders eg SAPS, OA, serious pathology (eg HH AVN, osteosarcoma)
• No definitive gold standard test
• Dx based on clinical exam, exclusion of other pathologies & normal GHJ radiographs
ultrasound( neovascularity of the RC interval has been identified in individuals with symptomatic FSCS)
• Clues for early identification – Night pain – Pain at rest – Painful to lie on affected shoulder – Pain easily aggravated by movt – Pain with quick movts – Age over 35 – Progressive & global loss of AROM/PROM (especially ER) with EOR pain (capsular pattern….)
Recall: Capsular Pattern of Restriction
A proportional limitation of passive movt of a joint
Each joint has a characteristic pattern of motion impairment
Capsular patterns appear when capsule is globally contracted
Shoulder CP: ER >abduction
Natural history
Recovery can be prolonged 2‐3 years – Av time 30.1 months (range 12‐42 months)
• Full pain free ROM may not be restored in everyone ‐ ongoing pain &/or stiffness common 50% of people with FSCS experienced pain &/or stiffness at an average of 7 years post onset – Usually mild
Define rotator interval
(RC interval: bound medially by subscapularis tendon & laterally by SS tendon; contains a cross sectional view of biceps tendon. Coraco-humeral ligament located in lateral aspect of RC interval above capsule)
GHJ Capsular Restriction & Scapula Mechanics
for frozen shoulder
GHJ Capsular Restriction & Scapula Mechanics
– Loss of capsular mobility results in compensatory /
adaptive dysfunctional scapula movt to maximise functonal shoulder elevation
• ie excessive scapula elevation & upward rotation
• Do NOT classify as “motor control” disorder!
– Any attempt to “correct” this will result in decreased range, increased pain & decreased fx
– As GHJ mobility Increases, scapula movt usually “normalises”
•In some cases, mal‐adaptive impairments of scapula control may persist & require intervention
FSCS Clinical Pattern Sheridan & Hannafin 2006
What are the stages of Frozen shoulder contracture syndrome
– Stage I (Inflammatory): pain & synovitis
• Diffuse hypervascular synovitis
– Stage II (Freezing): pain & synovitis with progressive stiffening
• Hypertrophic/hypervascular synovitis, capsular fibroplasia, scar formation, loss of capsular volume
– Stage III (Frozen): contracture & fibrosis of capsule
• Fibrosis of capsule, profound loss of capsular volume
– Stage IV (Thawing/Recovery): progressive improvements in ROM
Clinically, FSCS better divided into 2 stages
Stage 1 ‐ more pain than stiff (Stage I & II)
Stage II ‐ more stiff than pain (Stage III & IV
The Stiff Shoulder –
Global capsular restriction
Regional capsular restriction
GLOBAL Capsular Restriction
Presents similar to frozen shoulder but joint restriction 2 to another pathology or cause
Eg post # NOH, post RC repair, post‐immobilisation, post‐trauma
Usually no sig inflammatory phase – does NOT go through same “stages” as frozen shoulder
Restriction develops secondary to a lack of joint motion
Pain ‐> reduced movt Capsular pattern of restriction (as for frozen shoulder)
Prognosis better than frozen shoulder – quicker recovery++
REGIONAL Capsular Restriction
• NOT a capsular pattern of movt restriction
• Secondary to:
– Chronic RC MC impairment – failure to control HH centring
– Capsular reaction 2 to RC pathology (recall: RC blends with capsulo‐ligamentous structures)
– Tendency for antero‐superior translation of HH
• Commonly posterior shoulder tightness
– Structures blend therefore likely capsulo‐ ligamentous & m/s (IS, teres minor) components
• Quick improvements in mobility with STW!
• SGHL / CHL contracture (rotator interval)
o Glenohumeral joint OA
Typical patients
Symptoms
Radiology changes
• Typically older patients (> 70 years) – History of trauma or physical work++
• Deep, diffuse ache rather than sharp, localised pain
– Pain develops insidiously & is slowly progressive
– May have night pain & pain at rest
– Pain worse with movt & activity
• Progressive restriction of global GHJ mobility
– Can present similar to frozen shoulder
– Crepitus or grinding with movt
Radiology not sensitive to early degenerative change
• Radiographs demonstrate typical OA changes (later stages):
– Joint space narrowing
– Marginal osteophytes
– Sclerosis
– Later stages show glenoid erosions
• Usually involve posterior glenoid & can cause posterior displacement of HH
o Acromioclavicular joint pathology / injury
Traumatic (sprains and dislocations)
MOI
What structures provide stability to the ACJ
Describe the grading system of ACJ sprain/dislocation
Gr I - VI
Treatment for each grade
Traumatic: ACJ Sprain / Dislocations
• MOI: fall on point of shoulder or FOOSH
Injury to ACJ capsule & ligaments Injury graded I‐VI
Stability of ACJ provided by:
- coracoclavicular (CC) ligaments (conoid & trapezoid),
- acromioclavicular (AC) ligaments
- Joint capsule
Gr I =ACJ capsular sprain
Gr II =complete tear AC ligs with sprain of CC ligs
Gr III & V =complete tear CC ligs with marked displacement
– Gr V > displacement than Gr III
– Gr V more ST damage (m/s, skin, fascia, sometimes skin)
Gr IV=a/a with posterior clavicle displacement
Gr VI=a/a with inferior clavicle displacement into SA or SC space
Treatment
• Gr I‐III usually treated non‐operatively
• Gr IV‐VI (& III that fails to respond to conservative Rx) usually managed surgically
- immob in sling for pain relief (Gr I: 2‐3 days, Gr II or III: up to 6/52)
- Taping – support joint / minimise separation
- Graduated exercise program ‐ mobility & strength
- Monitor & address development of mal‐adaptive scapula mechanics
Symptoms of acromioclavicular joint pathology
Sprains/dislocations
Localised pain over ACJ
(Gr I & II more painful than Gr III)
- TOP over ACJ – ACJ palpation (high sensitivity) may be a valuable screen when negative
- Pain on movt especially horizontal adduction
- Gr II, III & V associated with palpable / visible step deformity (Superior subluxation of distal clavicle)
*Chronic or Atraumatic ACJ Pain
Cause
Atraumatic/degenerative
• May follow Gr II+ injuries • Typically a consequence of ACJ OA – Post‐trauma ‐> secondary OA – Primary OA – Spurs can develop on undersurface of ACJ • Contribute to primary SA impingement (abrasion from above)
• Discuss the indications for and the limitations of radiological imaging in shoulder pain disorders
True AP GHJ ( with neutral rotation)
– AP with internal rotation (Hill Sachs lesion)
– AP with external rotation (fracture or degeneration of greater tuberosity, reverse Hill Sachs lesion)
• Y or lateral view
• Axillary view
