Causes of px arising from shoulder:
• Rotator cuff disorder |
• Frozen shoulder |
• Instability disorder |
• AC joint disorder |
• GH joint osteoarthritis |
• Inflammatory arthritis |
• Septic arthritis |
Causes of px which arise from elsewhere:
• Malignancy |
• Referred pain from the neck, heart, or lungs |
• Polymyalgia rheumatica |
Red flags on Hx or examination:
• Trauma, pain & weakness, or sudden loss of ability to actively raise the arm (with or without trauma): suspect acute rotator cuff tear |
• Any shoulder mass or swelling: suspect malignancy |
• Red skin, painful joint, fever, or the person is systemically unwell: suspect septic arthritis |
• Trauma leading to loss of rotation & abnormal shape: possible shoulder dislocation |
• New Ssx of inflammation in several joint: suspect inflammatory arthritis |
Further investigations:
• Blood tests: if malignancy, poly myalgia rheumatica, or inflammatory arthritis are suspected |
• Testing for diabetes considered if pt with frozen shoulder |
• X-rays: if Hx of trauma; little improvement with conservative care; Ssx last more than 4 weeks; severe pain or restriction of movement; arthritis suspected |
Treatments:
• Initial management: explanation & education on diagnosis; analgesia if appropriate; MSK treatment |
• Corticosteroid injections may be considered, depending on the suspected cause & Ssx severity |
• If orthopaedic referral is indicated (suspected septic arthritis / dislocation), should not be delayed |
• Referral to 2° care considered if pain & function are not improving following conservative treatment for 3 months |
• Earlier referral considered if: pain is having significant impact on ADLs; recurrent shoulder instability; severe post-traumatic pain |
Adhesive capsulitis
• GREEN or YELLOW |
- Condition gradually develops |
• Intro: |
- Also known as Frozen shoulder
- Inflammatory condition causing stiffness & px in the shoulder joint
- Dx emphasises the gradual development of global limitation of shoulder motion
- Significant radiographic findings may not be present
- Assessing passive ROM crucial for Dx |
• Aetiology (risk factors): |
- Prevalence 2-5% in general pop
- Common in people starting 55yrs
- F>M (1.4:1)
- Non-dominant hand often affected
- Associated w/ autoimmune comorbidities: thyroid disorders, DM (poorer treatment outcomes)
Form classification:
- 1°: idiopathic, gradual onset, associated w/ other conditions (e.g. DM, thyroid disease, drugs, hypertriglyceridemia, or Cx spondylosis)
- 2°: result of shoulder trauma (e.g. rotator cuff tears, #, surgery, or prolonged immobilisation) |
• Pathophysiology: |
- Not fully understood
- Leading hypothesis: inflammation begins in joint capsule & synovial fluid
- Subsequent reactive fibrosis & adhesions in synovial lining
- Initial inflammation causes px
- Fibrosis & adhesions limit ROM |
• Clinical presentation: |
- Gradual onset of shoulder px
- Worsens over weeks - months
- Followed w/ significant limitation in shoulder ROM |
• Physical examination: |
- Reduced AROM & PROM
- Specifically affected movements: EXT rotation → ABD → INT rotation → forward FX
- Severe cases may loose natural arm swing during walking & muscular dystrophy
- TTP around the joint
- Distal neurology MUST remain intact
- RROM elicits px & marked limitation, resembling rotator cuff tear
- Apley scratch test: measure INT rotation
- +ve special tests: Need, Hawkins, & Speed's (indicating impingement or biceps tendinopathy) |
• Diagnosis: |
- Dx based mainly on clinical & physical findings
- X-rays considered for alternative Dx or underlying pathology
- Injection test can help differentiate adhesive capsulitis from other shoulder pathologies
- MRI may reveal characteristic findings: rotator interval synovitis, coracohumeral lig hypertrophy, loss of subcoracoid fat triangle, & thickening of the GH capsule (they're not specific) |
• Staging: |
3 clinical phases:
- Phase 1: painful phase is characterised by diffuse & disabling shoulder px, initially worse at night, along w/ increasing stiffness, can last 2-9 months
- Phase 2: frozen or adhesive phase involves a progressive limitation in ROM in all shoulder planes, the intensity of px gradually diminishes during this phase, typically lasts from 4-12 months
- Phase 3: thawing or regression phase is marked by gradual return of the ROM, recovery of ROM may take 12-24 months for complete restoration |
• Complications: |
- Residual shoulder px &/or stiffness
- Humeral fracture
- Rupture of the biceps & subscapularis tendons
- Labral tears
- GH dislocation
- Rotator cuff tear |
• Management: |
- SMT & STW
- IASTM/TFM
- Spencer technique
- NSAIDs
- Corticosteroids / steroid injections
- Arthroscopic capsular release
- Exercises phase 1: Codman pendulum, Cane - FX & ABD, Cross body stretch, Shoulder INT rotation - towel, EXT rotation doorway stretch
- Exercises phase 2: Side lying horizontal ABD, resisted shoulder EXT prone, Resisted shoulder FX
Indication for surgery:
- Pt fails a trial of steroids or NSAIDs
- No response to GH or SC injections
- No response respond to PT
Contraindications for surgery:
- Pt has had an inadequate course of steroids or NSAIDs
- Pt has not had any attempt at conservative therapy
- Acute infection
- Pt has a concomitant malignancy in the shoulder
- Pt has a neurological deficit or nerve complaint originating from the Cx spine |
• Ddx: |
- Cx radiculopathy
- AC arthrosis
- Bicep tendinopathy
- GH arthritis
- Fracture
- Calcifying tendinitis/synovitis
- Malignancy
- Polymyalgia rheumatica
- Shoulder impingement s. |
AC joint injury
• GREEN to RED |
- Sprain degree to torn degree |
• Intro: |
- Common among athletes & adolescents
- Around 40% of all shoulder injuries
- Mild injuries usually don't cause significant morbidity
- Severe injuries can result in substantial strength loss & function of shoulder
- AC injuries may be linked to clavicular #
- They can lead to impingement s.
- Neurovascular insults are a rare complication associated w/ AC injuries |
• Aetiology (risk factors): |
- Commonly occur after sporting events, car accidents, & falls
- Make up about 40% of all shoulder injuries
- Up to 10% of all injuries in collision sports (e.g. football, lacrosse, & ice hockey)
- AC joint: lateral process of clavicle meets the acromion process projecting off the scapula
- Stabilised by AC lig (anterior, posterior, superior, & inferior portion), where superior portion crucial for stability
- Mild injuries don't cause significant issues, but severe can lead to substantial strength & function loss
- Linked to clavicular #, impingement s., & occasionally neurovascular problems |
• Pathophysiology: |
- Most common: direct trauma to lateral aspect of the shoulder or acromion process w/ the arm in ADD
- Falling on an outstretched hand or elbow may also lead to AC separation |
• Clinical presentation: |
- Antero-superior shoulder px
Mechanism of injury:
- Blunt trauma to ABD shoulder
- Landing on outstretched arm
Px description:
- Radiating to neck or shoulder
- Aggravated by movement
- Worse when sleeping on affected shoulder |
• Physical examination: |
- Swelling, bruising, or deformity of AC
- TTP
- Restricted A&PROM due to px
- "Piano key sign": palpation of the distal clavicle demonstrates a feeling of "giving way"
- Cross-body ADD test
- BvR test
- Paxino's test
- AC differential test |
• Diagnosis: |
- X-rays are 1° for Dx
- US & MRI may be considered if Dx remains uncertain |
• Staging: |
Rockwood classification (gold standard):
I: AC ligament sprain; CC ligament intact; no radiographic abnormalities
II: AC ligament is torn; CC ligament sprain; clavicle has elevated but is not superior to the border of the acromion, or exhibits a less than 25% increase in the CC interspace compared to the contralateral
III: AC & CC ligaments are torn; clavicle has elevated above the border of the acromion, or there is an increase of 25-100% in the CC interspace compared to the contralateral
IV: AC & CC ligaments are torn; posterior displacement of the distal clavicle into the trapezius
V: AC & CC ligaments are torn; superior displacement of the distal clavicle by more than 100% in the CC interspace compared to the contralateral
VI: AC & CC ligaments are torn; inferolateral displacement in a subacromial or subcoracoid displacement behind the coracobrachialis or biceps tendon |
• Complications: |
- Residual joint px (30-50% of pts)
- AC arthritis (more common in surgical management)
- Following fixation: hardware irritation, infection, adhesive capsulitis, coracoid, & clavicular #
- Hook plate: acromion irritation, subacromial impingement, & osteolysis |
• Management: |
- Generally favourable prognosis
- Functional motion regain by 6 weeks & return to normal activity by 12 weeks
- Non-operative grade 1, 2 & 3; 3 operative if athlete / > displacement
- Acute (within 6 weeks): stabilisation & reduction of Ssx
- STW
- SMT (not shoulder)
- IASTM / TFM
- Exercises phase 1: scapular clocks & protraction / retraction
- Exercises phase 2: resisted shoulder EXT rotation, cane - FX, low row |
• Ddx: |
- AC distal clavicle osteolysis
- AC arthritis
- Acromion #
- Adhesive capsulitis
- Anterior humerus subluxation
- Complex pain s.
- Erb-Duchenne injury
- Glenoid labrum tear
- Os acromiale
- Rotator cuff injury
- Superior tabral tear
- Septic arthritis
- Shoulder dislocation |
AC osteoarthritis
• GREEN |
• Intro: |
- Common (spec. in 40 & older) & causes anterior / superior shoulder px
- Px exacerbated during overhead & cross-body activities
- 1° affects middle-aged pts due to degeneration of the fibrocartilaginous disc
- Many pts are asymptomatic, w/ findings often discovered incidentally on shoulder x-ray / MRI |
• Aetiology (risk factors): |
- Less common than knee / hip OA, but more common than GH OA
- Approx 54-57% of elderly pts exhibit x-ray evidence of degenerative changes in AC, though clinically relevant AC OA is less common
- Approx 20% of all shoulder px
- Common in 40 & older pts
Types of AC arthritis:
- 1° OA: articular degeneration w/o an apparent underlying cause, often occurring due to constant stress from repeated overhead lifting activities
- 2° OA: resulting from associated causes such as post-trauma (prevalent) or underlying disease (e.g. RA)
- Arthritic Ssx have been observed in Grade I & II sprains of the AC |
• Pathophysiology: |
- AC is a synovial joint connecting the axial skeleton & scapula
- Limited ROM characterises the AC
- Articular connection involves the distal clavicle's convex surface & the acromial facet's slight convex surface
- Fibrocartilage disc exists between the hyaline cartilage covered facets (akin to knee meniscus)
- Degenerative changes are part of the natural process
- In early adulthood, the fibrocartilage disc undergoes degeneration, leaving behind fibrous remnants |
• Clinical presentation: |
- Hx of trauma, e.g. direct impact on the joint or a FOOSH injury
- Occupational Hx, e.g. occupation that requires repeated overhead lifting activities
- Participation in sports that stress / injure AC, e.g. weightlifting, rugby
- Complaints of px at night during sleeping on affected shoulder
- Pt may experience popping, clicking, grinding, or catching sensation w/ movement of the shoulder
- Functional limitations ACJ px include difficulty w/ resisted-training activities that place the GH in an extended position, common in weightlifters AKA Weightlifter's Shoulder
- Damage to AC can be synchronous w/ damage to the supraspinatus tendon & osteophytes from the arthritic AC joint may contribute to subacromial impingement exacerbating & producing further shoulder px |
• Physical examination: |
- Pts typically maintain intact ROM, EXCEPT for specific movements: cross-body ADD, behind the back (scratch back), & overhead reaching, which exacerbate px - Localised superior shoulder px is common - TTP, possible accompanied w/ swelling due to distal clavicle osteolysis - Px can be induced in deltoid area through certain movements: forward FX to 90° w/ horizontal ADD (Cross-body test) or straight-ahead pushing (e.g. bench press) - Most sensitive tests: TTP over Acromioclavicular point & Paxino's test, & AC resisted EXT test |
• Diagnosis: |
- Dx relies on Hx, physical exam, imaging (x-ray, MRI), & diagnostic local anaesthetic injection
Imaging:
- Plain film & Dx local anaesthetic local injections are essential Dx tools
- X-ray & MRI provide comprehensive imaging of AC joint pathology
- US is effective in detecting signs of AC OA & is commonly used for imaging
- US-guided injections: +ve if Ssx reduction; -ve if persistent px post-injection suggesting alt shoulder pathologies (commonly rotator cuff injury) |
• Management: |
- Activity modification (avoid repetitive & overhead movements), NSAIDs, PT modalities, corticosteroid & local anaesthetic injections
- Surgery
Physical therapy:
- Px management using electro-modalities, SMT/STW
- Maintaining active ROM & strengthening scapular stabiliser muscles
- Rotator cuff strengthening exercises
- Postural correction - pec muscle stretching & retractors strengthening |
• Ddx: |
- Calcific tendonitis
- GH arthritis
- Adhesive capsulitis
- Rotator cuff impingement s. |
Tendinopathies*
"Tendinopathy is an umbrella term to decribe the tendon px, w/ an unknown cause" |
"Tendinitis describes a tendon in which inflammatory processes are present. However, studies show that tendons are rather in a degenerative state than in an inflammatory state." |
"Tendinosis describes the degenerative state of tendons & therefore, this term is more applicable"
• Eccentric exercises major role in treatment
- Promote cross-linking of collagen fibres
- Promote tendon remodelling
• Tendinosis can be described on a continuum |
Calcific tendonitis
• GREEN |
• Intro: |
- Self-limiting disorder, identified by calcium deposits in rotator cuff tendons (esp. infra & supraspinatus)
- Common & painful condition, that decreases ROM
- Visible signs of calcium deposits overlying rotator cuff insertion on shoulder x-rays |
• Aetiology (risk factors): |
- Up to 20% of pts are asymptomatic
- 40-60% of shoulder pts
- 30-60yrs
- F>M
Localisation:
- Supraspinatus tendon (80%): critical zone (most common)
- Infraspinatus tendon (15%): lower 1/3
- Subscapularis tendon (5%): pre-insertional fibres |
• Pathophysiology: |
- Unclear
Hypothesis include:
- Repetitive trauma of tendon → tendon degeneration → calcification
- Tendon necrosis → intracellular calcium accumulation
- Active process mediated by chondrocytes arising from metaplasia → calcium deposition
- Phagocytosis of metaplastic areas reforms normal tendon |
• Clinical presentation: |
- Night px, causing loss of sleep
- Constant dull ache
- Px increases considerably w/ AROM
- Decrease in ROM, or complaint of stiffness
- Radiating px up into suboccipital region, or down into the fingers |
• Physical examination: |
Cluster (+ve):
- Neer's test
- Hawkins-Kennedy test
- Drop arm test
- Jobe's test |
• Staging: |
Chronic (silent) phase: presence of the calcific deposit is asymptomatic & may be so for years
Acute painful phase: severe px, disability, & frequently nocturnal discomfort
Mechanical phase: tendon impingement being a prominent finding; px of less severe nature than the acute phase |
• Diagnosis: |
- Diagnosed through x-rays |
• Complications: |
- Adhesive capsulitis
- Rotator cuff tear
- Ossifying tendinitis |
• Management: |
- NSAIDs, PT, stretching & strengthening, steroid injections
- ESWT (most useful in refractory calcific tendonitis in the formative & resting phase)
- US-guided needle lavage
- Surgery (surgical decompression of calcium deposit)
Physical therapy:
- Mobs / drops
- ROM exercises to avoid articular stiffness
- Strength exercises to restore normal mechanics
- Commonly scapular dyskinesia needs to be treated at the same time |
• Ddx: |
- Incidental calcification: found in 2.5-20% of 'normal' healthy shoulders
- Degenerative calcification: found tendons w/ tear Hx; generally smaller; slightly older individuals
- Loose bodies: associated chondral defect; associated 2° OA |
GH dislocation
• RED |
• Intro: |
- Separation of the humerus from glenoid of scapula at the GH joint
- 50% of all joint dislocations
- Anterior dislocation most common
- Shoulder is an unstable joint due to a shallow glenoid that only articulates w/ a small part of humeral head |
• Aetiology (risk factors): |
- Directions: anterior, posterior, inferior, or anterior-superior
- Risk factors: Hx of shoulder dislocation, RC tear, Hx of glenoid fracture
- M>F
- Younger individuals, likely due to higher activity levels, more prone to redislocation
- Dislocation occurs due to a strong force or extreme rotation, e.g. blow to the shoulder or trauma from contact sports, motor vehicle accidents, or falls
- Fibrous tissue connecting the shoulder bones can be stretched or torn during dislocation, complicating injury |
• Pathophysiology: |
Anterior dislocation:- Up to 97% of shoulder dislocations - Mechanism: typically a blow + ABD + EXT rot + EXT - Exam findings: ABD + EXT rot arm, prominent acromion - Associated injuries: nerve damage, labrum tears, glenoid fossa or humeral head fractures (up to 40%) Posterior dislocation:- 2-4% of shoulder dislocations - Mechanism: hit to the anterior shoulder, axial loading of ADD + INT rot arm - Exam findings: arm held in ADD + INT rot, inability to EXT rot - Higher risk of associated injuries: surgical neck or tuberosity #, reverse Hill-Sachs lesions, labrum or rotator cuff injuries Inferior dislocation (laxation erecta):- Least common type (less than 1%) - Mechanism: hyperABD or axial loading on the ABD arm - Exam findings: arm held above & behind the head, inability to ADD the arm - Often associated w/: nerve injury, rotator cuff injury, tears in the internal capsule, highest incidence of axillary nerve & artery injury among shoulder injuries |
• Clinical presentation: |
- Pts may report: popping sensation, sudden onset of px w/ decreased ROM, sensation of joint rolling out of the socket
- Ask about PREVIOUS dislocations
- Nerves can get stretched out during shoulder dislocation, some pts may report stinging & numbness in the arm at the time of dislocation |
• Physical examination: |
- ROM diminished & painfull
- Anterior dislocation: arm ABD & EXT rot; in thin pts potentially prominent funeral head felt anteriorly, & void can be seen posteriorly
- Posterior dislocation: easy to miss (pt appears to only guard the extremity) because arm is in INT rot & ADD; in thin pts potentially prominent head can be palpated posteriorly
- Neurovascular exam (IMPORTANT): axillary nerve injury (40%)
- Special tests: apprehension test (anterior & posterior), sulcus sign (inferior instability), load & shift test (anterior & posterior), anterior & posterior drawer test |
• Diagnosis: |
- Assess for axillary nerve injury: innervates deltoid & teres minor, & sensation to lateral shoulder - Fractures of tuberosity & surgical neck may occur - Bankart lesion: disruption of glenoid labrum, w/ or w/o avulsed bone fragment - Hill-Sachs deformity: compression # of postern-lateral humeral head 1° w/ anterior dislocations - Reverse Hill-Sachs deformity: impaction # of antero-medial aspect of humeral head in posterior dislocations |
• Management: |
|
• Ddx: |
- AC injury
- Bicipital tendonitis
- Clavicle fracture
- RC injury
- Shoulder dislocation
- Swimmer's shoulder |
GH instability*
• YELLOW |
• Intro: |
- Includes dislocation & subluxation events
- Approx 1-2% of general population experience GH dislocation in their lifetime
- Shoulder instability events are common among young, active, athletic population
- Anterior shoulder instability accounts for over 95% |
• Aetiology (risk factors): |
Classification criteria:
- Uni- or multidirectional instability
- Traumatic or atraumatic
- Presence or absence of accompanying soft-tissue hyperlaxity
- M>F
- Rugby & football have particularly high incidence rates
- Anterior labral tears & Hill-Sachs lesions are frequently observed |
• Pathophysiology: |
GH anatomy:
- Complex, mobile, multiracial ball-and-socket articulation
- Allows motion in frontal, transverse, & sagittal planes
- Glenoid fossa articulates w/ humeral head, allowing 360° circumduction
- Movements at 4 distinct joints: SC, AC, GH, & scapuloTx
Stabilisers:
- Static: GH articulation, labrum, ligaments, RC interval structures, intra-articular pressure
- Dynamic: RC muscles, deltoid, scapular & periscapular stabilisers
Shoulder instability cascade:
- Excessive translation of humeral head on glenoid leads to px, weakness, dysfunction
- Anatomic risk factors identified
- Differentiation between joint laxity & instability crucial
Unidirectional instability:
- May result from acute trauma or low-energy instability events
- Soft tissue hyperlaxity may accompany
- Hill-Sachs lesion on humeral side common
- Glenoid bone loss prevalent, detected via CT scans
- Blunted osseous defects due to acute or chronic/recurrent processes
Multidirectional instability:
- Definition not precise; involves instability in multiple directions
- Often accompanied by capsulolabral injuries
- Soft tissue hyperlaxity associated w/ generalised hyperlaxity
Long-term implications:
- Altered biomechanics due to glenoid bone loss
- Scapular dyskinesia common, predisposing to instability
- Recurrent instability possible post non-operative/operative management
- Dislocation arthropathy: degenerative changes following instability events, possibly leading to GH arthritis |
• Clinical presentation: |
1st time dislocations:
- Recent high-energy trauma or collision is often reported as the cause
- Ask about: degree of trauma, sports activities & positions, discernment between true dislocation & subluxation, & the need for manual reduction
Chronic cases:
- Pts often present after ROM limitations impact daily activities significantly
- Detailed Hx of inciting instability events should be gathered
- Initial injury may be overlooked, leading to chronic instability/recurrence
- Heightened clinical suspicion is warranted in cases of seizures, polytrauma, or low-energy, recurrent subluxation |
• Physical examination: |
Cx exam:
- Rule out Cx radiculopathy in neck or shoulder pathology
- Evaluate neck posturing, muscular symmetry, palpable tenderness, & ROM
- Conduct Spurling manoeuvre, myelopathies testing, reflex testing, & neurovascular exam
Shoulder exam:
- Compare B shoulder girdles for asymmetry, muscle bulk, or atrophic changes
- Check for anterior fullness in chronic anterior instability
- Assess scapulothoracic motion & scapular winging
- AROM & PROM, noting limitation in complex instability cases
- Assess axillary nerve function, supraspinatus muscle, & sensory examination
Provocative tests:
- Assess global tissue laxity, GH translation, & hypermobility
- Anterior apprehension test: reproduce Ssx of anterior instability
- Jobe relocation test: alleviate Ssx
- Load & shift test: assess humeral head translation (Grade 1, 2, or 3)
Other exam considerations:
- Check for posterior & multidirectional instability
- Expect associated shoulder pathologies based on age (e.g. RC injuries in older pts)
- Note weakness or px of specific shoulder injuries (e.g. RC tears or Bankart lesions) |
• Diagnosis: |
- X-rays for comprehensive evaluation
- MRI & CT for advanced imaging |
• Complications: |
- Redislocation following surgical fixation
- Nerve injuries (esp. axillary n.)
- Infection (surgery)
- Implant-related problems |
• Prognosis: |
- Depends on various factors - Instability severity index score (ISIS) to guide shoulder instability management - Risk factors for recurrence: age, gender, joint hyperlaxity, sport participation level/type, Hx of instability, & osseous lesions (10-point scoring of ISIS) 5-year overall success rates:- 94% w/ 1-2 risk factors (ISIS score ≤ 3) - 85% w/ ISIS score of 4-6 - 55% w/ ISIS score >6 |
• Management: |
- Rehab program aim: enhance scapular stability; correct postural or functional deficits; increase RC function; improve proprioception - Closed-chain exercises help stability w/o increasing shear force - Phase 1 (rehab): decrease px, regain ROM, improve functional coordination - Phase 2 (exercises): improve strength, coordination, proprioception - Derby shoulder instability programme for recurrent posterior instability: stepwise exercise progression - Scapular stability exercises focus on improving retraction & EXT rotation - RC deficits, especially subscapularis, are crucial to address - Forward shoulder posture may benefit from SMT in EXT rotation - Controllable functional instability usually managed conservatively; non-controllable cases may need surgical repair - Six-month conservative care trial appropriate before surgical intervention for non-traumatic posterior instability |
• Ddx: |
- Labral defect
- SLAP lesion
- Bankart lesion
- Hill-Sachs lesion
- Fracture
- Inflammatory arthropathy
- Shoulder impingement
- RC tendinopathy
- Biceps tendinopathy
- Suprascapular n. entrapment
- Quadrilateral space s.
- Cx spine referral
- Radiculopathy |
GH internal rotation deficit (GIRD)
• GREEN |
• Intro: |
- Commonly results from repetitive over-head throwing
- Results in loss of IR
- Functional deficit, not a specific injury |
• Aetiology (risk factors): |
- Throwing motion ABD + ER + EXT w/ high velocities
- High amount of stress on static & dynamic stabilisers of shoulder
- Throwers often have a component of pathologic laxity or micro-instability (deposition for injuries) |
• Pathophysiology: |
- Chronic tensile loading of posterior capsule leads to micro-tears & scarring
- Resultant tissue changes contribute to loss of INT GH rotation
- Limitation contributes to various shoulder, elbow, & wrist conditions
- Sequellae inc: scapular dyskinesia, anterior shoulder impingement, RC s., & labral lesions
- Limited shoulder ROM can also result from these conditions |
• Clinical presentation: |
- Vague posterior shoulder px
- Need for prolonged warm-up due to shoulder stiffness
- Loss of throwing velocity, described as dead arm
- Ssx exacerbated in the late cocking phase of throwing, typically localised to the posterior shoulder
- Rare radiation of discomfort extending into the arm |
• Physical examination: |
- Increased EXT rotation & decreased INT rotation - NOT related to MSK injuries or px in overhead throwing athletes
- TrPs: infraspinatus & teres minor
GIRD Dx criteria:
- At least 20* deficit of IR in dominant arm (compared B)
- TTP in posterior shoulder musculature |
• Management: |
- Target improving shoulder ROM (early focus), reduce muscle stiffness, & increase flexibility
- Stretching targets tightness in posterior capsule & INT rotators - pecs, biceps, subscapularis, infraspinatus, teres minor, & levator
- Crossbody stretching may be beneficial
- After pain-free ROM, follow w/ incremental strengthening of GH & scapular stabilisers
- TrPs like infraspinatus & teres minor (EXT rotators)
- SMT - IR & inferior glide
- Rest from throwing & physical therapy for 6 months |
• Ddx: |
- Shoulder Impingement s.
- RC s.
- Biceps tendinopathy
- Labral lesion |
Glenolabral articular disruption (GLAD)*
• YELLOW or RED |
• Intro: |
- Soft tissue shoulder injury subtype
- Involves a tear to anterior-inferior labrum & adjacent glenoid articular cartilage damage
- Uncommon but established post-trauma cause of shoulder px
- Associated w/ stable GH joint; full ROM w/o apprehension or subluxation
- GLAD lesions seen in isolated or recurrent dislocations, challenging clinical Dx
- Imaging required for confirmation |
• Aetiology (risk factors): |
- Rare condition
- Est. 1.5-2.9% of cases of traumatic labral tears
- Younger M, consistent w/ general traumatic labral pathology
- Result from shoulder joint trauma, often involving forced ADD from a position of ABD + EXT rot, e.g. FOOSH
- Injury mechanism also inv. forceful ADD from throwing
- Anterior GH instability is a common injury mechanism associated w/ GLAD |
• Pathophysiology: |
- Affects the labrum & underlying glenoid cartilage in the GH joint
- GH: synovial ball & socket joint formed by the humeral head & glenoid fossa of the scapula
- Labrum function: adds depth to fossa & attachment point for long head of biceps tendon & GH ligaments
- Anterior labroligamentous complex: anterior-inferior GH ligament & labrum
- Function: prevents anterior dislocation & maintaining shoulder stability
- Injury mechanism: forceful ADD of the humeral head against the glenoid fossa, potentially accompanied by shear force, resulting in tears to the labrum & varying degrees of cartilage damage
- Despite the damage, the anterior labroligamentous complex often remains intact → shoulder joint remains stable in GLAD lesions
- Association between GLAD lesions & anterior shoulder instability |
• Clinical presentation: |
- Younger male, w/ clear onset of px after the event
- Potentially anteriorly, possibly diffusely
- Pt may localise px to deep-seated anterior joint
- Clear Hx of FOOSH, mechanism ADD force onto an ABD + EXT rot shoulder |
• Physical examination: |
|
• Diagnosis: |
- Imaging, especially MRA, crucial for Dx
- Challenging to detect on non-contrast MRI or CTA
- Findings: superficial tear to the anterior-inferior labrum w/ an underlying glenoid cartilage defect (from superficial to trans-chondral)
- MRA demonstrates contrast tracking the labral tear & filling into the chondral defect or under a damaged articular flap |
• Complications: |
- Linked to episodes of anterior shoulder instability
- Higher failure rates in arthroscopic Bankart repair w/ GLAD lesions
- Correlation between GLAD lesions & reduced GH stability
- GLAD lesions as biomechanical risk factor in shoulder instability by reducing joint concavity depth
- Risk of OA following GLAD injury (hypothesis) |
• Management: |
- Conservative: time, NSAIDs, & PT (especially for older pts)
- Incidental findings on imaging may complicate Dx in older pts due to common age-related cartilage & labral degeneration
- Treatment approach depends on the size & nature of the chondral defect & labral injury |
• Ddx: |
- Common traumatic labral tears, tearing of the labrum & associated ligaments partially or completely off the glenoid, most commonly the anterior-inferior labrum (Bankart lesions)
- Anterior-inferior instability lesions that include a glenoid rim # - bony Bankart lesions
- Perthes lesion: labral complex injury, but the labrum is still attached to the glenoid via a periosteal sleeve
- Anterior ligamentous periosteal sleeve avulsion: another labral injury, but it displaces medially on the glenoid neck
- (HAGL) or Bony HAGL: this time, the anterior-inferior GH ligament is avulsed from the humeral rather than labral attachment |
Polymyalgia rheumatica (PMR)*
• YELLOW or RED |
- Red if signs of vascular arteritis |
• Intro: |
- Rheumatic disorder 1° affecting white adults >50 - Characterised by px in neck, shoulder, & hip areas - Inflammatory condition w/ elevated erythrocyte sedimentation rate (ESR) & C-reactive protein (CRP) - Coexistence w/ or development of Giant cell arteritis (GCA) possible - Dx challenges inc. distinguishing PMR from other conditions - Does not lead to RA development |
• Aetiology (risk factors): |
- 100,000 / year
- White >50
- Second most common inflammatory autoimmune rheumatic disease (after RA)
- Etiology not well understood
- Some genetic predisposition
- Infection contribute: mycoplasma pneumonia, parvovirus B19, & Epstein-Barr virus (EBV)
- Some connection between PMR & diverticulitis, suggesting a role for changes in microbiota & chronic bowel inflammation |
• Pathophysiology: |
- Immune-mediated disorder
- Elevated inflammatory markers are common
- PMR pts have decreased number of circulating B cells (correlates w/ ESR & CRP) compared to healthy pts |
• Clinical presentation: |
- Symmetrical px & stiffness: affects shoulders, neck, & hip girdle
- Morning stiffness: worst in the morning, worsens after rest or inactivity
- Restricted shoulder ROM: common
- Upper body complaints: px & stiffness in upper arms, hips, thighs, upper & lower back
- Rapid onset: Ssx develop within day - 2 weeks
- Impact on quality of life: px impairs sleep & ADLs, e.g. getting out of bed, showering, driving, etc
- Inflammation sites: GH & hip joint, subacromial, subdeltoid, & trochanteric bursa
- Systemic Ssx: fatigue, malaise, anorexia, weight loss, low-grade fever (in some cases)
- Peripheral involvement: arthritis in 1/4 of pts, carpal tunnel s., distal extremity swelling w/ pitting edema, distal tenosynovitis |
• Physical examination: |
- Diffuse tenderness over shoulder
- Restricted AROM
- Normal PROM
- Restricted Cx & hip movements
- Muscle tenderness: neck, arms, & thigh
- Intact muscle strength despite complaints of weakness
- Normal sensory & reflexes (helps rule out mimicking conditions, e.g. peripheral neuropathy)
- Gait changes due to px & stiffness, e.g. shortened stride length, slow gait speed, stiffness, difficulty initiating movement, antalgic gait, decreased arm swing, & trunk lean |
• Diagnosis: |
Labs:
- Elevated ESR (>40mm)
- Elevated CRP
- Liver enzymes, especially alkaline phosphate, occasional elevated
- Serologic test (ANA, RF, Anti-CCP AB) negative
- CPK value within normal range
Imaging:
- US: assess subacromial/subdeltoid bursitis, biceps tenosynovitis, & GH synovitis
- MRI: depicts bursitis, synovitis, & tenosynovitis, more sensitive for hip & pelvic girdle findings; pelvic MRI often shows B peri-tendinous enhancement of pelvic girdle tendons & occasional low-grade hip synovitis
- PET: shows FDG uptake in shoulders, ischial tuberosities, greater trochanters, GH, & SC joints
Provisional classification criteria for PMR:
Age 50 or older w/ B shoulder aching & abnormal CRP/ESR, + specific points from:
- Morning stiffness >45 min duration
- Hip px or restricted ROM
- Absence of rheumatoid factor or anti-citrullinated protein antibodies
- Absence of other joint involvement
- US findings (if available) |
• Complications: |
- PMR pts have an increased risk of CV diseases
- Premature arteriosclerosis due to chronic inflammation is the probable cause of premature coronary artery disease (CAD)
- Some increased risk of lymphoplasmacytic lymphoma
- Higher likelihood of developing inflammatory arthritis (factors: small joint synovitis, younger age, & +ve anti-CCP) |
• Management: |
- Excellent prognosis w/ prompt Dx & appropriate treatment
- Medication
- Vitamin D & calcium supplementation for long-term steroids
- Pt should be educated on temporal/optic arteritis & how to act |
• Ddx: |
- RA
- GCA
- ANCA related vasculitis
- Inflammatory myositis & statin-induced myopathy
- Gout & CPPD
- Fibromyalgia
- Overuse or degenerative shoulder pathology (e.g. OA, RC tendinitis & tendon tear, adhesive capsulitis)
- Cx spin disorders (e.g. OA, radiculopathy)
- Crown dens s.
- Hypothyroidism
- Obstructive sleep apnea
- Depression
- Viral infections (e.g. EBV, hepatitis, HIV, parvovirus B19)
- Systemic bacterial infections, septic arthritis
- Cancer
- Diabetes |
• Temporal arteritis (TA): |
- 1 in 5 pts develop TA
- Systemic inflammatory vasculitis of arteries
- Scalp is painful to touch (hair brushing)
- Prominent, hardened & tender superficial temporal artery
- HA
- Claudication masticatoria
- Preliminary stage to optic arteritis (threat to visual ability) |
Rotator cuff injury*
• GREEN to RED |
- Grade 1, 2, 3 |
• Classification of strains: |
- Grade 1 (green): few torn/stretch muscle fibres w/ normal strength
- Grade 2 (yellow): several injured muscle fibres w/ muscle px, tenderness, mild swelling, bruising & loss of strength
- Grade 3 (red): complete tear of muscle w/ a possible audible sensation & a total loss of muscle function, severe px, bruising & swelling
- Referral depending on grade |
• Intro: |
- RC injuries range from tendinopathy to complete tears
- Rotator cuff: subscapularis (INT rotator), supraspinatus (ABductor), infraspinatus (EXT rotator), & teres minor (EXT rotator) |
• Aetiology (risk factors): |
- Most common tendon injury in adults
- Approx 30% of adults >60 have a tear, 62% in those >80
- Age is 1° factor for RC disease, being degenerative & progressive
- Risk factors: smoking (increases severity), family Hx, poor posture (kyphotic-lordotic, flat-back, swayback), trauma, hypercholesterolemia, & overhead activities
- Partial tears are prone to further propagation, factors inc. tear size, Ssx, location, & age
- Larger tears more likely to deteriorate structurally, w/ actively enlarging tears having higher likelihood of developing Ssx
- Anterior tears are more likely to progress to cuff degeneration |
• Pathophysiology: |
- Macro-trauma leads to acute tears, commonly in younger pts, resulting in complete tears
- Micro-trauma causes tendon degeneration, leading to degenerative tears
- Acute tears are typical in younger pts, while degenerative tears occur in older pts
- Sufficient tendon degeneration can make a complete tear possible w/ less force
- Multiple possible mechanisms: chronic degenerative tear, chronic impingement, acute avulsion injuries, iatrogenic injuries |
• Clinical presentation: |
- Typically begins w/ px, which can be acute or gradual
- Athletes often adapt biomechanics until they can no longer do their sport w/o px
- Pts may experience increasing px & difficulty w/ overhead activities & lifting heavy objects
- Px can radiate into the deltoid muscle area & may be felt when lying on the affected side
- Younger pts often have overuse tendinopathy
- Older pts may have OA contributing to the condition |
• Physical examination: |
- Tenderness at muscle insertion
- Muscle atrophy
- Abnormal scapular motion
- Special tests: Jobe (empty can) test, resisted EXT rotation, belly press test, drop arm test, & EXT & INT rotation lag sign |
• Diagnosis: |
- Plain radiography
- US - good for evaluating RC
- MRI - gold standard |
• Complications: |
- Retearing the cuff repair
- Adhesive capsulitis
- Inability to regain motion
- Cuff strength |
• Management: |
- Surgical & conservative treatment largest improvement at 12 months
- Surgery generally recommended for complete tears in pts <40, followed by rehab
- Conservative: PT, NSAIDs, subacromial corticosteroid injections
- STW
- SMT Cx & Tx
- GH mobs
- Nerve floss - brachial plexus
- Exercise phase 1: Codman pendulum, YTWL scapular depression, GH INT rotation, corner pectoral stretch
- Exercises phase 2: low row, eccentric supraspinatus, eccentric scapular stabilisers, eccentric shoulder ER's |
• Ddx: |
- SLAP or other labral tears
- Subacromial impingement from bursitis, os acromiale, bone spurs
- AC OA
- Biceps tendinitis
- Cx radiculopathy |
Rotator cuff tendinopathy*
• YELLOW |
• Intro: |
- RC injuries vary from minor contusions & tendonitis to chronic tendinopathy, partial tears (PTTs), & full-thickness tears (FTTs)
- They can impact diverse pt groups, from recreational athletes (weekend warriors) to elite athletes
- RC pathology is observed across all age demographics |
• Aetiology (risk factors): |
- Subacromial impingement s. (SIS) is the most common cause of shoulder px, RC tendonitis is often seen associated
- Occur acutely due to trauma or chronically from repetitive overuse activities
- 5-10% in pts <20, & over 60% in pts >80
- Acute RC tendonitis often affects athletes due to direct trauma, poor throwing mechanics, or FOOSH
- Chronic RC tendinopathy can result from extrinsic compression (mechanical impingement) or intrinsic mechanisms (cuff degeneration)
- Extrinsic compression can be caused by degenerative bursa, acromial spurring, or presupposing acromial morphologies
- Intrinsic degenerative theories suggests cuff degeneration compromises joint stability, making the cuff susceptible to extrinsic compressive forces
- Risk factors: vascular changes, age, sex, & genetics |
• Pathophysiology: |
Acute RC tendonitis can be caused by:
- Direct blows to the shoulder
- Poor throwing mechanics in overhead sports
- FOOSH
Tendinopathy develops from repetitive RC injury, leading to:
- Recurrent pathological cycle
- Acute or chronic tendonitis
- Increasing levels of tendinopathy & tendinosis
- Potential progression to PTTs &/or FTTs
Exact pathogenesis of RC tears is controversial, but likely involves:
- Extrinsic impingement from surrounding structures
- Intrinsic degeneration within the tendon itself |
• Clinical presentation: |
- Acute RC tendonitis: Hx of trauma or acute exacerbation on a chronic condition
- Chronic RC tendinopathy: either acute on chronic Hx/mechanism or a gradual, atraumatic onset
- Ssx may worsen w/ overhead activities
- Px, especially at night, is common
Thorough exam includes:
- Sports participation (including specific position played)
- Occupational Hx & current status
- Hand dominance
- Hx of shoulder &/or neck injury/trauma
- Relevant surgical Hx |
• Physical examination: |
Cx exam:
- Rule out Cx radiculopathy (Spurling's test)
- Evaluate neck posturing, muscular symmetry, tenderness, & ROM
- Special tests: Spurling's, sensation testing, reflex testing, & neurovascular exam (7 P's)
Shoulder exam:
- Shoulder girdle symmetry, posturing, & muscle bulk
- Check for scapular winging & skin abnormalities
- Palpate for tenderness
- AROM & PROM
- Consider RC tendonitis w/ anterolateral tenderness
- Test motor strength C5-T1
Special tests:
- Supraspinatus (SS): Jobe's & drop arm test
- Infraspinatus (IS): Strength test & EXT rotation lag sign
- Teres minor (TM): strength test & Hornblower's sign
- Subscapularis (SubSc): IR lag sign, passive ER ROM, lift-off test, & belly press
- EXT / subacromial impingement: Neer impingement sign, Near impingement test, & Hawkin-Kennedy test
- Internal impingement: pt supine, shoulder brought into terminal ABD & EXT rotation; +ve if px reproduced |
• Diagnosis: |
- Imaging should be obtained in all pts w/ acute or chronic shoulder px
- Plain radiographs
- US (should be used more due to their specificity)
- MRI (provides more accurate tear details) |
• Complications: |
Non-operative:
- Persistent px / recurrent Ssx
- Setting of PTTs: risk of tear propagation, lack of healing, fatty infiltration, atrophy, & retraction
- Risks for tear progression: initial presence of FTT, medium-sized cuff tears (1-3cm), smoking
- Setting of chronic/atrophic tears: DJD & RC atrophy
Surgical:
- Most effective for pts who failed 4-6 months of conservative care
- Risks of surgery: recurrent px/Ssx, infection, stiffness, neurovascular injury, & risks associated w/ anaesthetic use
- Subacromial decompression/acromioplasty: deltoid dysfunction or anterosuperior escape |
• Management: |
- Majority of pts w/o FTTs improve w/ non-operative management
- NSAIDs, rest/activity modification, cortisone injections
- STW RC muscles
- Cx & Tx SMT
- GH mobs
- Nerve floss - brachial plexus
- Exercises Phase 1: Codman pendulum, YTWL scapular depression, GH IR, & Corner pec stretch
- Exercises Phase 2: low row, eccentric supraspinatus, eccentric scapular stabilisers, eccentric shoulder ER's
- Surgery |
• Ddx: |
Impingement:
- External / subacromial
- Subcoracoid
- Calcific tendonitis
- Internal (inc. SLAP, GIRD, little League shoulder, posterior labral tears)
RC pathology:
- Tendonitis (acute), Tendinopathy (chronic or acute on chronic)
- PTTs vs FTTs
- RC arthropathy
Degenerative:
- Advanced DJD (often associated w/ RC arthropathy)
- GH arthritis
- Adhesive capsulitis
- AVN
- Scapulothoracic crepitus
Proximal biceps:
- Subluxation (associated w/ subscapularis injuries)
- Tendonitis & tendinopathy
AC joint conditions:
- AC separation
- Distal clavicle osteolysis
- AC arthritis
Instability:
- Unidirectional instability - seen in association w/ an inciting event/dislocation (anterior, posterior, inferior)
- Multidirectional instability (MDI)
- Associated labral injuries/pathology
Neurovascular conditions:
- Suprascapular neuropathy (can be associated w/ paralabral cyst at the spinoglenoid notch)
- Scapular wining (medial or lateral)
- TOS
- Quadrilateral space s.
Other conditions:
- Scapulothoracic dyskinesia
- Os acromiale
- Muscle ruptures (pec major, deltoid, lat dorsi)
- Fracture (acute injury or px resulting from long-standing deformity, malunion, or nonunion) |
Scapulothoracic dyskinesis*
• GREEN |
• Intro: |
- Altered position & motion of the scapula
- Also known as dysrhythmia, dyskinesia,or SICK scapula syndrome
- Scapular wining, exists but denoted a distinct condition typically following Tx or spinal accessory n. injury
- Observed in overhead athletes & pts w/ shoulder issues like RC disease, GH instability, impingement s., & labral tears, as well as in healthy pts
- No clear relationship between SD & shoulder px, even though some pts present w/ shoulder px
- Theory: SD might predict future shoulders even in the absence of current Ssx |
• Aetiology (risk factors): |
Shoulder-related:
- Shoulder pathologies associated w/ SD (AC instability, shoulder impingement, RC injuries, glenoid labrum injuries, clavicle #)
- Inflexibility of the pec minor & short head of biceps
- Stiffness of posterior GH capsule
Neck-related:
- Mechanical neck px s.
- Cx n. root-related s.
Posture-related:
- Excessive Tx kyphosis & Cx lordosis
- Athletes show these are more related causes SD |
• Pathophysiology: |
Scapular motions:
- Upward/downward rotation
- Internal/external rotation
- Anterior/posterior tilt
Scapular translation:
- Upward/downward sliding on the Tx
- Medial/lateral sliding around the curvature of Tx
Common scapular patterns:
- Scapular retraction: EXT rot + posterior tilt + upward rot + medial translation
- Protraction: INT rot + anterior tilt + downward rot + lateral translation
- Shrug: upward translation + anterior tilt + INT rot
Normal overhead elevation:
- Minimal INT/EXT rot until 100°
- 1° scapular motion: upward rot
- 2° scapular motion: posterior tilt
Scapulohumeral rhythm:
- Coordinated movement between scapula & humerus for efficient arm movement
- 2:1 ratio between GH elevation & scapular upward rot
- Consistent pattern during scapular plane elevation: upward rot + posterior tilt + EXT rot + clavicular elevation + retraction
Altered mechanics in SD:
- Increased scapular anterior tilt
- Increased scapular INT rot
- Altered scapular upward rot |
• Clinical presentation: |
- Pts w/ SD can be symptomatic or asymptomatic
Ssx can be one or combination of the following:
- Anterior shoulder px
- Posterosuperior scapular px (may radiate into ipsilateral para spinous Cx region or radicular/thoracic outlet-type Ssx in the affected UL)
- Superior shoulder px
- Proximal lateral arm px |
• Physical examination: |
- Assess AC & SC for instability
- Infraspinatus strength test
- Manual resistance of the arm at 130° of FX (for serratus anterior)
- Manual resistance of the arm at 130-150° of ABD (for lower & middle traps)
- Extension of the arm at the side (for rhomboids)
- Low row test
- Scapulohumeral rhythm test
- Quadruped rock
- Lateral scapular slide test
- Scapular dyskinesia test
- SICK scapula sign |
• Diagnosis: |
Classification of dyskinesia types:
- Type 1: inferior angle prominence (i.e. anterior tilt of scapula)
- Type 2: medial border prominence (i.e. winging of the scapula)
- Type 3: early scapular elevation or excessive/insufficient upward rot during arm elevation |
• Complications: |
- SD diminishes subacromial space & leads to decreased RC strength, impingement Ssx, & eventual RC damage
- 100% of pts w/ shoulder impingement demonstrate dyskinesia
- 5% of pts w/ dyskinesia have neurologic injury/damage (spinal accessory, long Tx, suprascapular)
- SD can occur from core & hip ABD weakness
- SD becomes more apparent w/ dynamic testing, particularly during the lowering phase of arm movement
- Recognition & rehab should begin independent of (generally absent) Ssx |
• Management: |
- STW: upper traps, pec minor, biceps
- SMT: Cx & Tx
- Scapular mobs
- Treatment aims at restoration of scapular retraction, posterior tilt & EXT rot
- Exercises Phase 1: trap stretch - sitting, YTWL scapular depression
- Exercises Phase 2: low row, burger w/ band |
Subacromial bursitis
• YELLOW |
• Intro: |
- Bursa is a fluid-filled sac
- Lubricatesjoints & body surfaces prone to wear & friction
- Subacromial bursa is surrounded by the acromion, coracoid, coracoacromial ligament, & deltoid muscle fibres
- Inflammation of this bursa can lead to subacromial bursitis |
• Aetiology (risk factors): |
- Around 0.4% of primary care visits
- F=M
Common aetiologies:
- Subacromial impingement (especially in older pts)
- Repetitive overhead activities / overuse (athletes, factory workers, manual labourers)
- Direct trauma
- Crystal deposition
- Subacromial hemmorhage
- Infection
- Autoimmune disease (e.g. RA) |
• Pathophysiology: |
- Aetiologies can cause inflammation of the subacromial bursa, leading to increased fluid & collagen formation
- Fluid is often rich in fibrin & can become hemorrhagic
Bursitis has 3 phases:
- Acute: marked by local inflammation w/ thickened synovial fluid, resulting in painful movement, especially w/ overhead activities
- Chronic: constant px due to a chronic inflammatory process, which can weaken & eventually rupture surrounding ligaments & tendons. Require attention to tendinitis as they may coexist
- Recurring: can result from repetitive trauma or routine overhead activities, & it may also be seen in pts w/ inflammatory conditions (e.g. RA) |
• Clinical presentation: |
- Px in the anterolateral aspect of the shoulder
- Possible causes: trauma (fall w/ direct impact), repetitive overhead activities (sports, lifting)
- Impingement s. as a common cause
- Mechanism: decreased subacromial space due to overhead activities
- Effect of arm ABD: brings humerus closer to acromion, reducing subacromial space
- Function of subacromial bursa: protects supraspinatus muscle from wear between humeral head & acromion
- Result of repetitive activity: irritation & inflammation of the bursa
- Consideration of tendon pathology: supraspinatus tendinitis or tear may coexist w/ impingement s. |
• Physical examination: |
- TTP at anterolateral aspect of shoulder below acromion
- Localised px, doesn't usually radiate (if it does, consider Cx pathology)
- Warm or boggy skin at site, but no erythema typically
- Px on resisted ABD of arm beyond 75-80°
- Compression of subacromial bursa at undersurface of acromion during motion |
• Diagnosis: |
- X-rays may be used to rule out other pathologies (e.g. fractures, dislocations, OA, etc)
- MRI: burial fluid accumulation visible
- US: evaluates the thickness of the bursa |
• Complications: |
- Not associated w/ many complications
- Repeated steroid injections: theoretical risk of introducing an infection into skin/joint
- Risk of damaging RC muscles w/ recurrent injections |
• Management: |
- Good prognosis for pts w/ conservative care, even w/ surgery
- Rest, NSAIDs, PT, & corticosteroid injections
- Surgery for pts non responsive to conservative care |
• Ddx: |
- Impingement syndrome
- RC tendinitis/tear
- Biceps tendinitis
- Adhesive capsulitis
- AC joint OA |
Subacromial impingement syndrome (SIS)*
• GREEN |
• Intro: |
- SIS is the inflammation, irritation, degradation in subacromial space structures
- Shoulder impingement s. is considered most common cause of shoulder px
- Shoulder px often persists or recurs
- 54% of pts experience persistent Ssx after 3 years |
• Aetiology (risk factors): |
- Common in overhead sports (handball, volleyball), & manual labourers
- Incidence rises w/ age (especially 60s)
- Shoulder external impingement distinguished from internal impingement by RC anatomy
Extrinsic risk factors:
- Heavy loads
- Infection
- Smoking |
• Pathophysiology: |
- Normal shoulder movement narrows subacromial space, causing px
- Unclear whether tendon damage or narrowed space causes impingement
- Described by location (external/internal) & cause (1°/2°)
Anatomic borders:
- Acromion
- Coracoacromial ligament
- AC joint
- Humeral head
External (subacromial) impingement:
- Mechanical encroachment of soft tissue in subacromial space
- 1° impingement: structural narrowing (e.g. abnormal acromion)
- 2° impingement: onset during motion due to RC weakness |
• Staging: |
Neer's classification:
- Stage 1: edema, haemorrhage from overuse
- Stage 2: fibrosis, irreversible tendon changes
- Stage 3: tendon rupture/tear due to chronic fibrosis |
• Clinical presentation: |
- Px upon lifting the arm or lying on the affected side
- Pts may report loss of motion, nighttime px, weakness, & stiffness
- Onset is gradual over weeks to months, w/o a specific traumatic event
- Px is typically felt over the lateral acromion w/ radiation to the lateral mid-humerus
- Inquire: onset, quality, exacerbating factors, interventions tried, & prior injuries
- Important: overhead & repetitive activities
- Relief: rest, NSAIDs, ice
- Ssx often return w/ activity |
• Physical examination: |
- Inspection, palpation, A & PROM, & strength testing of neck & shoulder
- B comparison
- Common weakness: ABD &/or EXT rotation
- Scapular dyskinesis during arm forward elevation
- Tenderness over the coracoid process of affected arm
Special tests for shoulder impingement:
- Hawkins test - subacromial (external)
- Neer sign - anterior px = subacromial; posterior px = internal
- Jobe (empty can test)
- Painful arc of motion
Special tests for shoulder instability:
- Sulcus sign
- Anterior apprehension
- Relocation test - internal |
• Diagnosis: |
- Dx made from physical exam
- Imaging used to confirm & rule out other issues |
• Complications: |
- Due to structural damage within subacromial space
- Altered biomechanics
- Avoidance of use w/ subsequent atrophy
- Potential pathologies that may result: RC tendonitis/tear, bicipital tendonitis/tear, or adhesive capsulitis |
• Management: |
- Most pts resolve within 2 yrs w/ conservative care (initial approach before considering surgery)
- Restoring ROM is crucial, avoid aggravating movements e.g. elevation & INT rotation
- Tape used enhance recovery & decrease px
- Steroid injections
- Surgery
- STW (RC), SMT (Cx/Tx), GH mobs, nerve floss (brachial plexus)
- Exercises Phase 1: Codman pendulum, YTWL scapular depression, GH INT rotation, Corner pec stretch
- Exercises Phase 2: low row, Brugger w/ band |
• Ddx: |
- Adhesive capsulitis
- RC tear
- AC OA
- AC sprain
- Trapezius muscle spasm
- Biceps tendonitis
- Biceps tendon rupture
- Calcific tendonitis
- GH arthritis
- Distal clavicle osteolysis
- Cx radiculopathy
- TOS |
Hypermobility syndromes (HMS)
• GREEN |
• Intro: |
- Generalised articular hypermobility, w/ or w/o subluxation or dislocation
- Also known as joint hypermobility s. & benign hypermobility joint s.
- Primary Ssx: excessive laxity of multiple joints
- Differs from localised joint hypermobility & other disorders e.g. Ehlers-Danlos s, RA, lupus, & Marfan s.
- May occur in chromosomal & genetic disorders like Down syndrome, & metabolic disorders e.g. homocystinuria & hyperlysinemia
- Lab tests used to exclude other systemic disorders when HMS is suspected |
• Aetiology (risk factors): |
- Most prevalent in children & tends to decrease w/ age
- Joint mobility is at its highest at birth, decreasing in children around 9-12 yrs
- Adolescent girls hypermobility peak at 15, decrease after, influenced by hormonal changes
- F>M
- More prevalent in ASIA, Africa, & Middle East |
• Pathophysiology: |
- Involves systemic collagen abnormality
- Joint hypermobility & tissue laxity are linked to abnormal collagen ratios
- Collagen types I, II, & III are decreased in the skin
- Dx criteria include joint abnormality
- Affects cardiac tissue, smooth muscle in female genital system, & GI system
- Impairs joint position sense |
• Clinical presentation: |
Joint instability & trauma:
- Recurrent ankle sprains
- Meniscus tears
- Acute or recurrent dislocations or subluxations of various joints (shoulder, patella, MCP joints, TMJ)
- Traumatic arthritis
- Bruising
- Fractures (chronic or non-traumatic)
- Chondromalacia
Soft tissue disorders:
- Tendinitis
- Epicondylitis
- RC syndrome
- Synovitis
- Juvenile episodic synovitis
- Bursitis
MSK conditions:
- Scoiliosis
- OA
- Congenital hip dislocation
- Delayed motor development
- Flat feet & sequelae
Neurological Ssx:
- Nerve compression disorders - carpal tunnel, tarsal tunnel, TOS
- Raynaud s.
- Clumsiness
- Chronic HA
Px & sleep issues:
- Exercise-related / post-exercise-related px
- Nocturnal leg px
- Low nocturnal sleep quality
- Joint swelling
- Back px
- Unspecified arthralgia or effusion of affected joint
Other systemic effects:
- Fibromyalgia
- Chronic fatigue s.
- Functional GI disorders
- Immune system dysregulation
- Pelvic dysfunction
- CV dysautonomia
- Exocrine glands dysfunction
- Little changes of the skin
- Greater risk of failures in tendon, ligament, bone, skin, & cartilage
- Enhanced flexibility
- Ankylosing spondylitis (axial spondyloarthritis) |
• Physical examination: |
- ROM
- End feel
- Beighton score
- Paradoxical breathing evaluation |
• Diagnosis: |
Major criteria:
- Beighton score of ≧4/9
- Arthralgia for >3 months in >4 joints
Minor criteria:
- Beighton score of 1-3
- Arthralgia in 1-3 joints
- Hx of joint dislocation
- Soft tissue lesions >3
- Marfan-like habitus
- Skin striae, hyperextensibilty or scarring
- Eye signs, lid laxity
- Hx of varicose veins, hernia, visceral prolapse
Requirement for Dx of HMS:
- 2 major criteria
- 1 major criteria + 2 minor criteria
- 4 minor criteria
- 2 minor criteria & unequivocally affected 1st-degree relative in FHx |
• Complications: |
- Px & stiffness
- Clicking
- Dislocations
- Recurrent injuries
- Digestive problems
- Dizziness & fainting
- Fatigue |
• Management: |
- Education
- Abdominal brace exercise
- Active mobs exercises
- Strengthening exercises - muscle surrounding the joint
- Proprioceptive exercises
- Control neutral joint position
- Re-train dynamic control
- Motion control
- NSAIDs for px management |
• Ddx: |
- Ehlers-Danlos syndrome
- Fibromyalgia
- Chronic fatigue syndrome
- Depression |
|
Created By
Metadata
Comments
No comments yet. Add yours below!
Add a Comment
More Cheat Sheets by bee.f