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6002 Shoulder Cheat Sheet by * Must know

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


• 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

- Condition gradually develops
- 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)
- 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)
- 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)
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
- Residual shoulder px &/or stiffness
- Humeral fracture
- Rupture of the biceps & subsca­pularis tendons
- Labral tears
- GH dislocation
- Rotator cuff tear
- Spencer technique
- 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
- Cx radiculopathy
- AC arthrosis
- Bicep tendinopathy
- GH arthritis
- Fracture
- Calcifying tendinitis/synovitis
- Malignancy
- Polymy­algia rheumatica
- Shoulder imping­ement s.

AC joint injury

- Sprain degree to torn degree
- 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
- 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
- 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
- X-rays are 1° for Dx
- US & MRI may be considered if Dx remains uncertain
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
- 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
- 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
- SMT (not shoulder)
- Exercises phase 1: scapular clocks & protra­ction / retraction
- Exercises phase 2: resisted shoulder EXT rotation, cane - FX, low row
- 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

- 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
- 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
- Dx relies on Hx, physical exam, imaging (x-ray, MRI), & diagnostic local anaest­hetic injection
- 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)
- 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
- Calcific tendonitis
- GH arthritis
- Adhesive capsulitis
- Rotator cuff imping­ement s.


"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

- 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
- Supras­pinatus tendon (80%): critical zone (most common)
- Infras­pinatus tendon (15%): lower 1/3
- Subsca­pularis tendon (5%): pre-in­ser­tional fibres
- 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
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
- Diagnosed through x-rays
- Adhesive capsulitis
- Rotator cuff tear
- Ossifying tendinitis
- 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
- 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

- 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
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
- 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
- AC injury
- Bicipital tendonitis
- Clavicle fracture
- RC injury
- Shoulder dislocation
- Swimmer's shoulder

GH instab­ility*

- 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
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
- 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)
- X-rays for compre­hensive evaluation
- MRI & CT for advanced imaging
- Redisl­ocation following surgical fixation
- Nerve injuries (esp. axillary n.)
- Infection (surgery)
- Implan­t-r­elated problems
- 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
- 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
- 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)

- 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)
- 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
- 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
- Shoulder Imping­ement s.
- RC s.
- Biceps tendinopathy
- Labral lesion

Glenol­abral articular disruption (GLAD)*

- 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
- 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:
- Px may be elicited on ABD & EXT rot
- Force ADD may produce 'popping' sensation
- Special tests: Crank test; O'Briens test; Anterior Appreh­ension test; Passive Compre­ssion test
- High associ­ation between GLAD & anterior shoulder instab­ility
- 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
- 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)
- 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
- 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)*

- Red if signs of vascular arteritis
- 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
- 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
- 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
- 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)
- 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)
- 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
- RA
- 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*

- 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
- 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
- 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
- Plain radiography
- US - good for evaluating RC
- MRI - gold standard
- Retearing the cuff repair
- Adhesive capsulitis
- Inability to regain motion
- Cuff strength
- 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
- 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
- SLAP or other labral tears
- Subacr­omial imping­ement from bursitis, os acromiale, bone spurs
- Biceps tendinitis
- Cx radicu­lopathy

Rotator cuff tendin­opathy*

- 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
Acute RC tendonitis can be caused by:
- Direct blows to the shoulder
- Poor throwing mechanics in overhead sports
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
- 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
- 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)
- 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
- 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
- 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
- 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
- Advanced DJD (often associated w/ RC arthropathy)
- GH arthritis
- Adhesive capsulitis
- Scapul­oth­oracic crepitus
Proximal biceps:
- Sublux­ation (assoc­iated w/ subsca­pularis injuries)
- Tendonitis & tendinopathy
AC joint condit­ions:
- AC separation
- Distal clavicle osteolysis
- AC arthritis
- 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)
- 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*

- 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 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
- Mechanical neck px s.
- Cx n. root-r­elated s.
- Excessive Tx kyphosis & Cx lordosis
- Athletes show these are more related causes SD
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
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
- 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
- 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

- 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)
- 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
- 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
- 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
- Good prognosis for pts w/ conser­vative care, even w/ surgery
- Rest, NSAIDs, PT, & cortic­ost­eroid injections
- Surgery for pts non responsive to conser­vative care
- Imping­ement syndrome
- RC tendinitis/tear
- Biceps tendinitis
- Adhesive capsulitis
- AC joint OA

Subacr­omial imping­ement syndrome (SIS)*

- 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
- 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
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
- Dx made from physical exam
- Imaging used to confirm & rule out other issues
- 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
- 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
- Adhesive capsulitis
- RC tear
- AC sprain
- Trapezius muscle spasm
- Biceps tendonitis
- Biceps tendon rupture
- Calcific tendonitis
- GH arthritis
- Distal clavicle osteolysis
- Cx radiculopathy

Hyperm­obility syndromes (HMS)

- 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
- 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:
- End feel
- Beighton score
- Parado­xical breathing evaluation
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
- Px & stiffness
- Clicking
- Dislocations
- Recurrent injuries
- Digestive problems
- Dizziness & fainting
- Fatigue
- 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
- Ehlers­-Danlos syndrome
- Fibromyalgia
- Chronic fatigue syndrome
- Depression


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