Shoulder MSK Flashcards
(20 cards)
Should we stay in
Stiff
Weak
Stable
Irritable
STIFF
Frozen shoulder
OA
Muscle guarding
RC
Sinister patho
Frozen shoulder main areas affected
Three main areas effected:
- Rotator interval – Gap between supraspinatus tendon and subscapularis tendon/muscle
- Coraco-humeral ligament
- Subscapular recess – soft tissue runs under subscap
Frozen shoulder explained:
Fibrosis of Glenohumeral joint capsule (Around three main structures)
Increased activity of fibroblasts and myofibroblast (tissue remodelling cells) leading to capsular thickening and fibrosis.
Research unsure why this inc. in activity starts
Frozen shoulder RF and S/S
**RF: DM, Thyroid issues, Previous episode, Secondary to trauma, Hypercholesterolaemia
Age 40-60 (50-56 most commonly)
Women need longer treatment – link between menopause and changes in hormone levels for inflammatory processes
**Symptoms:
Capsular pattern: Lateral rotation, Abduction, Medial rotation
No crepitus, Limited trauma, Diffuse pain close to deltoid tuberosity
Lateral rotation 50% that of the other shoulder
Reduction in both AROM and PROM
Poor response to treatment
Pain and stiffness dominate stages
Research disputes previous three stages
**Pain dominate phase:
Extreme Pain
Night pain
**Stiffness phase:
Reduced ROM
Stiffness even under aesthetic (EUA)
OA
Degenerative changes of OA
Manual workers for long period of time, post-trauma, hereditary
Insidious onset
Grumbly and gradual progressive history
Over 60 unless trauma
Reduced ROM + crepitus
Boney end feel
RC
Degenerative changes due to massive rotator cuff tear (2 or more torn tendons)
RC not working properly – Superior migration of Humeral Head into sub-acromial space – subsequent-degenerative changes of joint surfaces
History of trauma or known RC tear
Muscle wasting
Poor AROM/PROM +/- crepitus
Weakness on testing as well as reduced ROM and pain
X-ray showing reduced sub-acromial space
Sinister pathology
AVN, Fracture, Locked Posterior dislocation, Osteosarcoma, Tuberculosis
Determine mechanism of injury is key
Locked Posterior dislocation – Missed 50% of the time, can’t get out of IR
TB: foreign travel particularly South Asia, increased risk in HIV, DM, Smoking, poor nutrition or increased alcohol
AVN risk factors: STARS (Steroids, Trauma, Alcohol, Radiation, Sickle cell) + Lack of ER due to bony collapse
WEAK
RC tear
Nerve injury
Nerve injury
Axillary nerve – Deltoid, teres minor
Suprascapular nerve – Supraspinatus, Infraspinatus
Long thoracic nerve – Serratus anterior
Spinal accessory nerve – Traps, SCM
Most likely traumatic
Mechanism can be low grade on accompanied by sensation change
Muscular wasting – late stage
Rucksack or heavy bag – brachial plexus
STABLE
Traumatic instability
Atraumatic instability
Muscle patterning
SLAP lesion
Traumatic instability
Dislocation due to trauma
Anterior much more common
High energy force applied to GHJ causing humerus to disengage with glenoid – commonly Abd +ER position for Anterior Dislocation
Multiple dislocations following Bankart or Hill-Sachs lesions
Bankart lesion – Tear in labarum between 3-6 o’clock Or can be bony Bankart lesion – inferiorly and anteriorly, fractures bone as well as tearing labarum
Hill-Sachs Lesion – Posterior humeral compact after major shoulder dislocation
The more dislocations increase the likelihood of Bankart or Hill-Sachs lesion
Once lesion has occurred dislocations are more common.
Why surgery is common in traumatic/structural changes.
Instability tests: Load and shift, AP/PA glides
Nerve injury chance rises with how long dislocation lasts for
Atraumatic instability
Dislocation without trauma
Altered proprioception or neuromuscular control
Born loose or worn loose
Born loose e.g. hypermobile EDS
Warn loose – repeated activity leading to adaptive changes
Mechanism of injury clear
Multiple dislocations in short period of time
More likely Bi if born loose
Structural changes – small labral tears, given potential high frequency of dislocation
Muscle patterning
Little trauma, alteration in muscle requirement (pecs, delts lats pull shoulder out of joint) Rare but psychological links)
Very rare subspecialty of shoulder instability caused by significant changes to neuro-muscular requirement
Abnormal recruitment of muscular system leading to dislocation and instability.
Party trick as a child now become habitual can’t stop doing it. Strong links to stress and phycological issues.
Dislocation history in non-threatening positions
Pop shoulder in and out on command
Increased tone of pecs, lats and delts
SLAP lesion
Superior labrum anterior to posterior tear
Anchor = Attachment to superior labarum
Rope = RC/LHB tendons
Traumatic event involving LHB tendon
In under 40 tendon remains strong and pulls anchor out creating a SLAP lesion
Over 40: More likely that tendon snaps - RC or BLH tendon tear
Most likely to occur following high force trauma
Often overhead position or FOOSH
Clear link between trauma and onset
More common under 40
Deep seated ache
May or may not feel unstable/cause clicking and clunking
Likely to experience loss of power
IRRITABLE
Tendinopathy
Biceps LH tendinopathy
Calcific tendinitis
ACJ dysfunction
Parsonage turner syndrome
Tendinopathy
Underloaded tendon – sudden increase in activity
Impingement doesn’t exist – decompression surgery doesn’t work
Could be secondary issue e.g. sub acromial pain
Tendinopathy rather than tear – strong but painful – tear weak
Special tests may or may not be helpful e.g. empty can, Hawkins Kennedy
Biceps LH tendinopathy
Has inter and extra-capsular portions
LHB shown to be working harder when other pathologies are present
A small amount of irritation causes an increase in tendon fluid content for a tendon held in a tight space
Most common: Secondary to overuse as a result of other pathologies
More rare: Primary over-use of LHBT e.g. moved house or heavy eccentric loading
Anterior shoulder pain
Pain on palpating the tendon
Pain on palpation of LHB
Px taking off jacket
Widespread shoulder pain
Pain with larger shoulder movements
Speeds test
Obrien’s test – more when thumb in down
Uppercut test
Calcific tendinitis
Most commonly supraspinatus
Calcium deposits thought to be part of ageing process or as an inflammatory response to tendon change or aggravation
Bodies protective measure – naturally stops movement
Extremely painful – sudden and unprovoked
Most common 40-60, Women>men
Night pain
Can react as a flare up to sudden activity
USS best diagnosis
Steroid injection or surgical removal if it doesn’t heal on its own – reabsorption stage more painful
ACJ dysfunction
Local pain to the ACJ
OA most common – AC one of the fastest advancing OA in the body
Biomechanical – change in biomechanics
Instability – disruption of stabilising structures
Clear location of pain
Pain/AROM over 100deg
Scalf test, ACJ squeeze, Obrien’s test
Step deformity
Best imaging is MRI
