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Karteikarten von gault.kirsten, aktualisiert more than 1 year ago
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Erstellt von gault.kirsten
vor etwa 9 Jahre
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| Frage | Antworten |
| What is the most popular graft for ACL reconstructions? | Patellar Tendon Graft |
| Why is the patellar tendon graft the most popular graft for ACL reconstructions? | Due to easily performed interference screw fixation and the rapid bone to bone healing to the graft -Less likely to fail than hamstring |
| Why is the patellar tendon graft not useful | -Possible OA -Patella Baja 5-10% -Decreased knee flexion during stance -Women and for people who kneel |
| What are the negatives to hamstring recon? | -Graft Laxity -Patellar tendon joined to tunnels within 6 weeks (compared to hamstring at 8 weeks) -However if fixation is standardised there are no differences in laxity |
| What are the stats for recons for ACL's | For every 100 patients 2 per year (20%) will suffer a further cruciate ligament injury regardless of patellar or hamstring |
| Following a patellar graft, what are you also likely to injure? | Contralateral ACL |
| What are the factors that determine surgery vs. conservative management? | Degree of instability Presence of meniscal lesions Patients veel of activity Patients age |
| What is the stats for OA post ACL recon? | 10-87% |
| What did the Mueffells' study in regards to conservative vs. surgical post ACL | -Insufficient evidence to show that reconstructing the ACL is better surgically than conservative -Higher OA surgically -Higher meniscectomy surgically -No differences in functional outcome -Instability in conservative group is present |
| At what time period are ACL's at their most vulnerable to tears? | 6-8 weeks The ligament is revascularising, however the pain goes so the patient is ready to go DO NOT LET THEM DO ANYTHING THEY SHOULD NOT BE DOING |
| Why are open kinetic chain exercises not appropriate at 6 weeks? | Due to the patient not being able to achieve terminal end range, therefore OKC are not appropriate |
| What are the goals for weeks 0-2 for ACL | -Educate and manage pain -Protect graft, however do not stay in bed all day -0-90 degrees flexion -co-contraction work -Gait progression |
| Weeks 2-6 ACL recon | -Educate and manage pain -0 degrees extension- 90-120 degrees flexion -improve gait -co-contraction -muscle conditioning -STATIONARY CYCLE -SWIMMING NO KICK |
| Weeks 7-12 ACL recon | -Educate and manage swelling -Near full knee ROM -Normal gait -SQUATS -SIDE STEPS -DEAD LIFTS -LL conditioning -Cycle and swimming (No kick) -Walk treadmill |
| Weeks 13-26 ACL recon | -3 hours/ week exercise -RUNNING -JUMPING -CONTROLLED AND CAREFUL RUNNING HOP -SQUATS -LUNGES -HURDLE DRILLS -Proprioception -Bike -STATIONARY SPORTS (weeks 16- gold and tennis) |
| Weeks 26+ ACL recon | -Running and agility -Fartlek training -Interval training -NM control -Squats -Swimming -Ski Machine -Team scratch match |
| Functional outcome measures RTS for ACL | -Single hop -6m hop -Triple hop -Figure 8 hop -Must have 100% contralateral symetry |
| What is the major problem post- ACL tear | -Feelings of rotational instability of the lateral tibiofemoral compartment |
| What are the three types of Polar Classification of Instability | Type One- atraumatic/ structural (TUBS) Type Two- atraumatic/ structural (micro-trauma) Type Three- Musculoskeletal patterning disorder/ non-structural (AMBRII) |
| What are the benefits of Polar Classification of Instability | -Allows patients to be between poles -Recognises the stages as a continuum -Recognises instability as a continuum -Takes into account the shifting nature of pathology -Graduation from traumatic to atraumatic causes |
| Ottawa Ankle Rules: | -Top midline distal 6cm of fib or top of lateral malleolus -Top midline distal 6cm of tin or top of medial malleolus -Unable to WB at time of injury and unable to walk 4 steps -Top base of 5th metatarsal -Top of navicular |
| Dorsiflexion restriction | AP glide of talus -Patient in supine |
| Plantar-flexion restriction | PA glide of talus -Patient in prone with feet on bed - |
| What joint is involved with lack of dorsiflexion/ plantar flexion for AP and PA glide of talus | Talocrural joint |
| Why would you perform a medial/ lateral glide of the calcaneus? | Lack of eversion and inversion |
| What joint is involved with medial and lateral glide of calcaneus? | Sub-talar joint |
| What ligament is stressed in the anterior drawer test? | ATFL Anterior band of deltoid ligament |
| What ligament is stressed in the talar tilt test? | -Ankle in PG= CFL -Ankle in 20 degrees PF= CFL and ATFL |
| Rupture to Achilles Tendon- Clinical Presentation | -Pain on resisted tests -Irritability -Pain on eccentric and concentric loading |
| A 30 year old man has trouble squatting 6 weeks post fractured tibia- the movement is only slightly painful and irritability is low -WHICH DIRECTIONS OF ACCESSORY GLIDE MAY BE RESTRICTED? | -AP glide will be restricted (DF) |
| How would you determine if a loss of ankle DF is due to soft tissue or stiffness to the joint | Muscle- muscle length test Joint- reduced PAMS; AROM and PROM |
| What is the role of the talocalcaneal ligament complex | Stabilises the sub-taler joint (supination sprain) |
| Ligaments of antero-lateral ligament | ATFL CFL Talocalcaneal ligament |
| Medial ankle complex | Tibionavicular ankle complex Tibiospring Ligament Tibiocalcaneal Ligament |
| Low ankle sprain mechanisms of injury | -Supination injury -PF, inversion and adduction |
| Pronation sprains | Injuring distal TFJ/ syndesmosis -deltoid ligament |
| Lateral ankle sprains- why are they more common | Size and extent of ligament support- deltoid ligament is larger -Loose pack position of TCJ -Speed of NM protective response -Side of lateral vs. medial malleolus- the MM block inversion of the calcaneus and talus to a lesser extent that the LM block eversion |
| Mild supination sprain | Ligaments are stretched |
| Moderate supination sprain | Ligaments are torn slightly |
| Severe supination sprain | Ligaments torn completely |
| Grade 1 supination sprain | Partial ATFL and CFL -10-12 days RTS |
| Grade 2 supination sprain | Complete ATFL and/or partial CFL -RTS 2-3 weeks |
| Grade 3A supination sprain | Complete ATFL and CFL and/or partial PTFL -6 weeks return to sport NORMAL STRESS RADIOGRAPHS |
| Grade 3B | Complete ATFL, CFL and/or PTFL 10 weeks RTS -Stress radiographs more than 3mm of difference |
| Which grade is most likely to have reinjury | Grade 1 or 2 |
| High ankle sprain- Ankle syndemsosis | -Fibrous joint in which two adjacent bones are linked by a strong membrane -Realtively uncommon injury MECHANISMS- external rotation (pronation) of the foot or hyperdorsiflexion |
| Weber A fracture | -Break in the fibula -Below talar dome |
| Weber B fracture | -Medial malleolus may be broken -Torn deltoid ligament |
| Weber C fracture | Above the level of the malleolus Syndemosis disrupted Medial malleolus fracture w/ deltoid torn usually requires ORIF |
| Mechanisms of injury for syndemosis injuries | -Forces external rotation (widening the mortise) -Powerful abduction -Hyperdosriflexion with the talus forcing the malleoli apart |
| Symptoms of syndemsotic injury | Focal pain above the ankle May radiate superiorly No significant swelling or bruising Poor tolerance of WB -SQUEEZE TEST WILL SHOW GAPPING |
| Four landmarks for significant swelling of ankle (oedema) | 1. Navicular tuberosity 2. Distal tip of lateral malleolus 3. Distal tip of medial malleolus 4. Base of fifth metatarsal |
| Rehabilitatio for ankle sprain | Early ankle ROM Proprioception day 1-2 Local muscle strengthening Gradual return to function i.e. normalise gait pattern, brace, taping, return to sport is guided by pain and swelling |
| Chronic ankle instability | -Functional ankle instability- giving way -Mechanical instability- excessive inversion and/or laxity BOTH Mechanical instability, perceived instability and recurrent sprain |
| CAI- clinical features | History of ankle trauma Recurrent giving way and or ankle sprains Feelings of instability, hollowness or weakness Manual stress tests= POSITIVE Time in SLS- less than 26 secs -More than 10% difference in jump landings -Hopping test fails |
| Talar dome fracture/ lesion -Mechanism of injury | -Atypical sprain event with dominance of compression and shearing forces Severe pain with WB post injury Poor tolerance of compression Persistent ache at rest Generalised TC joint swelling Injury fails to resolve in expected manner Recurrent effusion |
| Post-traumatic synovitis | -Observable swelling -Usually mild -Pain at EROM -Focal top along joint line -Thickened odematous synovium at joint margins |
| Medial tibial stress syndrome | Pain at attachment of posterior compartment muscles to tibia Especially tib post Comes under the broad heading of exercise-related leg pain "tenoperiostial stress reaction through overt bony stress fractures of the tibia" |
| Causes of medial tibial stress syndrome AKA SHIN SPLINTS | Intrinsic- -Excessive uncontrolled pronation -Muscle tightness -Running technique Extrinsic- -High and unaccustomed training loads -Hard training surfaces -Poor footwear |
| What is the most important predictor of ingoing instability in ankle sprain patients | -Perceived ankle instability is more than mechanical instability |
| SPRICEMM | Support Protect Rest Ice Compression Elevation Movement Medication |
| POLICE | Protection Optimal Loading Ice Compression Elevation |
| Grade 1 tear what management?Gra | SPRICEMM and POLICE |
| Grade 2 | SPRICEMM and POLICE |
| Grade 3 tear- what management? | SPRICEMM and conservative or surgical |
| Plantar Fasciosis | Non-inflammatory stress reaction to the plantar aponeurosis of the medial calcaneal tubercle DEGENERATIVE |
| Symptoms of plantar fasciosis | Gradual onset of burning sensation Common in running athletes or sedentary people who begin high training schedule Post rest stiffness Symptoms easing with activity Tender on medial calcaneal palpation -Loss of DF, PF -Calf weakness -Sub-optimal hip control also... |
| Compartment Syndrome | Pain secondary to the muscle and nerve schema -Caused by increased compartment pressure during exercise and results in poor vascular flow -Relieved with rest -TOP on compartment |
| Three compartments of compartment syndrome | Anterior- deep fibular nerve Lateral- superficial nerve Deep posterior- tibial nerve |
| Purpose of the foot posture index | Quantifies degree of supination/ pronation Considers all regions of the foot (RF/STJ), mid-foot, forefoot in three planes (transverse, frontal and sagittal) |
| FPI Normal score | 0-5 |
| FPI Pronated score | +6-+9 highly pronated 10+ |
| FPI Supinated foot | -1 to -4 highly supinated -5 to -12 |
| FPI criteria | -Talar head palpation -Curves above and below the malleoli -Calcaneal inversion/ eversion -Talo-navicular congruence -Medial arch height -Forefoot abduction/ adduction |
| Talar head palpation | Lateral- -2 Medial- +2 |
| Curves above and below the malleoli | Curve below the malleoli= straight -2 Curve below the malleoli= concave +2 |
| Inversion/ eversion of the calcaneous | Inversion from achilles= -2 Eversion from achilles= +2 |
| Talo-navicular congruence | Talo-navicular congruence- concave= -2 Talo-navicular congruence- bulging out= +2 |
| Medial longitudinal arch | Arch high= -2 (supinated) Arch very low and flat= +2 (pronated) |
| Forefoot abduction and adduction | No lateral toes visible= -2 (supination) No medial toes visible= +2 (pronation) |
| Tendinopathy (COOK) | Pain Decreased exercise tolerance Reduction in function Repetitive energy storage and release and excessive compression appear to be key factors |
| Intrinsic factors that cause tendinopathies | Genes Age Circulating and local cytokine production Sex Biomechanics Body composition |
| Three stages of tendinopathy | Reactive tendinopathy Tendon disrepair Degenerative tendinopathy |
| Reactive tendinopathy | Acute tensile or compressive overload Thickening portion of tendon Excessive load Unaccustomed physical activity Falling directly onto the tendon Initial changes in ground substance Increased stiffness More common in younger people |
| Imaging for reactive tendinopathy | Tendon is swollen in fuisform manner |
| Treatment for reactive tendinopathy | Reduce load Modifcation of FITT Cycling Weight training NSAID's |
| Tendon disrepair | Attempt at tendon healing similar to reactive tendinopathy but with greater matrix breakdown Increase in vasculatiry and assoc. neuronal growth |
| Imaging for tendon disrepair | Matrix and collagen disorganisation |
| Tendon disrepair clinically | Chronically overloaded tendons in the young However can include many ages Or old people with stiff tendons |
| Treatment for tendon disrepair | Eccentric exercises |
| Degenerative tendinopathy | Matrix and cell changes Areas of cell death Matrix disorganisation Little capacity for reversibility of pathological changes Degenerative pathology with some normal tendon CAPACITY FOR HEALING IS SEVERELY REDUCED |
| Imaging of degenerative tendinopathy | Hyperechoic regions with decreased tendon size |
| Degenerative tendinopathy clinically | Older people Elite athletes with chronically overloaded tendons Middle-ages, recreational athlete with focal nodular areas with or without thickening |
| What exercises are best for the acute stages of tendon healing? | Isometric exercises |
| Once a patient has begun to be less irritable with their tendinopathy, what exercises will they undertake? | Eccentric (for high demand RTS) and concentric (for concentric sport deficits) exercises |
| Stretch shortening training | -Eccentric lengthening of muscle action with elastic energy storage -Concentric muscle action coupled with released of elastic 2-5 mins of session with 2-5 days of recovery |
| Examples of stretch shortening exercises: | Jumping DL/SL trampette DL bunny hops SL hop Triple extensions Walk, jog, running -- DL borad jumps SL hopping Box jumping |
| Criterion for SSC training | Late stage rehab progression Tolerating high-intensity tendon loading Low irritability Pain free walking But can begin some early form of gentle SSC if non-irritable |
| In Sherry et al. study on hamstring strains who is prone to getting hamstring strains? | Males more than females Field sports more than courts |
| In Sherry et al. study on hamstring strains what are the risk factors for hamstring strains? | Increased age Decreased quads flexibility muscle imbalances |
| In Sherry et al. study on hamstring strains what are the likely mechanisms for injury? | Terminal swing of gait Biceps femoris experiencing the greatest strain |
| In Sherry et al. study on hamstring strains what are the best methods for reconditioning the injured hamstring? | -Eccentric training -NM control of muscles of lumbopelvic region -Trunk stabilisation and NM control exercises -Warmup is critical |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 1A | Fatigue induced muscle disorder -Dull diffuse, tolerable pain in involved muscles |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 1B | DOMS -Swelling, stuff muscles, limited ROM, pain on iso contraction |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 2A | Spine-related neuromuscular disorder -Aching muscle firmness, increasing with continued activity -No pain at rest |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 2B | Muscle related NM disorder -Cramp like pain, swelling, pressure pain and aching |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 3A | Minor partial tear -Well-defined localised pain, palpable, stretch induce pain aggravating |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 3B | MOderate/ partial muscle tear -Stabbing, sharp pain well-defined and localised -Patient experiences a sharp snapping sound on experience |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS TYPE 4 | Sub-total muscle tear/ tendinous avulsion -Dull pain at the time of the injury -noticable tearing 'snap' |
| In Mueller-Wohlfahrt et al. study on muscle terminology and classification WHAT IS CONTUSION | -Dull pain at time of injury -Iccreasing pain due to haematoma -Definite external mechanism |
| According to: The association of scapular kinematics and glenohumeral joint pathologies by Ludewig and Reynolds WHAT IS SHOULDER IMPINGEMENT DEFINED AS? | Compression Entrapment Mechanical Irritation of the rotator cuff structures and/ or long head of biceps tendon |
| According to: The association of scapular kinematics and glenohumeral joint pathologies by Ludewig and Reynolds WHAT CAUSES SHOULDER IMPINGEMENT? | 1. Anatomical reductions in available space beneath the coracoacromial arch or within the supraspinatus outlet area 2. Intrinsic tendon degeneration from eccentric overload, schema, raging or inferior tissue properties 3. Scapular or humeral movement alterations compromising the rotator cuff tissues through sub acromial impingement |
| According to: The association of scapular kinematics and glenohumeral joint pathologies by Ludewig and Reynolds WHAT CLINICAL SIGNS ARE SEEN WITH SHOULDER INSTABILITY? | -Less scapular upward rotation at beginning of elevation/ faster at end -Significantly more scapular winging -Significant differences in scapulohumeral rhythm |
| According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE MAIN REASONS PEOPLE EXPERIENCE SHOULDER PAIN? | -Rotator cuff pathology -Sub acromial bursa |
| According to Rotator Cuff Tendinopathy by JS Lewis HOW WOULD YOU DESCRIBE SHOULDER DIAGNOSIS? | -High sensitivity -Low specificity |
| According to Rotator Cuff Tendinopathy by JS Lewis WHY CANT THE CLINICAL ASSESSMENT PROCEDURES FOR ROTATOR CUFF TENDIOPATHY DIAGNOSE INDIVIDUAL TENDON OR OTHER STRUCTURES? | -Morphology of rotator cuff -The position and innervation of sub-acromial bursa -Lack of correlation between symptoms and contemporary methods of imaging |
| According to Rotator Cuff Tendinopathy by JS Lewis WHAT IS THE SHOULDER SYMPTOMS MODIFICATION PROCEDURE | -Series of four mechanical techniques that are applied while the patient performs the activity or movement that most closely reproduces the symptoms experienced |
| According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE FOUR CATEGORIES OR SHOULDER SYMPTOM MODIFICATION PROCEDURE? | 1. Humeral head procedure 2. Changing scapular position 3. Cervical and thoracic procedures (as structures within the spine may cause symptoms) 3. Thoracic kyphosis technique |
| According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE ADVANTAGES OF THE SHOULDER SYMPTOMS MODIFICATION PROCEDURE? | -Recognises the inadequacy of the present method of assessment and proposes that patient management may be guided by the response to symptom modification -The program is graduated according to the individuals needs and aims to restore normal function -Flexible and capable of modification and evolution |
| According to Rotator Cuff Tendinopathy by JS Lewis WHAT ARE THE DISADVANTAGES OF THE SHOULDER SYMPTOM MODIFICATION PROCEDURE? | -No means for determining the origin of the symptoms -Lacks validity |
| According to the J S Lewis' study on subacromial impingement WHAT IS SAPS? | -Based on the hypothesis that lacrimal irritation leads to external abrasion of the bursa and rotator cuff |
| According to the J S Lewis' study on subacromial impingement WHAT ARE THE MAJOR FINDINGS OF THE STUDY? | Lacks evidence in regards to: -The areas of tendon pathology and accordion irritation -The shape of the accordion and symptoms -The proposal that irritation leads to the development of tendinitis and bursitis -Imaging changes and symptoms of the condition |
| According to the J S Lewis' study on subacromial impingement STATS | 91% of partial thickness tears are on the inferior (articular or joint) side of the supraspinatus tendon 9% on the superior or bursal side |
| According to the J S Lewis' study on subacromial impingement WHAT IS THE EVIDENCE IN REGARDS TO POSTURE AND SAPS | There is little evidence to state that posture will lead to SAPS |
| According to the J S Lewis' study on subacromial impingement WHAT ARE THE THREE TYPES OF ACROMIAL SHAPE | -Type 1: Flat Type 2: Round Type 3: hooked |
| According to the J S Lewis' study on subacromial impingement WHAT ARE THE TYPES OF ACROMIAL SHAPE THAT WILL CAUSE SAPS | Type 2: round Type 3: hooked *however studies have disproved this theory* |
| What are the upward rotators of the scapular? | -Lower trapezius -Upper trapezius -Serratus anterior |
| What attaches to the inter tubercular sulcus? | Latissimus dorsi Trees major Pectoralis Major |
| What are the attachments of levator scapulae? | Medial spine of scapular to T7-T12 |
| Contribution of supraspinatus and middle deltoid to abduction | Supraspinatus- first 30 degrees of abduction Deltoid- remainder of abduction |
| Attachments of rotator cuff | Supraspinatus- superior facet Infraspinatus- middle facet Teres Minor- inferior facet Subscapularis- lesser tubercle |
| Ligaments of glenohumeral joint | Superior GHL Middle GHL Inferior GHL Coraco-acromial Ligament -Transverse humeral |
| External types of impingement | -Sub acromial -Sub coracoid- Structures possibly impinged= subscap tendon, LHB middle GHL |
| Internal types of impingement | -Posterior superior impingement (SS or IS , RC and posterior labrum/ deep IS/ SS) -Anterior superior impingement (Subscap and biceps) |
| Structures which can sub acromial pain syndrome | -supraspinatus tendon -long head of biceps -superior capsule -superior glenohumeral ligament -sub acromial bursa |
| Functional outcome measures to allow for testing for chronic ankle instability | No effusion Full ROM Pain free walking Normal walking gait Straight line running |
| What are the benefits of eccentric training? | Allows for heavier weight |
| Extrinsic causes of shoulder region pain | -Cervical spine referral -Thoracic spine referral -Heart--> Left side -Live--> Right side -Gall bladder--> right side -Spleen--> Left side -Apical lung tumors |
| Why is there lack of specificity in shoulder tests? | -Morphology of RC (all have one insertion) -Position and inversion of sub acromial bursa- richly innervated and blends with bursa -Weakness on testing (weakness during testing shows pain rather than actual structural pathology -Pain/ weakness during testing can be influenced by spinal, scapular or head position |
| What is primary impingement of the shoulder? | True structural narrowing leading to impingement of structures in sub acromial or sub coracoid spaces |
| What is secondary impingement of the shoulder? | Functional narrowing leading to impingement of structures due to: -Sub-topimal/ impaired RC function/ GHJ MC impairment -Instability -Hypomibility -Poor scapula kinematics -Sub-optimal postures in spine |
| Sub acromial impingement- encroachment of which structures? | -SA spur/ osteophytes -Calcified caraco-acromial ligament -ACJ arthropathy -Malunion of ACROMIAL or greater tuberosity |
| Structures potentially impinged in SAPS | -Sub-acromial bursa -SUperior GH: -RC tendons -LHB |
| Symptoms of SAPS | -Pain w/ overhead movements -Loaded shoulder IR -EOR -Pain with loading RC due to failure of RC to keep the HH centred |
| Possible causes for sub-optimal RC function | -Structural pathology of RC -Pain inhibition of RC -Disuse of RC -Disuse/ reconditioning leading to weakness or loss of endurance of RC -Muscle fatigue -Abnormal GHJ mobility leading to sub-optimal RC function -Sub-optimal spinal/ scpaula postures and scpaula kinematics -If RC is impaired--> poor HH control during loading or movement//> excessive superior or antero-superior HH translation (therefore impingement) |
| Consequences of gross of subtle GHJ hypo mobility | Inability to centre HH -Loss of ER ROM (this affects the ability of greater tuberosity to clear coraco-acromial arch during shoulder elevation) which means there is a risk for secondary impingement |
| Normal scapular position | Upward rotation 2 degrees IR 33 degrees Anterior tilt 8 degrees |
| How can scapular mechanics change | Pain Soft tissue tightness over activity Altered function of scap force couples- reduced strength, endurance and sub-optimal timing Sub-optimal thoracic postures |
| Excessive medial border winging | -Secondary to sub-optimal serratus anterior -results in lack of normal upward rotation and posterior tilt (i.e. the coraco-acromial arch fails to rotate out of the way) |
| Excessive downward rotation- muscles involved | -Overtight levator scap or rhomboids -Weak serratus anterior and upper and lower traps |
| Excessive anterior tilt- muscles involved | Tight pectoralis minor -Results in scap IR, DR and anterior tilt |
| Alterations in scpaular kinematics common in patients w/ impingement, RC pathology, GHJ instability, GHJ hypomobility | -Upward rotation -Posterior tilt -Increase in IR (medial winging) |
| Result of flexed/ kyphotic thoracic postures | -Lengthened/ reconditioned scap upward rotators -Tight pec minor and major -Restriction in UR and post tilt -Decreased thoracic extension ROM -LITTLE EVIDENCE TO SUPPORT |
| Is impingement a diagnosis or clinical sign? | CLINICAL SIGN |
| Acromial irritation model- limitations | -Common location of RC pathology doesn't support this model (most RC pathology (i.e. 90%) occurs on deep articular side) -Acromial shape and relationship to pathology doesn't support this model -Acromial shape- SA spur formation may be secondary not primary |
| Why does 90% of RC pathology occur on intra-articular/ deep side | -Deeper side fibres relatively weaker and fail earlier than large acromial side fibres -Pathology due to intrinsic tendon degeneration or failure without direct mechanical irritation |
| Risk factor predisposing to RC tears | -Increased age -SMoking -Hypercholesterolemia -Family predisposition -High BMI |
| Classification of RC tears | -Partial thickness tear (start in the deep articular side)--> the progresses to involve subscap -Full thickness tear |
| Diagnosis of RC tear | -Age more than 60 -Night pain -Abduction weakness (initiation) -ER weakness -Positive impingement signs -Imaging (however symptoms do not always correlate) -Antero-lateral shoulder pain |
| Calcific tendinopathies | -Causes of calcium deposits in RC unknown -Unclear if assoc. with tendon degenerative process -Usually supraspinatus -More common in those above 30 -Deposits chemically irritate the tendon leading to inflammatory process and therefore pain! -The size of the deposit is not always linked to pain -usually managed conservatively |
| Joint Laxity | Degree of translation which falls within physiological range and is asymptomatic -Increased of developing shoulder pathology is higher |
| Joint instability | Abnormal symptomatic motion -Abnormal motion of HH relative to the gleaned during active shoulder motion -Feelings of looseness, slipping, shoulder falling out, apprehension, lack of power, sense of displacement |
| Multi-directional joint instability | -Instability in atleast 2 direction -TRUE JOINT INSTABILITY= instability in posterior and anterior w/ inferior component |
| Anterior instability | -Hand behind head -Abduction -ER |
| Inferior instability | Carrying objects/ lifting things when HH gets pulled down |
| Posterior instability | Pushing something out front or when throwing (VERY COMMON) |
| General classifciation system TUBS | Traumatic Unidirectional Bankart Surgery |
| General classification system- AMBRII | Atraumatic Multidirectional Bilateral Rehab- restore optimum NM control -Inferior capsule shift- tightening -Interval RC closer and reconstructing |
| Mechanisms of injury for anterior dislocation | -Forced abduction and internal rotation |
| Posterior dislocation- MOI | More than 90 degrees flexion -Adduction -IR (i.e. falling on outstretched arm) |
| Structures affected w/ anterior dislocation | -Inferior glenohumeral ligament -Antero-inferior glenoid labrum (Bankart lesion) -Axillary nerve injury- reduced sense of lateral sensation and deltoid weakness -RC possibly (more if over 40) |
| Structures affected w/ posterior dislocation | -Bankart lesion (tearing labrum) -Bony bankart (pulling glenoid rim as well) -Hills Sach's lesion (compression) -Bennet lesion (calcification of posterior band of inferior GH ligament) -RC damage |
| Common symptoms w/ non-acute instability | -In direction of symptoms -Feelings of apprehension -Less firm ER -RC weakness -Laxity tests positive -Impairments of static and dynamic scapula and GHJ motor control |
| Adhesive capsulitis -aka frozen shoulder | -GLOBAL limitation of GH motion resulting from contracture and loss of compliance of GHJ capsule |
| Clinical features of adhesive capsulitis | -Females more than males -40-60 yrs -Diabetic population (meaning to do with immune system) -Thyroid disorders assoc. -Unknown cause -10-30% become bilateral -Night pain -Pain w/ quick movements -Pain lying on shoulder -Pain at end range of movement |
| Stages of adhesive capsulitis | 1. Inflammatory- pain and synovitis 2. Freezing- pain and synovitis w/ progressive stiffening LOSS OF CAPSULAR MOVEMENT- ER, abd, IR, flexion 3. Frozen- contracture and fibrosis of capsule (min pain) 4. Thawing- recovery @2 years however uncertain timeframe (min pain) |
| Closed packed position of shoulder | Abduction and external rotation |
| Open packed position of the shoulder | 50 degrees abduction, slight horizontal adduction, external rotation |
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