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Sports Science Y3 S1 > Sports Inuries > Flashcards

Sports Inuries Flashcards

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1
Q

Medial ligament of the anlkle role and attachments

A

Deltoid ligament.
Navicular, talus, calcaneus.
Resists eversion.

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2
Q

Lateral ligament of the ankle role and attachments

A

ant and post talofibular and fibulocalcaneal.

Resists inversion.

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3
Q

What is the sequence of prevention?

A

Measures to prevent sports injuries. Firstly the extent of the promblem must be identified and described. Secondly the factors and mechanisms identified. Thirdly introduce measures based on aetiological factors and mechanisms. Evaluate through repeating first step.

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4
Q

What is a sports injury

A

Any physical complaint sustained by practising or competing in a sport that causes a reduction in future training/ competition or an athelet to seek medical attention

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5
Q

Broad classification of sports injury

A

Time loss injury or medical attention injury

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6
Q

Some potention consequences of sport injury

A

Pain, Financial

Repetitive muscle straign, osteoarthritis, bone fracture, lig reupture, tendonopathy

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7
Q

What is epidemiology

A

The study of disease in relation to populations

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8
Q

What is incidence

A

The number of new cases per 1000 people within a set population in a set time period.

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9
Q

What factors could cause variation in studys?

A 
Definition of sports injury
Variation of methods to count injuries
Variation of populations
The way incidence is expressed
MEthod used t establish the population at risk
Representativeness of sample.
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10
Q

Why is prospective better than retrospective

A 
Can measure many exposures
Count number of episodes
No Recall bias
Single standard of diagnosis.
Can prove temporal sequence
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11
Q

What is a stress fracture

A

Hariline fractures that cant be imaged via Xray

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12
Q

Variate in how you measure the nature of a sports injury

A

Acute (traumatic) vs chronic (overuse)

Tendonitis vs tendopathy. Failure to heal.

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13
Q

Difference between contusion vs laceration

A

Skin cut vs un cut

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14
Q

How is severity measured? 6 criteria

A

Time loss (working or sport), medical/ economic cost, nature of injury, nature of treatment, permanent damage.

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15
Q

How is severity measure in terms of days lost?

A

<7 minor
8-21 moderate
>21 severe

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16
Q

Describe the spectrum of tissue regenrates

A

Fastest to slowest

Bone, muscle, tendon, ligament, meniscus, cartilage

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17
Q

Costs of sports injuris

A

Direct (medical) and indirect

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18
Q

Difference between systematic review and meta analysis

A

Synthetic output of one value, not all included

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19
Q

Describe intinsic factors

A

Know as capacity (as increases, risk of injury decreases)

Includes psych - A (competitive and self critical) and C personalities (struggle expressing emotion e.g. always nice)

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20
Q

Whats the difference between relative risk and odds ratio

A

Relative risk = (exposure case/ Total exposure)/ (non exposure case/ Total non exposure)
= exposure risk/ non exposure risk

OR =
(exposure case/ Exposure non case)/ (non exposure case/ non exposure non case)

If disease is rare then OR= RR as is normally the case.

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21
Q

Why is a association not always causal

A

unknown factor may cause both
Confounder
Also an unknow factor may cause one thing that causes another

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22
Q

RFs for sports injuries

A

Loads

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23
Q

Describe the causation model

A

Intrinsic factors predispose an athlete. Exposure to extrinic factors result in a susceptible adult.
An inciting event/ mechanism of injury causes an injury

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24
Q

Difference between mechanism and diagnossi

A

Mechanism- Process of how an injury occured, macro (being tackled from behind) or micro e.g. hyperextension of a joint, inversion.
Diagnosis - Outcome of mechanism e.g. straign, rupture, break

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25
Q

What does the injury incidence assessment depend on?

A

Definition of the sport injury in question
Method using to establish pop at risk (how to define exposure group)
Method used to count injuries (e.g. diagnosis)
Representativeness of sample
The way incidence is expressed e.g. hours/years

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26
Q

What is the sequence of prevention? What factors should be ascertained?

A

Prevalence/ extent WHAT
Aetiology - RFs and mechanism WHO WHY HOW
Preventative measure based on factors/ mechanisms introduced
Evaluate through repeating first step.

Measures

How many
Nature - acute vs chronic
Where
Type
Who
Severity
Situation - trianing/comp
Process (mechanism) - contact vs non contact
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27
Q

First step of sequence of prevention. Best practice

A

Comparable measure e.g. 1000 hours of sport participation (variable measure)

Can be retro or prospective. Bare in mind the representativeness of sample.

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28
Q

Second step of sequence of prevention from Van Mechelen 1992 (review of concepts)

A

often uses an epidemiological model.
Stress/ capcity model (must be inbalance) intrinsic effects capacity and stress (extrinsic) also mechanism needs to be addressed.

Another model = relationships between factors and determinants of sports behaviour e.g. athlete manipulates stress and alters capacity and risk of injury. Factors include load, personal equipment, physical and human factors and intrinsic factors - all lead to sports behaviour.

Only 1st talked about in lecture

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29
Q

Findings from Taimela et al 1990 - intrinsic RFs

A

Intrinsic factors
Aged 15-16 and Senior but sport dependent
Men more at risk - due to more vig exercise?
Certain lesions recur e.g. sprain, dislocation
Individuals at higher risk or injury a cause
Height and weight being high
lack of fitness
muscle weakness, joint looseness, poor flexibility
Reaction times
Life stress
Loqwer IQ

Can decrease by
Coaching
anatomical considerations
motor performance requirements
Psychological factors
Avoid stress
treatment and rehab to avoid recurrence
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30
Q

Findings from Bahr & Holme (2003) Metholodical sport injuries

A

For moderate to strong associations 20-50 cases are needed, small to moderate need 200 injured subects. Lots are too small to detect moderate associaions.
Prospective cohort the best.

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31
Q

Findings from Bahr, R., & Krosshaug, T. (2005). Understanding injury mechanisms: a key component of preventing injuries in sport. British Journal of Sports Medicine, 39(6), 324-329.The importance of the mechanism (not just intrinsic and extrinisic factors). Including a description of whole body and joint biomechanics at the time of injury.

A

Ability to design specific prevention programmes is limited by lack of knowledge of cause. Needs a multifactoral approach to understand all the factors involved in this
The importance of a comprehensive model which accounts for all events leading to injury including mechanism (not just intrinsic and extrinisic factors, also situation, player and opponent behaviour). Including a description of whole body and joint biomechanics at the time of injury.

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32
Q

Explain common problems with SEM in the army

A

Many fail to improve with physio and then there is no evidence for the next step e.g. PRP- platelet rich plasma
Many injuries
Most downgraded (get worse)

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33
Q

Difference between origin and insertion

A

Origin close and insertion distal.

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34
Q

Does a tendon lengthen or schorten during muscle contraction?

A

Stay the same

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35
Q

Why can running in boots be an RF for achillies tendinopathy?

A

Compression of tendon is a RF

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36
Q

Describe the microstructure of a tendon

A

Covered in epitenon (surrounded by peratenon)
Tertiary fibre bundle
Fascicle (secondary fibre bundle) - covered in endotenon
Subfascilcle (primary fibre bundle) - endotenon
Fibre
Fibril
High alligned collagen composed of the above
Initiates movement of joints and stabalises joints

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37
Q

Movement that precipitates achillies tendon rupture

A

repetition and overuse,
eccentric activities, and quick cutting motions that
involve rapid acceleration / deceleration
These injuries upset the balance between mobility
and stability and results in abnormal loading that
could damage other soft tissues and cause pain
and osteoarthritis in long run.

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38
Q

Cause of subacromial impingement (painful arc)

A

Posture causing tendon (rotator cuff) impingement

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39
Q

Describe tendinopathy pain

A 
Morning stifness/ pain (shortening)
Pain commencing and after activity. Eases with warm up
Pain on palpation
Pain at specific site
Insidious onsett
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40
Q

Causitive factors of tendinopathy intrinsic (achillies) (RFs)

A

Giat
Heavy heel strike
Double heel lift

Motor patterning

BMI

Previous injury

Age

Posture/Allignment

DM/ dyslipidaemia

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41
Q

Causitive factors for tendinopathy extrinsic

A

Training errors
Frequency
Intensity
Energy storage activities

Footware
Exercise
Medication e.g. fluroquinolones or steroid

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42
Q

Describe the continuum model

A

Replaced the inflammatory tendinities model.

excessive load leads to reactive tendinopathy.
Optimised load leads to gradual strengthening and adaptation with normal tendon.
Lack of load leads to stress shielded (normal load may then cause this to become reactive).
Further load causes tensdon dysrepair.
Further load cuases degenerative tendinopathy
The further from normal tendon means the harder it is to return so treament revolves around modified load.

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43
Q

What does disrepair look like?

A

Increased cellularity and ground substance (occurs initially).
Focal area of disorganised collagen.
Neurovascular ingrowth (cause of pain?)
Explains why NSAIDs may not help

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44
Q

Describe the pathology of acute/ reactive tendinopathy

A

Increase in small proteoglycans and ground substnace (NSAIDs)
Non inflam response secondary to acute tensile or compressive overload - too much too soon
Tenocyte proliferation (become more chondroid)
No neovascularisation
Some collagen disruption from water

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45
Q

Describe the cause of pain in acute tendinopathy

A

Hypoxic - increased tissue fluid

Hypersensitivity of tenocytes

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46
Q

Describe how long acute tendinopathy may last for

A

a few days

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47
Q

Describe pathology of dysrepair tendinopathy

A

Focus of holes of collagen disorganisation
More ground substance
Upregulation of neo vascularisation factors e.g. VEG F
Myofibroblasts
MOre chondrocytic cells

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48
Q

causes of Pain in dysrepair tendinopathy

A 
new vessels with nerves (more factors e.g. glutamate and substance P)
Pain centralisation (thinks it's more important than it is)/ neuronal sesnitivity
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49
Q

Degenerative tendinopathy pathology

A 
Significant matrix disorganisation
cell death - apoptosis - hypoxia due to more cells
Increased type III.
Hyaline degeneration
Tenocyte echaustion
Very disorganised
Little reversibility
older people
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50
Q

Difference in swelling in types of tendinopathy

A

Fusiform in reactive and dysrepair possible (and in reactive on degenerative).
Nodular in degen

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51
Q

Response to load in different types

A

sensitive in acute
less sensitive in dysrepair
Occasional grumbles in degen

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52
Q

Treatment for reactive

A

Rest/ unload (stress shielding)
Use ice
Adress compressive loads (concentric) and positions

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53
Q

What does rehabilitation address?

A

ROM
Pain
Contractile deficits
Movement patterns

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54
Q

Describe some outcome measures used in achillies.

A

Victoria Institute of sport A/P/H (VISA A)
Not good for less than 6 weeks
Achillies tendinopathy measure

VAS, NRS (numerical rating scale

Daily symptom report
General pain
Pain on walking
pain on activity

FAA (army) - occupational score

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55
Q

Causes of pain in degenerative

A

hypoxic
Centralisation
Neural

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56
Q

Describe the appearence of denerative on ultrasound and H&E

A

Hypoechoic areas and los of textured appearence on US
BV lumens visible
Doppler and BVs
Also in dysrepair but larger areas and more vessels with focal swelling in degenerative

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57
Q

Describe a progressive loading stage 1

A

Isometric contraction e.g. sitting or standing
Stimulate collagen synth and adress deficits.
30-60secs 4-5 times a day 4-5 secs
Avoid pain and compression

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58
Q

Describe a progressive loading stage 2

A

Concentric or eccentric medium load
Open and close chain if possible (fixed joint vs unfixed distal)
Stage 1 on days off

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59
Q

Describe a progressive loading stage 3 and options

A

HSL - Heavy slow resistance- through entire range. often less frequent option and more useful between dys and degen. Often increase %of 1RM working at but always till failure/ bad form

Eccentric training (Alftedson programme)

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60
Q

Describe a progressive loading stage 4

A

Pliometrics
Ensure no pain
Controlled intro to sport (can quikcly overloda)
Energy storage loading (jumping)
Minimal pain during/after high load tests
Started When single leg strength is equivalent

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61
Q

Summarise total program

A

Progressively add stages but add sparsely at first and increase frequency
May add ESWT.
Return to sport on high load days but continue monitoring

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62
Q

Other things considered in treatment other than load

A 
Biomechanics
Flexibility
Lumbar spine
Neural mobility
Associated injury

Ensure
coontinued education, maintain strength and gradula intro of novel activity

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63
Q

Other less conventional treatments

A

Steroid injection
LA injection (p
Dextrose injection
PRP/ autologous blood injection

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64
Q

Describe the functions of ligaments

A

Keep articulating surfaces together (limit mobility)
Minimise unwanted joint movement
Provide joint stability

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65
Q

What is viscoelasticity? how is this clinically relevant?

A

Can stretch slowly under tension but return to original shape.
Rapid strectching however can rupture e.g. grass

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66
Q

What is the Beighton score? genetic variation in stretching?

A

Degree of hypermobility assessed.
Natural stretchiness not from stretches e.c.t.
Less flexible with age.
1) Hands on floor
2) Elbows extent backwards
3) Knee that bends backwards
4) Thumb that touches forarm when bent backwards
5) little finger 90 deg when bent backwards

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67
Q

What is the cut off score for Beighton?

Problems with score?

A 
2 means hypermobility of joints likely
Often in studies >=4
(7-15% have >=4)
Higher score - higher risk of hypermobility and risk of injury -dose.
Binary score so score or don't
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68
Q

Describe the hypermobility questionnaire? Cut off

A

1) Hands on floor
2) Bend thumbs to touch forarms
3) As a child contort or do splits
4) As a child shoulder or knee dislocate more than once?
5) Consider yourself double jointed?

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69
Q

How do scores relate to hypermobility syndrome?

A

Don’t necessarly as asymptomatic often

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70
Q

Difference between structure of tendon and ligament

A

Ligaments have a more wavey appearence and slightly less parallel than tendons allowing lengthening (spring) fibroblasts les parallel.

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71
Q

Grades of ligamnet tear

A

1- Stain or streched but still competent and able to stabilise a joint
2- Partially torn and partially able to stabalise - healing is possible and promising
3 - complete tear, no stability

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72
Q

Treatment of ATFL tear?

A

Conservative

train muscle, strenght, speed, proprioception

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73
Q

Why might women be more prone to ACL injury?

A

More hypermobile, more valgus positon??

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74
Q

Where is the pain in tendonopathy?

A

Normally at attachment but achillies can be in the centre

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75
Q

Pathology of underloading and tendon

A 
Hyalin degen
Matrix disorganisation
Angiofibroblastic hyperplasia
Angiofibroblastic hyperplasia.
Mostly reversible in animals
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76
Q

Treatment for reactive… drugs?

A

3 days for peak body response
De-load
but can load without energy storage and release e.g. cycling, strength based weights training.
NSAIDs good for pain but may delay healing as inhibit tenocyte prolif. Ibuprofen favoured

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77
Q

Treatment for late tendon dysrepair/degeneration?

A

Stim cell activity and protein production via massage (friction) ESWT, US, Surgery??, Prolotherapy (blood and glucose??), injection itself may bemefit, Polidocinol sim to placebol,
Aptotinin - acollegenase inhibitor no evidence
Sclerosing agenets
GTN for pain
4-6weeks eccentric will change pain
Pain in exercse ok - wont affect outcome

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78
Q

General points about dislocation

A 
Xray for fracture
May need diazepam or GA to relocate
Early protection
Early mobilization
Muscle strengthening
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79
Q

Grade 3 tear and pain?

A

May be none as sensory fibres can be divied

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80
Q

MCL injury mechanism

A

Valgus force on partially flexed knee

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81
Q

MCL symptoms

A

1 - no swelling
Pain - localised tenderness to medial condyle/ tibial plateu
Pain but no laxity on test

2 - swelling possible (capsule tear)
Some laxity but distinct endpoint

3 - Instability, gross laxity without endpoint, lack of full extension, ACL tear often, swelling

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82
Q

MCL treatment

A 
Conservative.
Hinged brace (immobilisation is bad)
Rehab - ROM, strengthening, proprioception, graded exposure to sport 2-4week for mild, 6-10 for severe.
Other:
Cryo
Electrotherapy
Manual 
Gait re-education
Patient education
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83
Q

PCL function

A

Resists posterior draw of tibia and external rotation
Stronger than ACL
Often underdiagnosed

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84
Q

PCL damage associated injuries

A

LCL/ popliteus

1/4 have meniscal damage

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85
Q

PCL features

A

History
skiier
Poorly defined back of knee or calf
No swelling as extrasynovial

Exam
Posterior draw test
Posterior sag

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86
Q

PCL mechanism

A

Direct blow to anterior tibia when flexed

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87
Q

PCL investigation

A

Xray - avulsion

MRI if posteriolater cornal damage is suspected

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88
Q

Treatment of PCL

A

Conserve
Rebab - quad heacy
immobalise for 2-3 weeks if complete rupture
Good functional result

Surg
Sig posterolateral damage

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89
Q

Medial ligament incidence and treatment

A

Stronger than lateral and inversion rarer.

Same treatment as alteral but takes twice as long

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90
Q

Pott’s fracture symptoms, management and treatment

A

One or more malleoli (local pain)
May be pain at distal attachment of ligs
Xray needed
Conserve - cast immobilisation for 6 weeks
Surg- repair mortise via internal fixation

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91
Q

Maisonneuve fracture

A 
Fracture of proximal fib with complete rupture of AFTL and interosseus membrane
High impact sports
Xray often misses
Can reduce spontaneously
Refer to ortho
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92
Q

4 zones of lig to bone

A 
Lig
Fibrocartilage
Mineralised fibro
Bone
Superficial fibres to periosteum
Depp directly to bone at acute angles
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93
Q

3 stages of lig repair

A

Heamatoma formation
Reparative phase - fibroblast prolif and matrix
Remodelling - reallignment of collagen over years

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94
Q

Future treatments of ligs

A

Growth factors - PDGF in mice
Gene transfer to reduce undesired proteins
Cell therapy - mesenchymal stem cells
Mechanical factors e.g. allignment with strethc
Scaffolding materials e.g. alginates and collagen
Many disciplins that need to work together e.g. histology, clinicians, biomechaics, molecular bio, immunology

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95
Q

Describe valgus/ varus

A

Valgus is knee in toe out - lateral force (external rotation)
Varus is medial force

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96
Q

What is the mechanism of ACL damage

A

Valgus (abduction) or varus (adduction) force, contact or non contact

Valgus load
MCL stretched and lateral meniscus compression
Contraction of hamstring pulls lateral femoral condyle posteriorly and tibial internal rotation.
ACL ruptures at 4ms
Without this there is no resistance to extrenal rotation and this occurs until 170ms

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97
Q

Function of ACL

A

Stability
Reist anterior translocation
Resist internal rotation

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98
Q

Symptoms/ sings of ACL injury

A

ASymptomatic
Popping sound or feel
Sudden sharp pain
Loss of full extension or flexion (contracture)/ locking of joint
Swelling (haemarthrosis) within hrs (menisucs days) as more vascular
Stiffness
Anterior tibial translation

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99
Q

Potential injured structures from ‘knee in toe out’

A

ACL, LM, MCL

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100
Q

Potential injured structures from ‘knee out toe in’

A

ACL, MM, LCL

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101
Q

What is distraction/ compression

A

Into or away from - cause of knee damage but rare

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102
Q

Describe biomechanics of what happens in ACL injury

A

(Valus force causes) neutral abduction to 10-13 deg with external rotation at 5 degree at IC.
Rotated internally 8 degree during first 40ms then external fotation of 17.
High peak verticle ground reaction force is associated.
Likely injury occurs at 40ms.
Knee felxion and minimal valgus loading could prevent this. (study of 10 handball/ basketball players)

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103
Q

How do we know about biomechs of ACL injury?

A

From model based image matching (MBIM) motion analysis technique - skeleton matched frame by fram using animation software

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104
Q

What is genus valgum and varum

A

Posture that is naturally in or out - feet appear closer or more separate

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105
Q

What is the lachman test? Limitation?

A

knee plexed to 30 deg
hold thigh and with other hand apply anterior force to tibia.
Muscles need to be relaxed so ask patient to look away
Cant do if swelling/ immediately as wont be positive

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106
Q

What is the anterior draw test? Looking for? cause of false neg?

A 
Knee flexed to 90 degee
Apply anterior force to tibia
Signs of anterior subluxation
False negative - injured and tibia already forward (like anterior sag)
Note if end point
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107
Q

Describe the pivot shift test. limitations?

A

Hip flexed to 30
internally rotate tibia to 20 deg then apply valgus force - feel for subluxation by flexing
Reduction of a subluxeed tibia with further flexion as the IT band goes from extensor to flexor

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108
Q

How is ACL diagnosed?

A

Clinically or via MRI - solid black band - torn then ligher in coler +/- disorganisation or breakage
Arthroscopy

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109
Q

Aims of ACL treatment

A

Return to normal joint staboloty, ROM, muscle function, physical activity levels

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110
Q

Describe surgical techniques to repair torn ACL

A 
Wait until no swelling
Uses graft - drill 2 holes, one in femur and tibia
Pass graft through holes
Fix with screws
Autograft - patella or hams
Allograft - infection, cost, but lower OA, decreased morbidity? No RCTs, only if no visible autograft
Xenograft
Arthroscopy or arthotomy
No evidence of prosthesis
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111
Q

Describe petalla graft

A 
PBP
Central third used
140% of strength
Bone to bone healing better
Worse scan
Can damage nerves around patella
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112
Q

Describe hamstring graft

A 
70% of strength
Double or single bundle
semitendinosis +/- gracillis
Scar is only a hole
treat as a pulled hamstring.
4 stand much better, same clinical outcome as BPB
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113
Q

Describe bone to tendon healing

A

Progressive mineralisation of interface
Many cells acutely due to recruitment of healing cells
after 6 weeks incorporation - bone grows into outer tedon
Decreased cellularity due to matrix remodeeling and reestablishment of collagen fibres

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114
Q

What factors may enhance bone to tendon healing

A

Cells

  • stem cells
  • Transforming growth factor beta 1 - grown from stem cells
  • bone morphogenic proteins 2 (BMP2)
  • Mesenchymal stem cells

Biomaterial

  • Deminaralised bone matrix
  • Injectable phosphate cement

Biophysical

  • Low intensity pulse ultrasound (LIPUS)
  • Shock wave therapy
  • Ultra-sound guided shock wave therapy

Periosteum around tendon graft may help too

115
Q

Describe Bridge enhanced ACL repair (BEAR)

A

Sutures to hold a sponge with proteins from ruptured ends of tenson.
Blood added to sponge via needle and syringe
Tissue replaces sponge over time.

116
Q

Describe function of the menisci

A

Prevent damage to articular surfaces - shock absorber
Joint stability
DIstribute forces over a maximal area

117
Q

Symptoms of mensical injury

A

Medial- more specific pain
Lateral mre vague
24-48hr sweeling - synovial (difficult to heal)
Locking sensation due to jamming - ring changes shape with tear. Extension or flexion.

118
Q

Mecanism of injury in meniscal injury

A

Twisting, turning, cutting, robust in 20s
Normally knee out toe in.
Jumping more likely to be meniscal than ACL

119
Q

Indications for surgery of meniscal injury

A

Loss of full extensionq
Failure of conserve
Within 2 weeks of swelling going down

120
Q

Describe surgical proceedures for meniscal injury

A

Partial menisectomy
Arthroscopic meniscal repair
Otherwise long term contracture
Causes OAroportional to amount removed

121
Q

Describe the McMurray test

A

Hold knee in flexion with patient supine and hip in flexion
Passively rotate heel of foot causing internal and external rotation
Feel for clicking, popping sound
Look at face for pain
Lots of false positives
Not active - when symptoms occur

122
Q

Describe the Disco test

A

Patient to stand on one leg, flex knee and swing hips using arms - ensure its not just shoulder movement

123
Q

Describe the Thessaly test

A

Same as disco but hold hands and manually rotate - often painful but ask if it is their pain

124
Q

Investigations into meniscal injury

A

Xray useless

MRI 1.5 to 3T - 9T for rats

125
Q

Uses of static testing

A

inform about joint laxity but not stability (dynamic)
Measure dysplacement with force
Assess failure load in cadavas - 6 degrees of freedom 3 roational and 3 translational

126
Q

Uses of dynamic testing

A

JOint stability
Important clinically
Functional testing for grosss evaluation
C arm (biplanar xray motion analysis - cameras on treadmill - predict surgical outcome.
Can also look at stressors and treatments on ACL

127
Q

Use of computer modelling and simulation

A

Plan sur`gery

128
Q

Describe macroanatomy of ACL

A

Band like structure of dense CT
Lies lateral to midline
Posterior inner surface of the lateral condyle (hence resists external rotation - why knee does this after break)
Attaches to fossa anterior and lateral o the medial tibial spine.
Tibial attachment is stronger and thicker.
formed of anteriomedial bundle and PLB.
Non isometric - AMB lengthens in flexion and PLB shortens
Fascicles are parallel in extension and spiral in felxion

129
Q

3 zones of microstructure in ACL

A

1 proximal - less solid and cellular
2 fusiform, dense collagen and oxytalan (elastic), elastic fibres, orderly cells/ fibroblasts
3 many chondroblasts and fibroblasts, less collagen
Dense fibrous CT surrounds and prox to tibial attachment

130
Q

Describe innervation and vascularisation of ACL

A

Posterior articular branches of tibial nerve
Vasomotor
Proprioception (tension feeds to muscles to contract)
Nociceptors

Branches of the middle genicular artery

131
Q

Important factors with MBIM

A

Controls?
Time consumong
Subjective - single operator so better with most

132
Q

Extrinsic mechanisms of injury/ RFs

A

Contact (70% non)
Knee close to full extension with tibial rotaion internally (valgus)
Widened stance
Non contact
Increased valgus and foot pronation, less hip and knee flexion and hip abduction

Prior injury

133
Q

Effects of bracing prophylactically ACL

A

Decreases laxity but dalay jamstring so no effect dynamically

134
Q

Show surface interaction in non contact ACL

A 
More prev on grass
More in competition than practice
Cold weather has lower risk (traction)
MOre on synth/ rubber than wood
No strong assoc with shoe or field
135
Q

Intrinsic RFs for ACL

A

Increased thigh length
INcreased Q angle - quad angle to tibia (female)/ pelvis width
Decrease otch width of femor - small notch= small ACL? smaller in women
JOint laxity (female higher) sig factor
Ham flexibility - less control, delay in activation.
INcreased foot pronation and navicular drop
BMI and age (older than 11 in girls)
Estrogen - matches estrogen cycle, decrease ACL strength, OCP may prevent/ decrease laxity?
Genetics, physical and psychological?

			Greater risk due to
				Anatomic differences e.g. pelvis
				Hormonal differences - oestrogen
				Shoe-surface interface - friction, shoes and weather Neuromuscular factors - delayed or weak hams (females more quad dominant)
136
Q

Movements in pronation

A

Eversion, dorsiflexion and` adduction

137
Q

Types of knee stability assessment and purpose

A

Clinical - diagnosis
Intraoperative - surgical
Function - long term rehab

138
Q

What is the KT-1000

A

Objective measure of knee ant-post laxity in mm

139
Q

Intraoperative measures of knee laxity

A

e.g. computer assisted navigation system.
Integrated images into programm to give anles and location of bones in joint
Improves accuracy

140
Q

Describe fucntional tests - dynamic

A

Optical motion analysis with reflective skin marker and infrared
3 high speed cameras
Ground reaction force plates
Can obtain flexion angle, tibial rotation, valgus angle
Cutting and jumping movements
use visual cue to make spontaneous

141
Q

Examination of ACL

A 
3 tests also
Widespread tenderness
LAt joint tenderness
Medial joint line tenderness if MM.
Ant draw less specific than pivot shift
142
Q

ACL investifation

A

XRay for avulsion - measns ACL rupture
MRI useful f undecided vs bone bruise or tear.
Examination under anaesthesis (EUA) determine instability

143
Q

ACL conserv vs surg?

A

Recurrent, unstable or with activities of daily living

Wants to partake in high risk sport

144
Q

Treating combined MCL and ACL injury

A

Treat MCL first with brace for 6 weeks

145
Q

Rehab post surg ACL

A 
Protected mobilization
US
TENS - trancutaneous electric nerve stim
Strengthening
Slow back to weight baring
Rahab based on patient outcomes
6 months return to sport
Agility testing first
146
Q

Outcomes of conserve ACL treatment

A

Return to sport longer - most in first year
3-6% reinjure
OA
75% get OA due to medial mensical tears

147
Q

Describe epidemiology of ankle sprain injuries

A

Second most common injury after ACL

Mostly in team sports and court games

148
Q

Symptoms of ankle sprain

A 
Feel or hear a pop
Pain on palpation
Discolouration
Swelling (quickly)
Often stop but may continue
149
Q

Bones of foot

A

Cuboid lateral

Navicular and cuniforms medial (deltoid to the cuboid too)

150
Q

How much body weight through tib and fib?

A

5/6

151
Q

Joints at ankle and movements?

A

Talofibular/ talocrural = dorsi and plantar flexion.

Sub talar joit - inversion/ eversion

152
Q

Describe supination and pronation and possible functions

A 
Supination = plantarflexion and inversion. Generate power
Pronation = dorsiflexion and eversion. = adapting to surfaces
153
Q

Describe muscles of the lower leg

A 
Gastrocnemius and soleus
Tib post
- add to foot arch
- ankle plantar
- inversion
- deepest
Flexor hallucis longus
-supports arch of the foot
Flexor digitorum longus
-maintain balance
Tib ant
- Main dorsiflexor and inverter
Extensor hallucis longus and digitorum longus
Peroneus longus and brevis - eversion
Peroneus tertius in 90%
154
Q

relative incidence of different ligament injuries

A

LAteral 75%. Most common AFTL, then CFL then PFTL.
High ankle sprain 10% - syndesmosis spain = anterior inferior/ syndesmotic lig or Interosseous membrane
Medial sprain 5% - deltoid

155
Q

Investigation into ankle sprain

A

Xray is Ottawa ankle rules.

If not then from history and examination

156
Q

Describe the Ottawa ankle rules

A

Xray if:
Pain in mallolar zone and one of:
-tenderness posterior to lat malleoli in 6cm area.
- tender below 5th metatarsal
- unable to weight bare at time of injury and in a&e

OR pain in mid foot zone and one of (medial):

  • tenderness posterior to medial malleoli in 6cm area.
  • tender around navicular
  • unable to weight bare at time of injury and in a&e
157
Q

Describe sensitivity and specificity and relation to Ottawa

A

Sensitive is rate of false neg - tue pos/ (true pos+false neg)
Specificity is rate of false pos- true neg/ true neg + false pos

Ottawa - 100% sensitive
Specificity impaired due to swelling

158
Q

Mechanism of lateral sprain

A

supination/ inversion

159
Q

Mech of medial sprain

A

Plantarflexion/ eversion

160
Q

Mech or high ankle sprain

A

Dorsiflexion and inversion

161
Q

Mech of achilles tendon rupture

A

Forceful plantarflexion- usually voluntary

162
Q

Why is lat more common than medial ankle sprain?

A

fibia drops down during eversion to prevent it occuring - mortise side is longer

163
Q

Acute management of ankle sprain

A 
RICE
Compression (tubigrip - reduces 95% of BF) and elevation good fro pain but may only reduce blood flow temporaily, effects end when compression goes
NSAIDs probably useless
Crutches, early weight baring
Early treatment varied
164
Q

Different strengths of lateral ligaments

A

ATFL weakest then PTFL then CFL however CFL breaks more than PTFL (often due t front to back tearing

165
Q

Grading of lateral ankle sprains

A

Anatomical
1-3 depending on num of ligs
Severity
1 - no laxity, decreased ROM, point tenderness, swellin 2cm, >10deg loss of ROM

166
Q

Examination of ATFL

A 
Ant draw.
Hold foot and tib in neutral flexion
draw foot up so that anterior translation occurs.
Done in 10-20deg plantarflexion.
Dorsiflexed = more bony congruity
167
Q

Examination of CFL

A

Talar tilt test
Held in neutral
Invert the hind foot.
Wont work if plantarflexion as this is AFTL.
Feel for separation of art surfaces of tibia and talus

168
Q

Examination of high ankle sprain

A

x3 - pain in the distal lower leg is pos test.
1 -external rotaton test - knee flexed to 90, ankle neutral, rotate foot outward.
2- squeeze test - compress the tibia and fibula at mid-calf
3- Cross leg test - injured foot on knee of other leg, push down on knee of injured leg.

169
Q

Management of high ankle sprain

A

Walker boot - air cells filling the gap
Walk with crutches and avoid weight baring
Avoid restretching of the ligmanets to induce further injury
Limb rehab

170
Q

Management of minor fracture without limb deformity

A

Walker foot
Avoid beat baring
Rehab

171
Q

Management of major fracture or dislocation

A

Ortho for surg then walker boot after

172
Q

Long term management of ankle sprain of 1-2 grade

A

Early weight baring very important with gait assistive devices/ bracing if needed.
Early manual therapy - lymphatic drainage
Functional exercises - strength, ROM, proprioception/balance and stability.
Target hip and trunk flexors too.
Graded back to activity
Chinese traditional methods e.g. massage and acupuncture.
Pulsed shortwave Diathermy

173
Q

Prophlactic devices in ankle sprain and why the work

A

Neoprene, tapes, orthosis, aircast, lace up brace, taped with shoes.
Increase proprioception, maintain verticle langing, mechanical support

174
Q

Treatment of grade 3 ankle sprain

A

Surgery maybe better/ similar at preventing reinjury but may increase OA, less pain/
Often in sportsmen
Drill tunnel, place tendon graft.
May break fibula with tunnel.
Conserve - wobble board ect to tolerate rupture, no complications.
Conserve first then surgery.

175
Q

Why should immobilisation never be used?

A

Stifness, muscle atophy, loss of proprioception.

176
Q

Anatomy/ function of achilles tendon rupture

A

Gastroc and soleus to calcaneous

Very strong pushing off contraction

177
Q

Examination of achilles tendon rupture

A 
Palpation to feel for rupture
Thompson/ Simmons lest.
Patient lying or kneeling prone.
feet off end of bed
Examiners squeeze calf and should cause foot to plantarflex.
False neg due to plantaris

Repeat with active plantarflexion
Use US-partial rupture

178
Q

Management of achilles tendon rupture

A

Surgery - sew ends together or if at distal attachment drill hole and fix
Rehab following surgery
6 months back to sport
Walking boot for 12 weeks allowing some flexion both ways but angled so achilles is shorter with less strain
Early weight baring.
Rerupture rate higher without surgery but lower risk

179
Q

Risk factors intrinsic for inversion injury

A 
Previous injury
Obesity
Inferior single leg balance.
ROM of calcaneal eversion increase.
Reduced dorsiflexion ROM
180
Q

Risk factors extrinsic for inversion injury

A 
Shoes with air cells
Not stretching before exercise
No orthosis
Artificial turf for footy
Increased exercise
181
Q

How many people seek appropriate help?

A

Less than 30% of Hong Kong pop, some site 15%

182
Q

Discuss prognosis

A

10-30% have chronic probs e.g. synovitis, tendinitis, ankle stiffness, swelling, muscle weakness and giving way

183
Q

Risk of ankle instability

A

5x then risk
Increased talar curve
No external support
No balance or proprioception exercises

184
Q

How is chronic ank instab defined and types.

A

Giving way and/ or feelings of instability
Mechanical - abnormal laxity
Functional - normal laxity but abnormal function e.g. giving way.
Mech leads to func/ several subgroups

185
Q

Complications of chronic ank instab

A

Contributes to ongoing sensorimotor deficits and. Decreased PA and QOL - comorbidities
Post tramatic oA early in life.
Delayed peroneal reaction time, decreased evertor strength, inferior ankle proprioception, changes in gait and function, ankle replacement

186
Q

Treatment of chronic ank instab

A

Manual therpay, Mulligan athletic taping, dry needling maybe, comprhensive rehab program

187
Q

Prevention of ankle sprain methods

A

Prophylactic devices
Functional trainig e.g. woble, bands, ankle disc
Technical training e.g. landing in vollyball - jump straight
Change of game rules e.g. red card in footy, vollyball cant land past central line
Rugbby - reduce number of changes
Education - high cut shoes, People delay treatment, compliance important.
Device - intelligent anti sprain system - gyroscope measuring twisting

188
Q

Aetiology of lateral ankle sprain

A

LAnding on lateral side of foot
Creates a medial moment arm
Causes inversion/ supination as the medially deviated ground reaction force does not pass through the centre of the joint thus creating a twisting torque

2 - delayed peroneal reaction - 57-69ms when falling, longer with more dynamic movements or in patients with chronic ankle instability

189
Q

Methods to study injury mechanism

A

Athlete interview
Clinical studies e.g. Xray, arthroscopy, radiology, video analysis, motion analysis of non-injury simulations - injury like
In vivo studies - small spring gauge - ethics
Injuries during biomechanic experiments
Cadaver and dummy studies
Mathematical modelling (clincal relevence?)
MBIM

190
Q

Significant findings in MBIM in regards to ankle sprain

A

Often degrees of movement arn’t abnormal
However always a high peak inversion velocity.

  • Inversion in all
  • Most plantarflexed some dorsi (supination not only mechanism)
  • All internal rotation
  • All large velocity (lab <200 uninjured, video >200 with injury)
191
Q

How does MBIM work

A

Need dimensions of sport each from organisation.
Need a skeleton model scaled to players height.
Determine foot strike visually
Need 2 high def cameras
Ethics - athlete ID

192
Q

findings from compuational analysis

A

Fixed tibia in space with bones free to move. Found that ligament strain was observed. (this trying to prove temporatl sequance of abnormal movement and ligament damage?)

193
Q

Findings of static testing

A

INversion - damages CFL
Inversion + plantarflexion or internal roation - CFL and ATFL
Inversion + internal + plantarplexion - CFL and ATFL more.

Dynamic testing also concluded this - inversion a common theme

194
Q

Explain monitoring system for ankle device

A

Sensor - measuring ground reaction foce and therefore inversion torque
3 sensors in 3 positions.
Used a support vector machine (SVM) and plate to determine boundary between injured and non injured.
Inversion velocity >500deg/s
True value between 300-500.
Now uses a gyrope at heel - 300deg/s

195
Q

Describe the correction system

A

Initially air bag
Then MR flid - issues with hazardous
Functional electrical simulation - within 40 - 25ms for mechaninal system leaving 15ms for monitor.
In stocking
Limited in battery size - bluetooth takes a lot of energy.

196
Q

Common inuries in running

A

Knee and lower leg, not hip and ankle.
Track - hamstring
Rec - overuse injury

197
Q

RFs for running injuries

A

Increased Q angle >20deg, previous injury, decreased recovery/ increased intensity ect.

198
Q

2 approaches to biomechanics

A 
Theoretical - computersimulation e.g. opensim or anybody - rehab and jury research and performance sport
Experimental:
3D motion analysis
Force analysis
Electromyography
Imaging
199
Q

Describe the Gait cycle

A 
Initial contact
Loading response
mid stance
Terminal stance
Pre swing
inititial swing
mid swing 
terminal swing
200
Q

Aetiology of runners knee?

A

friction between IT band and lateral condyle of the femur

201
Q

Symptoms of runners knee

A

lateral tenderness at knee during stance phase.

Actively induced

202
Q

Difference between Kinetics and kinematics

A 
Kinetics = forces at joing
Kinematics = forces in movements
203
Q

Biomechanics of people with IT band syndrome

A

Increased hip adduction
Tibial internal fotation
Foot eversion?

204
Q

PFP pain - kinematics?

A

Less peak knee flexion, less hip addiction less of other stuff.
3 kinematic profiles individual specific

205
Q

Biomech findings in Achilles tendinopathy

A

Increased foot eversion ROM, velocity - whipping effect and repetitve damage

206
Q

Can a cambered road predispose to injury? why?

A

Yes - less supinated, more pronated foot in middle of road.

207
Q

What is the overuse injury hypothesis?

A

Healthy individuals perform movements differently each time - variability suggests a healthy motor system. Too much causes lack of control.
Increaseing and decreasing coordinative variability predispose to injury

208
Q

How can orthotics help?

A

Increase variability - e.g. in achillies and increase calcaneal angle (less eversion)

209
Q

What is kinematic coordination and how can this be studies?

A

How one segment/ joint works at the same time as another joint.
Either:
Spatial - where in space
Temporal - timing in one relative to same event in other
-vector coding
-continuous relative phsae
-discrete relative phase

210
Q

Describe forces as injury mechanisms

A

Excess force causes tissue damage

211
Q

Describe ground reaction forces of heel strike

A

Impact peak - initial force from IC.
Sharp decrease followed by contaction of muscles and peak force.
Slower decline than after impact peak.
MEasured in force (body weights)

212
Q

Describe VIP, VILR, VALR, FV

A

Vertical impact peak - after initial contact (not in bare foot runners)
VILR - Vertical instantaneous peak loading rate
Vertical average loading rate.
Both done between 20% and 80% of vertical force
FV: Peak vertical force

213
Q

Differences in VIP, VILR, VALR, FV in female injured runners

A

All higher apart from FV

214
Q

Describe acute:chroic workload ratio and clin sig

A

1:1 perfect ratio, increase in acute events then increasing risk of injury. As a beginner everything is acute

215
Q

How many people do heel strike? Who does forefoot and what is this? Same with mid?

A 
70-80%
Forefoot - sprinters, heel doesnt touch ground.
Mid foot (heel and ball at the same time) = increasing speed or running barefoot - not vertical impact peak
216
Q

How does forefoot run change towards the end? does this reuslt in less injuries?

A

Decreased plantarflexion
Decreased GN activation and sligh GN decreased activation
Impact peak returns.
Same number of injuries but more plantar surface and less knee and plantar fasciitis (strengthening of foot muscles).
More achillies tendonopathy (15% increase in average loading rate with NRFS)

217
Q

Limitation of OpenSim and muscle and tendon mech behaviour in vivo

A

Hard to indiviualise model (doesnt account for variation)
Hard to measure
Need right EMG analysis

218
Q

Running techniques used in rehab

A 
All gaints can be used
Orthoses
Kinematic retraining (gait)
Taping
Effects of stretching, foam rolling, strength training
219
Q

Biomech studying and causality of overuse injuries issue?

A

Difficult to causily link

220
Q

Structure of muscle

A

Muscle surrounded by epimysium
Made up of fascicles surrounded by perimysium
Made up of muscle fibres (cells) surrounded by endomysium.
Contain myofibrils made up of myofilaments (actin and myosin)

221
Q

Anatomy of hamstrings muscles

A

Origin at ischeal tuberosity
BF short head - posterior distal femor medial to linea aspera
Long head - fibula head on lateral side
Semitendinosus - medial aspect of proximal tibia of MCL
Semimembranosus - multiple attachments on posteriomedial side of knee (both bones)

222
Q

Describe grades of muscle strain and MRI findings

A

1 - slightly overstreched, some fibres involved, minimal loss of structural integrity of MT unit - no fibre disruption on muscle
or tendon on MRI
2- sig number of fibres involved, partial or incomplete tearing. MRI shows fibre disruption <50% of tendon/muscle width
3 - Complete tear/ rupture - usually close to MT junction as highest eccentric load

223
Q

Causes of muscle strain and normal location

A

Eccentric contraction, normally by MT junction as highest load. Musc

224
Q

How common is complete muscle tear?

A

Rare - often predisposed by tendinopathy

225
Q

Prevalence of hamstring strain in football and rugby

A

Most common injury.

Also common in tract and field

226
Q

Is there a limb dominance with hamstring strain?

A

no

227
Q

Most common locations of muscle strain injury

A

Hamstring, groin, quad, calf

228
Q

when can hip adductor, hip flexor and quad strain occur?

A

Adductor - passing inside of foot
Quad - Straightening knee for running, kicking, jumping
Hip flexor - striking or shooting a ball

229
Q

Recurrence rate of strain injuries?

A

Very high

230
Q

Mech of injury of hamstring strain injury

A

eccentric contraction, particularly high before foot strike/ terminal swing with hip flexion and knee extension, slowing extension caused by quads and assist in hip extension.
BF reaches 110% of normal length when running.
High in hurdles and forceful kicks.

231
Q

MTJ vs muscle belly location of strain

A

Muscle belly less common only if direct trauma or contusion

232
Q

Pathology of muscle strain leading to further damage? How can disorganisation and fibrosis be prevented?

A

BV damage leading to clotting and bleeding (discolouration).
Oedema.
Hypoxia - local ischeamia and further damage.
Myofibrils can regen if basal lamina and microstructure remains as a scaffold.
Early ROM can help reduce disorganisation and fibrosis.

233
Q

Intrinsic RFs for hamstring strain injury

A 
H/Q ratio (contentious)
Age - older
Previous injury
Bilateral asymmetry
Lack of flexibility
Core/ muscle weakness
Ethnicity - afrocarribean or black african.
234
Q

Extrinsic RFs for hamstring strain injury

A

Dehydration
Fatigue
No warm up

235
Q

Effect of biceps femoris aponeurosis size as an RF

A

Proximal Aponeurosis has no correlation with muscle size.
Ratio may be an RF with long head of BF.
Not proven.

236
Q

Signs and symptoms of hamstring strain injury

A 
Sudden sharp pain posterior thigh
Broad ecchymosis (or none)
Audible pop
Sudden limp/ stop playing/ hold hamstrings
Localised stifness, tightness, swelling
Change of ham shape
237
Q

Examination of hamstring strain injury

A

Stiff-legged gait - dont want to flex hip or extend knee as would stretch hamstring
Palpate for muscle belly rupture.
If sciatic a DD then straight leg rasise - tilt head and passively lit legs.
Contract hamstrings against resistance.
Hurdle test - foot onto high table - stretching hams - hip flexion and knee extenion.
Bent-knee strech test - maximally flex hip and knee, passively extend the knee

238
Q

Investigations into hamstring strain and predictions on return to sport

A

Xray - for proximal avulsion fracture
Dynamic ultrasonography - show fluid collecions representing oedema/ haemorrhage acutely.
MRI - Proximal tear - longer return
% of fibres damaged - directly linked with return to sport
Number of fibres involved -
more rapid return with isolated injury of long head of the biceps <50% cross sectional involvement and minimal perimuscular edema (grade 1)

239
Q

Explain biomechanical assessment of hamstring strain injury

A

Isokinetic dynamometer
Moves at same speed (ISOkinetic) e.g. 60m/s. Can determine torque produced throghout both concentric quad and eccentric ham and vice versa. Look at any muscular strength deficits.
Measures torque which is proportional to strength

240
Q

Ideal H/Q ratio? What is this? Other ratios?

A

at least 60%, ideally 75%
eccentric ham:Concentric quad .
conventional ratio = concentric ham:concentric quad

241
Q

Management of noninsertional hamstring strain injury

A

RICE - not running or jumping - inactive too long can stretch and scar hams

Later - activity modification, stretching, early physcial therapy, NSAIDs, massage, US, electrical stimulation
Shockware good for proximal injury tendinopathies
IM corticosteroid?
Regular gentle stretches
(if not fully recovered when return then x11 risk of re-strain)
Strengthening

242
Q

Management of complete hamstring tear

A

Surgery - proximal or complete tear.
Incision across gluteal crease - inferior line of buttock.
Suture tendon to bone
Fix orientation at flexion of hip
Braced with hip orthotic in 30-40deg of flexion to limit stress to the surgery site followed by rehab.
High satisfaction rate and 75% of strength on recovery.

243
Q

Rehab after surgical repair of hamstring strain injury

A

DVT - asprin
Start with toe touch and crutches
Progressively weight bare more with use of hip orthotic
Remove orthotic and full weight bare with isotonic exercises (not isometric) - can use aqua therapy
Dynami training and isometric stengthening - builds pressure.
Sport specific training
Allow full return when leg has 90% strength of other leg on isokinetic testing

244
Q

Complications of hamstring surgery

A

Sciatic nerve damage -neuropraxia - burning, weakness of foot
Cutaneous nerve damage
Infections of GI and GU
Rerupture and loss of strength.

245
Q

Hamstring strengthening exercises

A

Supine bent knee bridge walk out exercise - eccentric with buttock off ground

246
Q

Risks of steroid injection

A

Fat atrophy, skin hyperpigmentation, infection, future rupture, post injection pain

247
Q

Future treatments of hamstring strain injury

A

PRP - platelet rich plasma - contain GFs in granules, safe
Cell therapy - stem cells
Tissue engineering
Growth factors

248
Q

Management of proximal insertional injury, complications

A

If 3 muscle involved or 2 and >2cm of retraction then surgery - within 4 weeks, earlier the better, less good for chronic ruptures.
If not surgery then very aggressive rehab - also targets core, hip, quads.
consider steroid, PRP.
Symptoms often persist if not op used e.g.
Pain on sitting
Weakness in ham actions
Deformity
Sciatic nerve affected from fibrosis (surgical debridement needed

249
Q

Describe distal insertional injuries

A

BF or ST, ST then surg. BF conserve, if fails surg, MRI to confirm.

250
Q

Describe prevention of hamstring strain injuries

A

Nordic hamstring exercise (Fifa 11+ warm up programme - the 11)
Hold lower leg with person kneeling
Body slowly leans forwards into pressup
Keep thighs straight
Perform slowly but can speed up
1 set of 3-5 reps
40% reduction.
Eccentric exercices key
Functional positioning to absorb loadis before and during heel strike
Identify and correct imbalance and optimise neural timing

251
Q

Describe MTSS RFs and mechanism

A 
Flat or high foot arch.
Attachment of soleus to Medial tibia.
Repeated trauma to connective tissue muscle tissue
Training errors in 60% of cases
Too much too soon.
Landing on supinated foot - pronating furing loading causing eccentric contraction of soleus and damage. 
Change in shoes abruptly
Change in surface
Sports with sudden start stops
252
Q

Symptoms of MTSS, different from a stress fracture?

A

Dull ache, hurts when you press and on activity lower 2/3.
Stress fracture more pain that builds
Increase in chronicity may get pain at ambulation/rest

253
Q

Examination of MTSS

A

Look at calcaneous - in or everted
Look at arch - if flat - get to stand on tipotes - arch will appear unless bony fusion
Look at calf length assively due plantar (soleus) and dorsiflexion (gastroc)
Palpate medial boarder, look for oedema and warmth

254
Q

MTSS treatment

A 
Rest until pain free.
NSAIDs, ICE.
Use of orthotics, 
- Soft - proprioception
- Hard - mechanical -
- Both can prevent pronation
change shoes regularly
Non weight baring activity modification
Do up laces
Calf stretching 3x a day - gastroc or soleus.
Rahab:
-when pain free
-Start 505 OF PREVIOUS INTENSITY/ DISTANCE ON soft level surface
- Add 10% per week for 3-6 weeks
-Strength and balance training 
-Plyometrics
255
Q

4 joints of the shoulder joint complex

A

Glenohumeral
Acromialclavivular
Sternoclavicular
Scapulothoracic joint (not a true joint)

256
Q

Describe the 2 differences in causes of shoulder instability

A

trauma e.g. rugby

Flexibility e.g. gymnastics - mobile anyway and pops out.

257
Q

Describe the rotator cuff muscles

A

Supraspinatus

Infraspinatus and teresmajor (external rotation)

Subscapularis (internal rotation)

All stabalise

258
Q

Describe shoulder joint (subacromial) impingement syndrome, who is at risk and why?

A

Gym monkeys, swimmers, tennis players, builders (repeated overhead movements) - sqeeze soft tissues in subacromial space
Inflammation of subacromial bursa or supraspinatus tendon
Arthritis and swelling

259
Q

Why assess shoulder ROM? how?

A

Frozen shoulder - joint capsule scarring/ thickening

Abley scratch test- touch opposite scapula - over (abductionand external) and under (adduction and internal)

260
Q

How to assess of impingement signs

A

Examination

Hawkins test

  • shoulder flex 90 deg, elbow 90 deg
  • parrallel to groung
  • raise arms against examiner pushing down
  • pain = supraspinatus, popping sesnsaiton too

Neer’s test

  • 90deg at shoulder
  • internally rotated
  • Passive flexion
  • Hold scapula - prevent scapulothoracic gliding compensatory movement
  • pain = impingement
261
Q

How to rule out acromioclavcular joint dysfunction

A

Cross over/ scalf test

  • Arm 90deg over body
  • draw medially
  • Neg in impingement
  • forces acromium into distal end of clavical.
262
Q

Test for rotator cuff tear

A

Empty can test

  • Internal rotation, elevate arm again assessor resistance
  • infraspinatus/ teres minor
263
Q

History of AC joint dysfunction

A

Landing on outstretched arm

264
Q

How is impingement syndrome treated?

A

Conservative first then surgery.
ROM, strengthening, rest, posture, pain NSAID, injection of LA or steroid
Surery - arthoscopic repair - , removal of imping structure e.g. inflamed burse or bone spurs

265
Q

Treatment of rotator cuff tear

A

Conserve - Full ROM first then strengthening
Arthroscopic repair- using patch or salvage
Rehab/ Prehab
Control of movement
Stretching and flexibility.
PROMs - rated score - many live with and asymptomatic e.g. UCLA.
Arm immobilised for 6 weeks after surgery

266
Q

Describe tendinopathy at the elbow, causes

A 
Gold - both
Tennis
Epicondylitis or epicondalgia
common extensor tendon
Traumatic, repetitive stain
Tendinopathy
267
Q

Symptoms of tennis elbow

A

Pain, swelling. Present on extension, gripping stuff, twisting
Stiffness in morning
Weakness in forearm
Point tenderness of epicondyle
Middle more painful in tennis
Tennis, capenters or workmen with hammer get tennis

268
Q

Treatment of tennis elbow

A 
Activity modification
Stretches and strengthening (eccentric)
-e.g. usign rubber bar - injured hand in extension and uninured in flexion infornt of body and eccentric contraction.
Steroid injection?
New balls, lighter racket, diff strings.
Surgery extreme
269
Q

Physical examination of the elbow

A

Cozen’s test-
Extend elbow and wrist extension against aggressor
Chair lift test - grip back of chair and attempt to raise

270
Q

Prevention of tennis elbow

A 
Decrease playing time
Stay fit
Strengthen muscles of forearm, upper arm, shoulder and upper back
Increase stability of joints
Use appropriate equipement
tennis elbow bands (anecdotal)
271
Q

What is the volar plate?

A

Attachment of collateral to dense FC (underneath) gives congruity and maintains stability

272
Q

Extensor digitorum attatchments

A

Superficialis splits - attaches to middle phalange

Profundus - to distal phalange

273
Q

What is mallet finger?

A 
rupture of extensor tendon or tear.
flexion deformity
1/3 have avulsion
From blunt impact
Also known as blunt finger or baseball finger
274
Q

Signs and symptoms of mallet finger?

A

Pain
Swelling
flexion deformity

275
Q

Examination and investigations of mallet finger

A

Passive and active ROM assessment - entrapment of bony or soft tissue (need op)
Xray
Loss of extension

276
Q

Treatment of Mallet finger, risks, follow up

A

Early splinting with ring splint or aluminium splint for 6 weeks, if flexion then restart. If over extended then necrosis can occur. Follow up every 2 weeks - compliance
May still participate in athletic events.

Earlier treatment better
Spint in full extension for 6 weeks if no aulsion or avulsion les than 1/3 of joint
If no extension then ortho
Can continue to do athletics
Same follow up as mallet
May need later recocontraction
277
Q

Central slip extensor tendon injury describe

A

LAteral extensor tendon

PIP forcibly flexed when actively extended e.g. ball

278
Q

Examination of central slip extensor tendon injury

A

Hold in 15-30 deg of flexion
Ask to extend
Tenderness over dorsal aspect of the middle phalynx

279
Q

What deformity can central slip extensor tendon injury cause and why?

A

Boutonniere deformity.

INtact lateral bands slip inferiorly causing extention at MCP, flexion at PIP and extesion and DIP.

280
Q

What is Jersey finger?

A

Forced extension of DIP during active flexion - over stretched tendon.

281
Q

Symptoms of Jersey finger?

A 
Bruising
Early swelling
Pain
Pop or rip felt/ heard
Finger extended at rest
Bruising after 48hrs
Lump on palm of finger if torn tendon bunches
Ring finger commoest
282
Q

Examination of Jersey finger

A

Flexor profundus - hold MCP and PIP and ask to flex DIP.
Superficialis-
Hold other tendons and as to flexjust injured fingers

283
Q

Treatment of Jersey finger

A

Splinting may not help Surgical repair to reattach then palstic splint for 6 weeks

284
Q

Collateral ligament injury symptoms, examination and investigation and treatment

A

Forced lateral movement either way at IPJs
Often PIP- jammed fingers
Basketball
Pain at lig
Test by applying valgus or varus stress with joint at 30deg flex and MCP at 90
Compare lacity with other hand/ fingers
Xray for avulsion
If stable and no fracture then strapping - don’t leave little finger exposed.

Sports Science Y3 S1 (5 decks)

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