Sports Inuries Flashcards
Medial ligament of the anlkle role and attachments
Deltoid ligament.
Navicular, talus, calcaneus.
Resists eversion.
Lateral ligament of the ankle role and attachments
ant and post talofibular and fibulocalcaneal.
Resists inversion.
What is the sequence of prevention?
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.
What is a sports injury
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
Broad classification of sports injury
Time loss injury or medical attention injury
Some potention consequences of sport injury
Pain, Financial
Repetitive muscle straign, osteoarthritis, bone fracture, lig reupture, tendonopathy
What is epidemiology
The study of disease in relation to populations
What is incidence
The number of new cases per 1000 people within a set population in a set time period.
What factors could cause variation in studys?
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.
Why is prospective better than retrospective
Can measure many exposures Count number of episodes No Recall bias Single standard of diagnosis. Can prove temporal sequence
What is a stress fracture
Hariline fractures that cant be imaged via Xray
Variate in how you measure the nature of a sports injury
Acute (traumatic) vs chronic (overuse)
Tendonitis vs tendopathy. Failure to heal.
Difference between contusion vs laceration
Skin cut vs un cut
How is severity measured? 6 criteria
Time loss (working or sport), medical/ economic cost, nature of injury, nature of treatment, permanent damage.
How is severity measure in terms of days lost?
<7 minor
8-21 moderate
>21 severe
Describe the spectrum of tissue regenrates
Fastest to slowest
Bone, muscle, tendon, ligament, meniscus, cartilage
Costs of sports injuris
Direct (medical) and indirect
Difference between systematic review and meta analysis
Synthetic output of one value, not all included
Describe intinsic factors
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)
Whats the difference between relative risk and odds ratio
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.
Why is a association not always causal
unknown factor may cause both
Confounder
Also an unknow factor may cause one thing that causes another
RFs for sports injuries
Loads
Describe the causation model
Intrinsic factors predispose an athlete. Exposure to extrinic factors result in a susceptible adult.
An inciting event/ mechanism of injury causes an injury
Difference between mechanism and diagnossi
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
What does the injury incidence assessment depend on?
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
What is the sequence of prevention? What factors should be ascertained?
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
First step of sequence of prevention. Best practice
Comparable measure e.g. 1000 hours of sport participation (variable measure)
Can be retro or prospective. Bare in mind the representativeness of sample.
Second step of sequence of prevention from Van Mechelen 1992 (review of concepts)
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
Findings from Taimela et al 1990 - intrinsic RFs
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
Findings from Bahr & Holme (2003) Metholodical sport injuries
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.
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.
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.
Explain common problems with SEM in the army
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)
Difference between origin and insertion
Origin close and insertion distal.
Does a tendon lengthen or schorten during muscle contraction?
Stay the same
Why can running in boots be an RF for achillies tendinopathy?
Compression of tendon is a RF
Describe the microstructure of a tendon
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
Movement that precipitates achillies tendon rupture
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.
Cause of subacromial impingement (painful arc)
Posture causing tendon (rotator cuff) impingement
Describe tendinopathy pain
Morning stifness/ pain (shortening) Pain commencing and after activity. Eases with warm up Pain on palpation Pain at specific site Insidious onsett
Causitive factors of tendinopathy intrinsic (achillies) (RFs)
Giat
Heavy heel strike
Double heel lift
Motor patterning
BMI
Previous injury
Age
Posture/Allignment
DM/ dyslipidaemia
Causitive factors for tendinopathy extrinsic
Training errors
Frequency
Intensity
Energy storage activities
Footware
Exercise
Medication e.g. fluroquinolones or steroid
Describe the continuum model
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.
What does disrepair look like?
Increased cellularity and ground substance (occurs initially).
Focal area of disorganised collagen.
Neurovascular ingrowth (cause of pain?)
Explains why NSAIDs may not help
Describe the pathology of acute/ reactive tendinopathy
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
Describe the cause of pain in acute tendinopathy
Hypoxic - increased tissue fluid
Hypersensitivity of tenocytes
Describe how long acute tendinopathy may last for
a few days
Describe pathology of dysrepair tendinopathy
Focus of holes of collagen disorganisation
More ground substance
Upregulation of neo vascularisation factors e.g. VEG F
Myofibroblasts
MOre chondrocytic cells
causes of Pain in dysrepair tendinopathy
new vessels with nerves (more factors e.g. glutamate and substance P) Pain centralisation (thinks it's more important than it is)/ neuronal sesnitivity
Degenerative tendinopathy pathology
Significant matrix disorganisation cell death - apoptosis - hypoxia due to more cells Increased type III. Hyaline degeneration Tenocyte echaustion Very disorganised Little reversibility older people
Difference in swelling in types of tendinopathy
Fusiform in reactive and dysrepair possible (and in reactive on degenerative).
Nodular in degen
Response to load in different types
sensitive in acute
less sensitive in dysrepair
Occasional grumbles in degen
Treatment for reactive
Rest/ unload (stress shielding)
Use ice
Adress compressive loads (concentric) and positions
What does rehabilitation address?
ROM
Pain
Contractile deficits
Movement patterns
Describe some outcome measures used in achillies.
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
Causes of pain in degenerative
hypoxic
Centralisation
Neural
Describe the appearence of denerative on ultrasound and H&E
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
Describe a progressive loading stage 1
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
Describe a progressive loading stage 2
Concentric or eccentric medium load
Open and close chain if possible (fixed joint vs unfixed distal)
Stage 1 on days off
Describe a progressive loading stage 3 and options
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)
Describe a progressive loading stage 4
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
Summarise total program
Progressively add stages but add sparsely at first and increase frequency
May add ESWT.
Return to sport on high load days but continue monitoring
Other things considered in treatment other than load
Biomechanics Flexibility Lumbar spine Neural mobility Associated injury
Ensure
coontinued education, maintain strength and gradula intro of novel activity
Other less conventional treatments
Steroid injection
LA injection (p
Dextrose injection
PRP/ autologous blood injection
Describe the functions of ligaments
Keep articulating surfaces together (limit mobility)
Minimise unwanted joint movement
Provide joint stability
What is viscoelasticity? how is this clinically relevant?
Can stretch slowly under tension but return to original shape.
Rapid strectching however can rupture e.g. grass
What is the Beighton score? genetic variation in stretching?
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
What is the cut off score for Beighton?
Problems with score?
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
Describe the hypermobility questionnaire? Cut off
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?
How do scores relate to hypermobility syndrome?
Don’t necessarly as asymptomatic often
Difference between structure of tendon and ligament
Ligaments have a more wavey appearence and slightly less parallel than tendons allowing lengthening (spring) fibroblasts les parallel.
Grades of ligamnet tear
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
Treatment of ATFL tear?
Conservative
train muscle, strenght, speed, proprioception
Why might women be more prone to ACL injury?
More hypermobile, more valgus positon??
Where is the pain in tendonopathy?
Normally at attachment but achillies can be in the centre
Pathology of underloading and tendon
Hyalin degen Matrix disorganisation Angiofibroblastic hyperplasia Angiofibroblastic hyperplasia. Mostly reversible in animals
Treatment for reactive… drugs?
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
Treatment for late tendon dysrepair/degeneration?
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
General points about dislocation
Xray for fracture May need diazepam or GA to relocate Early protection Early mobilization Muscle strengthening
Grade 3 tear and pain?
May be none as sensory fibres can be divied
MCL injury mechanism
Valgus force on partially flexed knee
MCL symptoms
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
MCL treatment
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
PCL function
Resists posterior draw of tibia and external rotation
Stronger than ACL
Often underdiagnosed
PCL damage associated injuries
LCL/ popliteus
1/4 have meniscal damage
PCL features
History
skiier
Poorly defined back of knee or calf
No swelling as extrasynovial
Exam
Posterior draw test
Posterior sag
PCL mechanism
Direct blow to anterior tibia when flexed
PCL investigation
Xray - avulsion
MRI if posteriolater cornal damage is suspected
Treatment of PCL
Conserve
Rebab - quad heacy
immobalise for 2-3 weeks if complete rupture
Good functional result
Surg
Sig posterolateral damage
Medial ligament incidence and treatment
Stronger than lateral and inversion rarer.
Same treatment as alteral but takes twice as long
Pott’s fracture symptoms, management and treatment
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
Maisonneuve fracture
Fracture of proximal fib with complete rupture of AFTL and interosseus membrane High impact sports Xray often misses Can reduce spontaneously Refer to ortho
4 zones of lig to bone
Lig Fibrocartilage Mineralised fibro Bone Superficial fibres to periosteum Depp directly to bone at acute angles
3 stages of lig repair
Heamatoma formation
Reparative phase - fibroblast prolif and matrix
Remodelling - reallignment of collagen over years
Future treatments of ligs
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
Describe valgus/ varus
Valgus is knee in toe out - lateral force (external rotation)
Varus is medial force
What is the mechanism of ACL damage
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
Function of ACL
Stability
Reist anterior translocation
Resist internal rotation
Symptoms/ sings of ACL injury
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
Potential injured structures from ‘knee in toe out’
ACL, LM, MCL
Potential injured structures from ‘knee out toe in’
ACL, MM, LCL
What is distraction/ compression
Into or away from - cause of knee damage but rare
Describe biomechanics of what happens in ACL injury
(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)
How do we know about biomechs of ACL injury?
From model based image matching (MBIM) motion analysis technique - skeleton matched frame by fram using animation software
What is genus valgum and varum
Posture that is naturally in or out - feet appear closer or more separate
What is the lachman test? Limitation?
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
What is the anterior draw test? Looking for? cause of false neg?
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
Describe the pivot shift test. limitations?
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
How is ACL diagnosed?
Clinically or via MRI - solid black band - torn then ligher in coler +/- disorganisation or breakage
Arthroscopy
Aims of ACL treatment
Return to normal joint staboloty, ROM, muscle function, physical activity levels
Describe surgical techniques to repair torn ACL
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
Describe petalla graft
PBP Central third used 140% of strength Bone to bone healing better Worse scan Can damage nerves around patella
Describe hamstring graft
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
Describe bone to tendon healing
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
What factors may enhance bone to tendon healing
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
Describe Bridge enhanced ACL repair (BEAR)
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.
Describe function of the menisci
Prevent damage to articular surfaces - shock absorber
Joint stability
DIstribute forces over a maximal area
Symptoms of mensical injury
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.
Mecanism of injury in meniscal injury
Twisting, turning, cutting, robust in 20s
Normally knee out toe in.
Jumping more likely to be meniscal than ACL
Indications for surgery of meniscal injury
Loss of full extensionq
Failure of conserve
Within 2 weeks of swelling going down
Describe surgical proceedures for meniscal injury
Partial menisectomy
Arthroscopic meniscal repair
Otherwise long term contracture
Causes OAroportional to amount removed
Describe the McMurray test
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
Describe the Disco test
Patient to stand on one leg, flex knee and swing hips using arms - ensure its not just shoulder movement
Describe the Thessaly test
Same as disco but hold hands and manually rotate - often painful but ask if it is their pain
Investigations into meniscal injury
Xray useless
MRI 1.5 to 3T - 9T for rats
Uses of static testing
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
Uses of dynamic testing
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
Use of computer modelling and simulation
Plan sur`gery
Describe macroanatomy of ACL
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
3 zones of microstructure in ACL
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
Describe innervation and vascularisation of ACL
Posterior articular branches of tibial nerve
Vasomotor
Proprioception (tension feeds to muscles to contract)
Nociceptors
Branches of the middle genicular artery
Important factors with MBIM
Controls?
Time consumong
Subjective - single operator so better with most
Extrinsic mechanisms of injury/ RFs
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
Effects of bracing prophylactically ACL
Decreases laxity but dalay jamstring so no effect dynamically
Show surface interaction in non contact ACL
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
Intrinsic RFs for ACL
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)
Movements in pronation
Eversion, dorsiflexion and` adduction
Types of knee stability assessment and purpose
Clinical - diagnosis
Intraoperative - surgical
Function - long term rehab
What is the KT-1000
Objective measure of knee ant-post laxity in mm
Intraoperative measures of knee laxity
e.g. computer assisted navigation system.
Integrated images into programm to give anles and location of bones in joint
Improves accuracy
Describe fucntional tests - dynamic
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
Examination of ACL
3 tests also Widespread tenderness LAt joint tenderness Medial joint line tenderness if MM. Ant draw less specific than pivot shift
ACL investifation
XRay for avulsion - measns ACL rupture
MRI useful f undecided vs bone bruise or tear.
Examination under anaesthesis (EUA) determine instability
ACL conserv vs surg?
Recurrent, unstable or with activities of daily living
Wants to partake in high risk sport
Treating combined MCL and ACL injury
Treat MCL first with brace for 6 weeks
Rehab post surg ACL
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
Outcomes of conserve ACL treatment
Return to sport longer - most in first year
3-6% reinjure
OA
75% get OA due to medial mensical tears
Describe epidemiology of ankle sprain injuries
Second most common injury after ACL
Mostly in team sports and court games
Symptoms of ankle sprain
Feel or hear a pop Pain on palpation Discolouration Swelling (quickly) Often stop but may continue
Bones of foot
Cuboid lateral
Navicular and cuniforms medial (deltoid to the cuboid too)
How much body weight through tib and fib?
5/6
Joints at ankle and movements?
Talofibular/ talocrural = dorsi and plantar flexion.
Sub talar joit - inversion/ eversion
Describe supination and pronation and possible functions
Supination = plantarflexion and inversion. Generate power Pronation = dorsiflexion and eversion. = adapting to surfaces
Describe muscles of the lower leg
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%
relative incidence of different ligament injuries
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
Investigation into ankle sprain
Xray is Ottawa ankle rules.
If not then from history and examination
Describe the Ottawa ankle rules
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
Describe sensitivity and specificity and relation to Ottawa
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
Mechanism of lateral sprain
supination/ inversion
Mech of medial sprain
Plantarflexion/ eversion
Mech or high ankle sprain
Dorsiflexion and inversion
Mech of achilles tendon rupture
Forceful plantarflexion- usually voluntary
Why is lat more common than medial ankle sprain?
fibia drops down during eversion to prevent it occuring - mortise side is longer
Acute management of ankle sprain
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
Different strengths of lateral ligaments
ATFL weakest then PTFL then CFL however CFL breaks more than PTFL (often due t front to back tearing
Grading of lateral ankle sprains
Anatomical
1-3 depending on num of ligs
Severity
1 - no laxity, decreased ROM, point tenderness, swellin 2cm, >10deg loss of ROM
Examination of ATFL
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
Examination of CFL
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
Examination of high ankle sprain
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.
Management of high ankle sprain
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
Management of minor fracture without limb deformity
Walker foot
Avoid beat baring
Rehab
Management of major fracture or dislocation
Ortho for surg then walker boot after
Long term management of ankle sprain of 1-2 grade
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
Prophlactic devices in ankle sprain and why the work
Neoprene, tapes, orthosis, aircast, lace up brace, taped with shoes.
Increase proprioception, maintain verticle langing, mechanical support
Treatment of grade 3 ankle sprain
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.
Why should immobilisation never be used?
Stifness, muscle atophy, loss of proprioception.
Anatomy/ function of achilles tendon rupture
Gastroc and soleus to calcaneous
Very strong pushing off contraction
Examination of achilles tendon rupture
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
Management of achilles tendon rupture
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
Risk factors intrinsic for inversion injury
Previous injury Obesity Inferior single leg balance. ROM of calcaneal eversion increase. Reduced dorsiflexion ROM
Risk factors extrinsic for inversion injury
Shoes with air cells Not stretching before exercise No orthosis Artificial turf for footy Increased exercise
How many people seek appropriate help?
Less than 30% of Hong Kong pop, some site 15%
Discuss prognosis
10-30% have chronic probs e.g. synovitis, tendinitis, ankle stiffness, swelling, muscle weakness and giving way
Risk of ankle instability
5x then risk
Increased talar curve
No external support
No balance or proprioception exercises
How is chronic ank instab defined and types.
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
Complications of chronic ank instab
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
Treatment of chronic ank instab
Manual therpay, Mulligan athletic taping, dry needling maybe, comprhensive rehab program
Prevention of ankle sprain methods
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
Aetiology of lateral ankle sprain
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
Methods to study injury mechanism
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
Significant findings in MBIM in regards to ankle sprain
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)
How does MBIM work
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
findings from compuational analysis
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?)
Findings of static testing
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
Explain monitoring system for ankle device
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
Describe the correction system
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.
Common inuries in running
Knee and lower leg, not hip and ankle.
Track - hamstring
Rec - overuse injury
RFs for running injuries
Increased Q angle >20deg, previous injury, decreased recovery/ increased intensity ect.
2 approaches to biomechanics
Theoretical - computersimulation e.g. opensim or anybody - rehab and jury research and performance sport Experimental: 3D motion analysis Force analysis Electromyography Imaging
Describe the Gait cycle
Initial contact Loading response mid stance Terminal stance Pre swing inititial swing mid swing terminal swing
Aetiology of runners knee?
friction between IT band and lateral condyle of the femur
Symptoms of runners knee
lateral tenderness at knee during stance phase.
Actively induced
Difference between Kinetics and kinematics
Kinetics = forces at joing Kinematics = forces in movements
Biomechanics of people with IT band syndrome
Increased hip adduction
Tibial internal fotation
Foot eversion?
PFP pain - kinematics?
Less peak knee flexion, less hip addiction less of other stuff.
3 kinematic profiles individual specific
Biomech findings in Achilles tendinopathy
Increased foot eversion ROM, velocity - whipping effect and repetitve damage
Can a cambered road predispose to injury? why?
Yes - less supinated, more pronated foot in middle of road.
What is the overuse injury hypothesis?
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
How can orthotics help?
Increase variability - e.g. in achillies and increase calcaneal angle (less eversion)
What is kinematic coordination and how can this be studies?
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
Describe forces as injury mechanisms
Excess force causes tissue damage
Describe ground reaction forces of heel strike
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)
Describe VIP, VILR, VALR, FV
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
Differences in VIP, VILR, VALR, FV in female injured runners
All higher apart from FV
Describe acute:chroic workload ratio and clin sig
1:1 perfect ratio, increase in acute events then increasing risk of injury. As a beginner everything is acute
How many people do heel strike? Who does forefoot and what is this? Same with mid?
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
How does forefoot run change towards the end? does this reuslt in less injuries?
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)
Limitation of OpenSim and muscle and tendon mech behaviour in vivo
Hard to indiviualise model (doesnt account for variation)
Hard to measure
Need right EMG analysis
Running techniques used in rehab
All gaints can be used Orthoses Kinematic retraining (gait) Taping Effects of stretching, foam rolling, strength training
Biomech studying and causality of overuse injuries issue?
Difficult to causily link
Structure of muscle
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)
Anatomy of hamstrings muscles
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)
Describe grades of muscle strain and MRI findings
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
Causes of muscle strain and normal location
Eccentric contraction, normally by MT junction as highest load. Musc
How common is complete muscle tear?
Rare - often predisposed by tendinopathy
Prevalence of hamstring strain in football and rugby
Most common injury.
Also common in tract and field
Is there a limb dominance with hamstring strain?
no
Most common locations of muscle strain injury
Hamstring, groin, quad, calf
when can hip adductor, hip flexor and quad strain occur?
Adductor - passing inside of foot
Quad - Straightening knee for running, kicking, jumping
Hip flexor - striking or shooting a ball
Recurrence rate of strain injuries?
Very high
Mech of injury of hamstring strain injury
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.
MTJ vs muscle belly location of strain
Muscle belly less common only if direct trauma or contusion
Pathology of muscle strain leading to further damage? How can disorganisation and fibrosis be prevented?
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.
Intrinsic RFs for hamstring strain injury
H/Q ratio (contentious) Age - older Previous injury Bilateral asymmetry Lack of flexibility Core/ muscle weakness Ethnicity - afrocarribean or black african.
Extrinsic RFs for hamstring strain injury
Dehydration
Fatigue
No warm up
Effect of biceps femoris aponeurosis size as an RF
Proximal Aponeurosis has no correlation with muscle size.
Ratio may be an RF with long head of BF.
Not proven.
Signs and symptoms of hamstring strain injury
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
Examination of hamstring strain injury
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
Investigations into hamstring strain and predictions on return to sport
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)
Explain biomechanical assessment of hamstring strain injury
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
Ideal H/Q ratio? What is this? Other ratios?
at least 60%, ideally 75%
eccentric ham:Concentric quad .
conventional ratio = concentric ham:concentric quad
Management of noninsertional hamstring strain injury
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
Management of complete hamstring tear
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.
Rehab after surgical repair of hamstring strain injury
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
Complications of hamstring surgery
Sciatic nerve damage -neuropraxia - burning, weakness of foot
Cutaneous nerve damage
Infections of GI and GU
Rerupture and loss of strength.
Hamstring strengthening exercises
Supine bent knee bridge walk out exercise - eccentric with buttock off ground
Risks of steroid injection
Fat atrophy, skin hyperpigmentation, infection, future rupture, post injection pain
Future treatments of hamstring strain injury
PRP - platelet rich plasma - contain GFs in granules, safe
Cell therapy - stem cells
Tissue engineering
Growth factors
Management of proximal insertional injury, complications
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
Describe distal insertional injuries
BF or ST, ST then surg. BF conserve, if fails surg, MRI to confirm.
Describe prevention of hamstring strain injuries
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
Describe MTSS RFs and mechanism
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
Symptoms of MTSS, different from a stress fracture?
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
Examination of MTSS
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
MTSS treatment
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
4 joints of the shoulder joint complex
Glenohumeral
Acromialclavivular
Sternoclavicular
Scapulothoracic joint (not a true joint)
Describe the 2 differences in causes of shoulder instability
trauma e.g. rugby
Flexibility e.g. gymnastics - mobile anyway and pops out.
Describe the rotator cuff muscles
Supraspinatus
Infraspinatus and teresmajor (external rotation)
Subscapularis (internal rotation)
All stabalise
Describe shoulder joint (subacromial) impingement syndrome, who is at risk and why?
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
Why assess shoulder ROM? how?
Frozen shoulder - joint capsule scarring/ thickening
Abley scratch test- touch opposite scapula - over (abductionand external) and under (adduction and internal)
How to assess of impingement signs
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
How to rule out acromioclavcular joint dysfunction
Cross over/ scalf test
- Arm 90deg over body
- draw medially
- Neg in impingement
- forces acromium into distal end of clavical.
Test for rotator cuff tear
Empty can test
- Internal rotation, elevate arm again assessor resistance
- infraspinatus/ teres minor
History of AC joint dysfunction
Landing on outstretched arm
How is impingement syndrome treated?
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
Treatment of rotator cuff tear
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
Describe tendinopathy at the elbow, causes
Gold - both Tennis Epicondylitis or epicondalgia common extensor tendon Traumatic, repetitive stain Tendinopathy
Symptoms of tennis elbow
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
Treatment of tennis elbow
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
Physical examination of the elbow
Cozen’s test-
Extend elbow and wrist extension against aggressor
Chair lift test - grip back of chair and attempt to raise
Prevention of tennis elbow
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)
What is the volar plate?
Attachment of collateral to dense FC (underneath) gives congruity and maintains stability
Extensor digitorum attatchments
Superficialis splits - attaches to middle phalange
Profundus - to distal phalange
What is mallet finger?
rupture of extensor tendon or tear. flexion deformity 1/3 have avulsion From blunt impact Also known as blunt finger or baseball finger
Signs and symptoms of mallet finger?
Pain
Swelling
flexion deformity
Examination and investigations of mallet finger
Passive and active ROM assessment - entrapment of bony or soft tissue (need op)
Xray
Loss of extension
Treatment of Mallet finger, risks, follow up
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
Central slip extensor tendon injury describe
LAteral extensor tendon
PIP forcibly flexed when actively extended e.g. ball
Examination of central slip extensor tendon injury
Hold in 15-30 deg of flexion
Ask to extend
Tenderness over dorsal aspect of the middle phalynx
What deformity can central slip extensor tendon injury cause and why?
Boutonniere deformity.
INtact lateral bands slip inferiorly causing extention at MCP, flexion at PIP and extesion and DIP.
What is Jersey finger?
Forced extension of DIP during active flexion - over stretched tendon.
Symptoms of Jersey finger?
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
Examination of Jersey finger
Flexor profundus - hold MCP and PIP and ask to flex DIP.
Superficialis-
Hold other tendons and as to flexjust injured fingers
Treatment of Jersey finger
Splinting may not help Surgical repair to reattach then palstic splint for 6 weeks
Collateral ligament injury symptoms, examination and investigation and treatment
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.
