Classification of Injuries
Sports Injury Classification
Acute / Traumatic
•  extrinsic causes: direct blow, collision, impact
•  intrinsic causes: muscle forces, joint loadings
Acute vs Overuse Injuries
v  increasing frequency
of overuse injuries
v  acute injuries:
high velocity
uncontrolled impacts macro-trauma
Muscle Strains
v  among most common
sporting injuries
v  muscle fibres fail under
imposed demands
v  recurrent (particularly
hamstrings)
Muscle Strains
Grade I small # fibres ruptured, pain
localised, no strength loss
Grade II
large # fibres ruptured,
reduced strength, swelling
& pain limited movement
Grade III complete tear of muscle,
muscle-tendon junction,
significant strength loss, obvious
visual defect
Biomechanical & Anatomical
Factors in Muscle Strains
v  sudden acceleration
or deceleration v  neural innervation
Biomechanical & Anatomical
Factors in Muscle Strains
v  eccentric action mode
² force velocity curve
v  biarticular muscles pre-disposed
² hamstrings
² rectus femoris
² medial gastrocnemius
Applying Exercise Physiology Knowledge
Draw a Force-Velocity Curve on the Graph below
Contraction Force
200%
100%
Sarcomeres shortening
under load
Sarcomeres lengthening
under load
eccentric
0
concentric
Contraction Velocity
Biomechanical & Anatomical
Factors in Muscle Strains
v  agonist-antagonist imbalance
(e.g., quad - ham ratio)
v  muscle-tendon interfaces
(e.g., semitendinosus)
v  elasticity (cc, sec, pec)
Muscle Contusions
“Corks” v  forceful impact
v  localised (blunt) trauma
v  “common” (superficial) sites
v  vastus lateralis / biceps brachii
v  “other” (medial) sites
v  thigh adductors / med. gastroc
Muscle Contusions
“Corks” v mild - severe bruising v local fibre damage & bleeding
v edema & hematoma v ICE not HARM
v  myositis ossificans
Tendon Rupture
v Partial Rupture
Small to large # ruptured fibres,
pain and limited function
(equivalent to Grade I / II sprain)
v Complete Rupture
Total rupture of tendon, pain and
non-function of specific muscletendon unit (Grade III equivalent)
Biomechanics & Anatomy in
Tendon Rupture
v sudden acceleration
v jumping / landing
v unexpected loading
v stretch-shortening action
Biomechanics & Anatomy in
Tendon Rupture
v in vivo loading pattern
v excessive stiffness
v muscle-tendon “imbalance”
(e.g., Achilles tendon)
Tendon “Avulsions”
v detachment of tendon
v mallet finger
(extensor mechanism)
v jersey finger
(flex digit profundus)
Ligament Sprains
Grade I
Grade II
pain on stressing
ligament no increased joint
laxity
pain
increased joint
laxity with definite
end point
Grade III
pain + / - gross joint laxity
without a firm
end point
Ligament Sprains
v  Clinical continuum based on
ligament stress-strain curve ² Stress-Strain curve
v  Grade I - III “overstretching”
fibre model
² mild, moderate, severe
Stress - Strain Curve
Classic Ankle Inversion Sprain
Rupture of Joint Capsule / Ligaments
(AC Injury Examination under Anesthesia)
v AC Injuries: Type I - VI
(Rockwood classification)
v joint capsule
v acromioclavicular lig’s
v coracoclavicular lig’s
trapezoid
conoid
Ligament Sprains
v  single, debilitating episode ² e.g., Knee
² ACL
² ACL + L/MCL
² ACL + L/MCL + Meniscus
² ACL + PCL
Ligament Sprains
v  multiple, debilitating episodes
(chronic on acute) ² e.g., Ankle
² ATFL
² ATFL+CFL+PTFL
² Syndesmosis
² ATFL+CFL+PTFL+Deltoid
Joint Dislocations & Subluxations
v Clinical premise -“hypermobility”, assessed by multi-joint
“laxity”, predisposes to subluxation / dislocation injuries
Beighton Score
Joint Action ROM Elbow extension
> 10° Knee extension
>10° Thumb apposition to ant forearm
5th finger ext >90° Forward flexion
Palms flat on floor
/ knees straight
Total maximum possible score 9 Score
1
1
1
1
1
1
1
1
1
Joint Dislocations & Subluxations
v  dislocation: complete
dissociation of the
articulating joint
surfaces
v  subluxation: articulating
surfaces remain
partially in contact
Biomechanics & Anatomy in
Joint Injuries
v  direct impacts
v  distracting forces
Biomechanics & Anatomy in
Joint Injuries
v  injury to surrounding joint
capsule and structures with
luxations
v  luxation / laxity predispose
to impingement (e.g.,
acromion process) and
recurrent injury
Biomechanics & Anatomy in Joint Injuries
v  “unstable” joints / structures
more likely to dislocate
² shoulder (anterior)
² acromioclavicular joint
² fingers (PIP joints)
² patella (lateral)
v  “stable” joints however do
dislocate
² hip
² elbow
Acute Meniscus Injuries
v  Joint line pain
v  +ve McMurray’s test
v  Joint effusion / swelling
v  Popping or clicking within joint v  Giving way sensation / locking
v  Arthroscopic surgery
Acute Joint Injuries – Joint Effusion
v increased intra-
articular fluid v traumatic ligament,
bone or meniscal
injuries Acute Joint Injuries – Joint Effusion
v synovial fluid
v bloody effusion:
hemarthrosis Acute Articular Cartilage Injuries
v  fragments sheared from
articular surfaces (luxations) v  chondral & osteochondral
fractures common v  osteoarthritis link
v  typical changes seen on X-ray
include: joint space narrowing,
subchondral sclerosis,
subchondral cyst formation, and
osteophytes
v  better detection (MRI, CT) v  arthroscopic surgery
Bone Fractures
v common sporting injury
v direct trauma ² blow / collision
v indirect trauma ² twisting
v splint / stabilize
v medical referral
Bone Fractures
v closed fractures
v open fractures
² (compound)
v nerve damage
v vessel damage
v bleeding / shock
v infection
Simple & Complex Fractures
Peak Fracture Prevalence in
Adolescence
Collés Fracture
Biomechanics & Anatomy in Fractures
Avulsion fractures
Greenstick fractures
l internal forces
l incomplete break
l younger athletes
l younger athletes
Stress fractures
l repetitive forces
l pars interarticularis
Bone Bruising
•  Microtrabecular fracture /haemorrhage / oedema
in bone following traumatic insult
•  MRI shows bone marrow oedema
•  Evident for 12 - 14 weeks
•  Subperiosteal hematoma - bleeding beneath
periosteum. •  Interosseous bruise - bleeding inside bone
marrow is located. •  Subchondral bruise – between cartilage and bone
beneath, causing cartilage to separate from bone.
Growth Plate Injuries
Type I - epiphysis (E) completely
separated from metaphysis (M) Type II - E + growth plate (GP)
separated from metaphysis M
Type III - Fx thru E separates part
of E & GP from M
Type IV - Fx thru E, across GP
and into M
Type V - GP compressed / crushed
(prognosis poor)
Salter & Harris
Overuse Injuries
v repetitive microtrauma exceeds
tissue repair capacity
v  ⇑ prostaglandin E2 in tissues -
⇑
collagenase, ⇓ collagen synthesis
v upregulation of genes for
cartilage, down-regulation of
genes for tendon (rat) ⇒ tendon
morphology alters to more
cartilaginous.
Overuse Injuries
v important to identify /
consider risk factors (RF)
v addressing intrinsic /
extrinsic RF may help
prevent re-injury
v often recalcitrant to
treatment (months to
resolve)
Overuse Risk Factors
v Extrinsic Factors
² Training
Errors
Errors
² Surfaces ² Shoes ² Equipment
² Technique
Overuse Risk Factors
v  Intrinsic Factors
² Previous
Injury
of Flexibility
² Leg Length Discrepancy
² Malalignment
tibial torsion / vara
genu valgum / varum ² Lack
Overuse Risk Factors
v  Intrinsic Factors
² Malalignment
patella alta
pes planus / cavus
² Muscle Imbalance ² Muscle Weakness
In the News
Tendinopathies (Overuse)
v  pathology is tendon (collagen)
degeneration (tendinosis) not
inflammation
v  surrounding structures may
have inflammation
(paratendinitis)
Normal → Abnormal
Pathological Findings
Multiple tendons
(Supraspinatus, ECRB,
Achilles)
v Collagen disarray
v Absent cells, prolific cells
v Abnormal vessels & nerves
v Abnormal
extracellular matrix
Dealing with Tendinopathies (Overuse
Injuries)
v  History (onset, nature, potential causes)
v  Examination (anatomical structure, reproduce pain)
Diagnosis required!
v  Treatment
Relative rest / maintain fitness
Avoid aggravating activities
v  Pharmacology (NSAIDs??, GTN)
v  Rehab (eccentric strengthening)
Try to find intrinsic / extrinsic causes!
v 
v 
Removing Abnormal Vessels & Nerves
Joint “Diseases” in Children / Adolescents
(Chronic??)
v Osteochondritis (apophysitis / enthesopathy)
Articular
Non-articular
Physeal
v Osgood-Schlatter (tibia)
v Sever’s (calcaneus)
Articular Cartilage Injuries / OA
v  Many alternative medicines purported
to decrease pain. v  little supporting evidence for: vitamin
A, C, and E, ginger, turmeric, omega-3
fatty acids, chondroitin sulfate and
glucosamine. v  Glucosamine - 2010 meta-analysis
found no better than placebo.
v  S-Adenosyl methionine may relieve
pain similar to NSAIDs.
v  electrostimulation techniques - no
evidence it reduces pain or disability in
knee OA
Chondral Defects
v  Perera et al. 2012 - isolated chondral defects of knee (>1,000
cases) Autologous chondrocyte implantation, following
conclusions:
v  Smaller (<1cm2), well contained lesions may be suitable for
microfracture v  larger defects – ACI satisfactory procedure in 70–80% of cases.
v  Motivated patients (15–55 yrs) with single lesion & short (<1 yr)
history and no previous procedures have best outcome.
v  ACI - statistically significant improvement in objective and
patient reported clinical outcome scores with durable outcome
for as long as 10years.
v  clinical results of ACI and MACI techniques comparable and
percen hyaline cartilage (biopsy) appears to improve with time.
v  Lesions of the femoral condyles have superior results to those in
the patellofemoral joint.
microfracture
Osteochondral autograft/
allograft transfer
(mosaicplasty) – cartilage
plugs
ACI “tidemark” show filling
Stress Fractures (Reactions)
v Bone failure v (repetitive microtrauma)
v Repetitive stresses
² Bending
(muscle action)
² Compression (calcaneum)
² Tension (femoral neck)***
v Fatigued muscle ⇓ stress absorb
Stress Fracture Risk Factors
Intrinsic
v  Sex / Age
v  Menstrual irregularities
v  Decreased tibial bone width
v  Increased ext rot of the hip
v Extrinsic
v  Training change (type, frequency, intensity)
v  Footwear / Training surface
v  Equipment
Stress Fractures
v  Onset usually insidious v  Initially pain during exercise
v  Relieved by rest
v  Symptoms occur one month after
change in training regime
v  Prolonged pain as condition worsens
Imaging of Stress Fractures
Bone Scans
v  excellent sensitivity / poor specificity
v  50% athletes increased uptake in
asymptomatic sites
v  non-visualization of fracture
CT
v  visualise fracture
MRI (best performed within 3 weeks)
v  differential diagnosis (e.g., infection)
v  fracture lines appear as low signal
intramedullary bands
Stress Fractures
v  Modified rest
v  Avoid precipitating activity
v  Minimal weightbearing activity
v  Modify biomechanics v  Orthotics
v  Avoid risk factors v  Avoid ultrasound
v  Most heal ~6 weeks
v  Healed when
²  Absence
of local tenderness
precipitating activity
without pain
²  Perform