An overview and update

Tendinopathy Management in Sport

Mark Young - ECB Lead Physio

Tendinopathy: Forget the recipes learn to rehabilitate tendons

Pete Malliaras Tendon Specialist

Tendinopathies Masterclass
Jill Cook & Graham Smith

Jill Cook Otto Chan Nicola Maffuli Hakan Alfredson Craig Purdam James Moore

Normal function
Connective tissue Transmit tensile load
Muscle to bone

Store and release energy

Stretch shortening cycle

Highest tensile strength tissue in body

Healthy tendon will not rupture

Collagen 90%
Type I 95-99% Type III 1-5%

Ground substance 8%
Proteoglycans Glycosaminoglycan tail Increased at insertion

Bind water Compressive

Strength

Elastin 2%

Longer than you think Tendon rotates externally from origin

Flat/broad round flat/broad at calc Gastrocnemius forms lateral portion 2/3 of insertion from soleus Role of bent knee calf raise for insertional tendinopathy
S G

Thin layer of fatty tissue Buffering matrix

Connective / neural / vascular tissues

Some independent movement Rich in vascular structures

Greatest proximally Lowest density mid-portion

Usually termed as poor blood supply Sufficient blood supply in normal tendon EXCEPT: when compressed or overloaded

Neural and vascular structures travel together

Kagers Fat Pad Plantarflexion

Dorsiflexion

Compressive load No buffer between tendon and osseous structures

Fat pad
Rich blood supply and innervation American orthopaedic surgeon self arthroscopy

Paratenon
Innervated by sural nerve (not tendon itself)

Tendon aneural (if normal!)

Not beneficial in tendinopathy (important to differentiate paratenonitis/reactive tendinopathy Collagen density and neat orientation Tensile strength

Load is the only way to remodel tendon (Khan et al. 2009) Slow to respond Impact/SSC
CSA/stiffness takes approx 5 years

Slow, heavy training

Much quicker (8-12 weeks)

...itis ...osis ...opathy No inflammatory markers

Animal models Histopathology Gene markers In vivo microdialysis

Cell degeneration/ tenocyte activity

Granular material separates collagen fibrils

Ground substance increases

Increased collagen splitting disorganisation

Fat deposits form (form typical bump)

Lipid cells invade areas of collagen atrophy

Fat deposits calcify

Large deposits of calcium replace lipids

Neovascularisation
Aberrant vascular and neural ingrowth biochemicals ++

Interesting is it an overuse injury?

Subpopulation

The more we know, the more we dont know

Risk factors identified Continuum model

ankle DF Abnormal subtalar ROM PF strength pronation Tendon structure

Comorbidities
Obesity, HTN, cholesterol, DM Gender (postmenopausal women), age ?genes familial hx

No consensus on origin of pain

European vs. American debate
Neural invasion associated with neovascularisation Opportunistic? Pain generating?

Pain pathology Like most MSK

Produced by tenocytes and nerve endings Substance P, calcitonin gene related peptide, glutamate, Theoretical

Low risk of rupture in symptomatic tendinopathy Normal Assymptomatic tendinopathy Rupture Painful Tendinopathy

MRI not as much information

? If not sure of Dx

Ultrasound
Doppler can identify vascularisation Vascularisation should be from site of fat pad
Partial tears will be within the tendinous structure

False positives
Tendinopathy pain Only if fits with clinical diagnosis

Tendinopathy
Travel anterior posterior (from fat pad)

If present in any other region

Likely to be partial tear

Techniques to shear neovessels and neural structures

? Mode of action for eccentrics

Medical and surgical management (later slide)

Royal London Hospital Test

pain in PF than DF

Arc Sign
Passive DF/PF bump moves - tendinopathy

Local Palpation
Squish test Shear test

Compressive
H/S origin Gluteus medius Quads tendon Tibialis posterior Achilles insertion Plantar fascia

Mid-substance

Load
SSC and/or compressive overload

Load attentuation
Biomechanics/alignment Strength Flexibility

Neural / alignment Systemic

SSC Biomechanics Weakness Flexibility

Joint Soft tissue

Chiropractic / osteopathic approach Some prognostic risk factors identified

Hyperextension L3 = risk of patellar tendinopathy L5/S1 pathology and radiculopathy = risk of AT

Purely due to this? Or due to altered load as a result?

As mentioned in risk factors

Optimise kinetic chain Manage biomechanics

Saggital ankle Coronal hip

Strength
Weak muscle = tendon overload (glut med) Concentric/eccentric ratio and effect on HEP If unable to do 10 calf raises to EOR eccentrics not as beneficial

Flexibility
Too or related to tendinopathy

Hakan Alfredson
Swedish Orthopaedic Surgeon

Developed AT All ATs were surgically repaired Put on WAITING LIST (Wasnt happy!) Knew rupture would be sorted quicker and outcome not that bad Im gonna rupture it Got better Gave all pts on waiting list protocol and most did not require surgery

Alfredson (3 x 15) x 2 daily

55-89% midportion respond 33% insertional (67% if not taken past PG)

Heavy load 3 times per week Outcomes very similar Why rest collagen remodelling

Heavy load
Remodel tendon Young, active population

BW
Others factors ROM etc Older popn

Differential Dx Decline board required!! Need to join a gym!

50-70% respond to alfredson

Manual Therapy Ultrasound Taping Heel raises (insertional) Injections Shockwave Surgery

Identify primary driver(s) Young = Heavy Old = BW

Concentric deficit / atrophy = NO eccentrics

For compressive
Avoid EOR compressive positions Mid range isometric holds ++

Tendons need SSC even horrible ones! Restoring SSC = risk of recurrance Jumps/hops/plyometrics (or derivative of)

GRADUAL progression (wait 2-3 days)

Load driven High load demands Mixed presentation

Systemic driven

High load SSC focus

Eccentrics

Con-eccentric Aerobic Behaviour change

DL calf raise SL calf raise

Flexion and extension

SL eccentric Insertional AVOID

Flat shoes/barefoot Sitting with feet up Stretching DF

Knee extension Leg press (isometric if reactive) Split squat Decline squat

NOTE: 0-60 degree knee flexion initially Need HEAVY load

Clam adduction to midline

Isometric!!

Crab walk / Monster walks SL squat

AVOID Crossing legs, hanging on hip, deep squat, Stretching

Active inversion
200-300 reps!

TB inversion Calf raise as AT

Walking on tip toes AVOID: barefoot/stretches

10% plantaris (present in ~50% pop.)

Require surgery

Some sites are notoriously stubborn

Compressive tendinopathy much more resistant to conservative rehab than load based ESWT more effective

Systemic vs. Load driven Once tendon has become degenerative irreversible

Meds
Ibuprofen - tenocyte activity GTN patches good short term effects Prednisolone orally Combi pill doxycyclin/ibuprofen/omega 3

Injections
Corticosteroid peritendinous (elbow usually manages intratendon) Autologous blood/PRP Sclerosing High volume

Many docs will not inject due to rupture risk No evidence if not injected into tendon substance Pain models
Paratenon/bursa/fat pad

Good for:
Reactive tendinopathy Inflammatory peritendon (as above)

12/52 pain relief - rehab

1-2 ml of PRP from 5ml blood Into site of tendinosis / most hypoechoic Introduce growth factors into area
TGF-, FGF, PDGF

Polidocanol (2-3 ml) or dextrose Into area of neovascularisation Destroys neovessels/nerves

US guided 25ml hydrocortisone + 40ml saline Between tendon and fat pad

Mechanically remove neovessels and nerves

Slurp

High volume growing in popularity and seems to have least complications

Insertional/compressive tendinopathy Equivalent to eccentric loading in older population Need to be stable will make reactive tendinopathy worse

Best on hamstring/insertional AT and PT

Tendon scrape Tendon floss

Need to differentiate load vs. systemic If load what is primary problem Identify and manage risk factors Need to identify pain phase Loading strategies depend on variables Grade exposure to SSC Not all will repsond