Transcript Achilles-Tendinopathy-Handoutx

Achilles Tendinopathy
Normal Anatomy
• Origin- the mid calf
• Insertion – posterior aspect of
calcaneus
• Made up of soleus AND
gastrocnemius
• Made from water (approximately
80%) collagen, ground substance
and elastin
• Collagen in an organised structure
• Constantly going through a state of
degradation, synthesis and
remodelling
Normal Anatomy
• Where tendon joins the bone there is a
combination of tissues called an enthesis
organ
• Enthesis organ composed of bursa,
fibrocartilage, tendon, mineralised
fibrocartilage
• Enthesis compresses the tendon against
the bone to reduce tensile load on the
insertion, spreading the load
• Enthesis organ also provides a mechanical
advantage to the muscle tendon unit
• As tendon attaches onto bone the type of
tissue merges (Normal Tendon –
fibrocartilage – mineralised fibrocartilage
– bone)
Normal Anatomy
• Joint side of the Achilles tendon
subject to less tensile load, but more
compressive load
• Normally compressive tissue
(fibrocartilage) transitions into tensile
tissue (fibrous) from
• More fibrocartilage present on the
joint side deep to superficial
• Fibrocartilage designed to absorb
compressive forces
• Normal tendon cells exposed to
compressive forces and can become
more chondrocyte like (cartilage cells)
Pathology
• Pain and change in tendon cellular
structure in response to tissue
injury and overload
• Imbalance between the rate of
break down and rebuilding
• Therefore the structure of the
tendon changes reducing its ability
to cope with load
• Can be insertional or mid portion
• Can develop into partial or full
thickness tears
Mechanism of Injury
• Insidious
• Intrinsic
• Previous lower limb tendinopathy
• Recent injury
• Reduce plantarflexion strengthparticularly soleus
• Reduced neuromuscular control
• Reduce subtalar motion
• Reduced dorsiflexion
• Hypertension
• Diabetes
• Extrinsic
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Excess training volume
Sudden changes in loading
Excess training time
Hopping, running, jumping sports
Changing environment
Changing footwear
Pathophysiology
• Overload (tensile, compression or both)
to the tendon causes it to change
• Results in cell proliferation and activation
eventually producing large proteins
(proteoglycans)
• Continued cell production and protein
presence disturbs cellular matrix
• If load continues and the cell production
and protein presence destructs the matrix
further eventually leading to
neovascularity
• As pathology disturbs collagen structure
the tendon is well designed to take load
Why does it hurt?
• Poorly understood
• Local nociceptive driver
• Local pain
• Tendon cells communication with
nociceptors in response to
mechanical load
• Central mechanism
• bilateral symptoms
• Motor and sensory adaptions occur
centrally
• However unilateral isometrics do not
effect contralateral pain
Structure, Pain and Function
Stages
• Reactive
• Acute response to increased load or activity
• Tendon cells (tenocytes) detect load
• Respond to load by increasing number of cells and producing large water
binding proteins (proteoglycans)
• Increases water in the tendon
• Swelling occurs
Stages
• Disrepair
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Continued abusive load
Altered tenocyte activity occurs with continuation of protein production
Continued protein production disturbed extracellular matrix
Increased collagen type III
Disorganised and separated collagen
Potentially increased neovascularisation
Structural change can still be reversible
Stages
• Degenerative
• Large structural changes are present and are largely irreversible
• May have a cortical involvement linking to pain symptoms
• Continued presence of large proteins (proteoglycans) destroys matrix
significantly leading to cell death
• Tendon structure changes considerably loosing ability to accept load
• Neovascularisation occurs
• Symptoms can still be addressed however structure may never improve
• Increased risk of tear or rupture
Stages
Stages
• Stages can occur in combination
Subjective Examination
• Key of subjective is to determine the stage of tendinopathy and
determine the key factors that lead to abusive load
• Mid Portion
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Pain in the mid portion of the Achilles
Morning stiffness
Pain worse with activity
May ease off and then return or can
persist through activity depending on
stage
• History of increased training load,
change in environment, change in
footwear
• Insertional
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Pain at the insertion
Morning stiffness
Pain worse with activity
May ease off and then return or can
persist through activity depending on
stage
• Worse with activities that compress
the tendon in dorsiflexion
• History of increased training load,
change in environment, change in
footwear
Objective Examination
• Mid Portion
• Swelling/thickening mid portion
• Pain with hopping, jumping
• More pain on palpation in a
relaxed position versus a stretched
position
• Degenerative
• Pain with hopping, jumping
• Pain with high load plantarflexion
from a dorsiflexed position
• Pain at the insertion on palpation
• N.B Passive dorsiflexion should be
pain free
Objective Measure
• Assess pain irritability
• Use energy storage and release
activity (e.g hopping)
• Rate out of 10 NPRS
• Used throughout treatment to
monitor load of exercise
programme and progression
• Use the measure the same time
every day at home
Further Investigation
• US Scan
• MRI
• Usually a clinical diagnosis
• US Scan can be helpful to
determine stage of pathology
Management
Isometrics
• Useful for pain relief
• Literature focused on patellar tendinopathy at present
• Reduces cortical inhibition
• Isometric loading with the use of a metronome also shown to
improve strength and neuromuscular control
Slow Heavy Isotonic Resistance Exercise
• No difference between eccentric and eccentric-concentric
programmes
• Eccentric-concentric easier to perform initially and less provocative
than eccentrics alone
• Slow heavy load, mild discomfort ok as long as it settles quickly
• Use of a metronome beneficial for neuromuscular training to improve
corticospinal excitability changes
• Should include soleus strengthening as well as other muscles in the
kinetic chain
• Soleus shown to be very weak in Achilles tendinopathy
Reactive Tendinopathy
Reactive Tendinopathy Management – Part 1
• Reduce Pain
• Remove abusive load
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Decrease frequency (e.g train every 2nd or 3rd day)
Decrease length of loading (e.g shorten training)
Decrease load in training (e.g remove energy storage and release drills)
Decrease compressive loads (if a factor)
• Isometrics
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70-80% MVC 4 X 45 second holds, 3 -4 times daily, 2 mins recovery
Away from compression
Enough load for a challenge, fasciculation’s should not be present
Avoid exercises requiring postural control (i.e better to sit, lie down, or standing with support)
Done before training, playing
• Other Adjuncts
• Reduce pain without stimulating cell proliferation
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Orthotics (heel raise useful for insertional tendinopathy)
Manual therapy to surrounding regions
Short acting and non-colloidal corticosteroids useful
Frictions, electrotherapies, shockwave, eccentrics all provocative
PRP provocative
Reactive Tendinopathy Management – Part 2
• Maintain Strength
• Isotonic Exercise
• If less than 3/10 NPRS
• 4 x 6-8, 60 – 90 second rest
Degenerative Tendinopathy
Mechanotherapy
• Using optimal mechanical
loading
• Stimulates tendon to gradually
accept load
Stage 1 - Isometrics
• Indications
• More than 3/10 NPRS pain on
isotonic exercise
• Implementation
• 70-80% MVC 4 X 45 second holds, 3 4 times daily, 2 mins recovery
• Enough load for a challenge,
fasciculation’s should not be present
• Avoid exercises requiring postural
control (i.e better to sit, lie down, or
standing with support)
• Done before training, playing
• Completed throughout ALL stages
Stage 2 – Strength Phase (Isotonic Exercise)
• Indications
• Loaded isotonic exercise ≤ 3/10 NPRS
• Pain stable on morning testing (≤ 3/10 NPRS)
• A positive response to 24 hour reassessment using pain and
outcome measures
• Implementation
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4 x 6-8, 60 – 90 second rest
Slow, heavy, single and double leg
Address deficits in kinetic chain also
Add endurance
• Considerations
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Avoid compressive loads
Avoid speed
Encourage evening to avoid calf fatigue during the day
Increases the muscle capacity, strength and muscle bulk through
functional ranges of movement
Stage 3 – Energy Storage Phase
• Indications
• Pain is stable on morning test (may not be
zero)
• Symmetry in muscle bulk
• Good strength (e.g 25 x 1.5 x BW single leg
press for Patellar Tendinopathy)
• Implementation
• Slow, deceleration
• Slow change of direction
• E.g skipping, jumping, acceleration,
deceleration, cutting – exercise selection
dependent on sport and area of injury
• Functional Corrections
• Squats, lunges, standing leg standing
• Avoid compressive loads
• Keep pelvis level
• Regress exercise so that technique is
good
Stage 3 – Energy Storage Phase (cont)
• Implementation
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Every 2 -3 days and assess response
Must keep strength going
Isometrics on days off
Progressively develop volume and then
intensity of relevant energy storage exercise
• Considerations
• Add/change one thing at a time
• Break up absorption and propulsion phase
early, add these together later in stage 3
• Consider as much a neural reprogramming
as muscle/tendon function
• Consider endurance for sports that require
endurance
Stage 4 – Energy Storage and Release
• Indications
• Pain is stable on morning test (may not be zero)
• Symmetry in muscle bulk
• Good strength (e.g 25 x 1.5 x BW single leg press for
Patellar Tendinopathy)
• Implementation
• Quicker, faster tendon loading
• E.g skipping, jumping, acceleration, deceleration,
cutting – exercise selection dependent on sport and
area of injury
• Return to sport drills
• Every 2 -3 days and assess response
• Must keep strength going
• Isometrics on days off
• Considerations
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Add/change one thing at a time
Don’t add load and speed together
May mix phase 3 and 4 exercises
Consider tendon capacity
Plan B
• Short acting and non-colloidal
Corticosteroids
• Extracorporeal Shockwave
Therapy
• Platelet Rich Plasma Injections
References
• Asplund, C. A. and T. M. Best (2013). "Achilles tendon disorders." BMJ 346.
• Beyer, R., M. Kongsgaard, B. Hougs Kjaer, T. Ohlenschlaeger, M. Kjaer and S. P. Magnusson (2015). "Heavy Slow Resistance Versus
Eccentric Training as Treatment for Achilles Tendinopathy: A Randomized Controlled Trial." Am J Sports Med 43(7): 1704-1711.
• Cook, J. L. and C. Purdam (2012). "Is compressive load a factor in the development of tendinopathy?" Br J Sports Med 46(3): 163168.
• Cook, J. L., E. Rio, C. R. Purdam and S. I. Docking (2016). "Revisiting the continuum model of tendon pathology: what is its merit in
clinical practice and research?" British Journal of Sports Medicine.
• Malliaras, P., C. J. Barton, N. D. Reeves and H. Langberg (2013). "Achilles and patellar tendinopathy loading programmes : a
systematic review comparing clinical outcomes and identifying potential mechanisms for effectiveness." Sports Med 43(4): 267286.
• Malliaras, P., J. Cook, C. Purdam and E. Rio (2015). "Patellar Tendinopathy: Clinical Diagnosis, Load Management, and Advice for
Challenging Case Presentations." J Orthop Sports Phys Ther 45(11): 887-898.
• O'Neill, S., P. J. Watson and S. Barry (2015). "WHY ARE ECCENTRIC EXERCISES EFFECTIVE FOR ACHILLES TENDINOPATHY?" Int J
Sports Phys Ther 10(4): 552-562.
• Rio, E., D. Kidgell, G. L. Moseley, J. Gaida, S. Docking, C. Purdam and J. Cook (2016). "Tendon neuroplastic training: changing the
way we think about tendon rehabilitation: a narrative review." Br J Sports Med 50(4): 209-215.
• Rio, E., L. Moseley, C. Purdam, T. Samiric, D. Kidgell, A. J. Pearce, S. Jaberzadeh and J. Cook (2014). "The pain of tendinopathy:
physiological or pathophysiological?" Sports Med 44(1): 9-23.
• Rowe, V., S. Hemmings, C. Barton, P. Malliaras, N. Maffulli and D. Morrissey (2012). "Conservative management of midportion
Achilles tendinopathy: a mixed methods study, integrating systematic review and clinical reasoning." Sports Med 42(11): 941-967.