Recognising and understanding soft tissue injuries Flashcards
Tendon injuries in racehorses - epidemiology
- account for >35% of all injures to flat and
National Hunt horses - 53% of injuries during steeplechase races
- 15% of National Hunt horses affected in one
season - 97-99% affect the forelimb
- 75-93% affect the SDFT
Tendon injuries in event horses - epidemiology
- 43% of injuries sustained
– 33% SDFT, 31% suspensory ligament, 17% DDFT
Losses due to soft tissue injury
1 – Days in training
* Injured horses are likely removed
from training reducing revenues for trainers
2 – Presentations to racecourses
* Injured horses don’t race, reducing
entry fees and racecourse finances
3 – Wastage
* Some horses removed from racing
but continuing in other disciplines
* Some horses euthanised due to poor
prognosis
Stress vs strain
- Stress put on a tissue is the pressure per cross-sectional area
– Stress is proportional to the force you add on each end of that structure - Strain is the amount that the structure you’re stressing deforms under each unit of stress
Tendon loading curve
1 - Straightening of tendon crimp
2 - Elastic deformation
3 - Non-elastic deformation
4 - Failure/rupture
What is elastic deformation?
- every bit of energy put into the tendon it will bounce back and give you everything back you put into it
- here we sit in a happy system -> no energy being dissipated, no failure of tendon fibre
What is plastic deformation?
- where you have elongation of a substance and it’s never going to return quite to where you started
- caused some damage to the tissue but is still structurally fairly sound
The tendon loading and unloading curve
- Force strain % curve
- Looking at energy return
- Most of the energy is elastically returned
- Small amount (area between the lines) is transformed to heat
- Important factor for the SDFT, accelerates protein degradation
- Core of SDFT can reach 45oC
Some of the factors affecting structural properties
- crimp
- glycosaminoglycans (GAGs)
- cartilage oligomeric matrix peptide (COMP)
- collagen
Crimp
- Straightens out in the initial phase of tendon loading
- Distributed differently over the cross section of the tendon in older horses
- Reduces with age -> tendons become less elastic -> affects injury rates
- Important in the very early stage of the stress strain curve and in absorbing that early amount of energy
GAGs
- Important components of the extracellular matrix
COMP
- Correlates with elasticity of tendon
- Increased COMP, more elastic
- Reduces with age -> tendons become less elastic -> affects injury rates
Collagen
- Size and number of fibrils changes over time
- Collagen types and distribution can change over time
Is the blood supply to tendons good?
- No it is poor, particularly within sheaths and bursae
- Therefore, poor recruitment of inflammatory cells
Variation of collagen deposition in the DDFT
- In the mid metacarpal region – lots of type 1 collagen
with elastic properties - In the fetlock region – more type 2 collagen which is
resistant to compression - Chondroid metaplasia
Variation of collagen deposition in the suspensor ligament
- Evolutionarily the suspensory ligament should be
called the interosseous muscle - The proximal end of the ligament still retains some
muscle fibres and some fat – makes ultrasound challenging
Where are most SDFT injuries/pathologies?
- mid metacarpal region of the forelimb
(Occasionally hindlimb pathology is seen, and occasionally disease of the branches close to the insertion onto second phalanx)
Largely in horses that are working at speed
Where are most DDFT injuries/pathologies?
- within the digital flexor tendon sheath, pastern or within the hoof
- common where the DDFT changes direction
– where have chondroid metaplasia and it is more tough
– e.g. where it changes direction through the fetlock and down the pastern
– e.g. where it changes direction around the navicular bone and down to the tip of P3
(Occasionally seen in the mid- metacarpal region in the forelimb alongside severe check ligament injury)
Where are most suspensory ligament injuries/pathologies?
- at the proximal origin or at the branches of insertion onto the proximal sesamoid bones
- fairly even split of front vs back legs in sport horses
- tends to be different in the front vs back leg
– front leg tend to see acute soft tissue injury -> acute severe lameness, unilateral - hindleg tend to see bilateral degenerative disease.
(Occasionally lesions in the suspensory body are seen but rarely as solitary lesions)
Where are most inferior check ligament (AL-DDFT) injuries/pathologies?
- proximal third of the forelimb metacarpus, usually larger on the lateral side
(Hind limb injuries are VERY rare as it is small and vestigial, and some horses don’t have a hindlimb check ligament at all)
True acute traumatic soft tissue injuries
Interference/overreach injuries:
* Horses at speed can strike a loaded forelimb with a rapidly protracting hind limb leading to acute damage of a previously normal soft tissue
* Often skin lacerations are seen alongside
* Big problem in racing (and in trotting & pacing horses but don’t see these often in the UK)
Does micromanage precede acute soft tissue injury in most cases? If so, why?
Yes
- Increasing age
- working in non-elastic region of loading curve
- repetitive loading
- poor reparative and adaptive processes in tendon tissue
- matrix degeneration
- reduction in crimp
- reduction in COMP, increases in type 2 and 3 collagen, poor vascularity, tendon heating
all ^ these lead to an overload which causes a failure of lots of fibre.
Is prevention possible?
- adaptation of the tendon is very high in the neonate and injury risk is very low
– huge training window
– the most important thing for these young horses is probably to live at pasture in a group of young horses so that they’re active, inadvertently training the tendons
– therefore, someone who’s bred from 1 horse and has a foal that ends up living on its own in a slightly small paddock is probably at a high risk for soft tissue injury later down the line - adaptation of the tendon is minimal in adults and injury risk increases massively
– lost ability to train tendons in the adult
Preventative considerations for competitive horses
A competitive horse is going to be working above thresholds for microdamage and degeneration, so how can we adapt a training program:
* An established horse should not be routinely trained at or above the expectations of the horse during competition
* You cannot train adult soft tissues, only accelerate microdamage
* Must be balanced with the aerobic fitness of the horse, and psychological training of horse and rider
The use of boots
- can help to reduce interference injuries
- Solid boots reduce risk of direct trauma
- BUT – consider the implications these might have for the physiological heating effect
Track surfaces
- Vast area of research
- Findings are inconsistent but trends are identified within specific populations
- Consider material surface, moisture content, changes in composition during a race, differences between training and racing surfaces
BHA says:
- hard ground is more risky for bony and soft tissue injury
(- ensure if this is because the ground is harder or because they travel faster on hard ground)
SDFT injury clinical diagnosis
- An easy diagnosis by palpation/visual inspection
- Characteristic “palmar bow” seen to the profile of the tendon
- Heat, pain, swelling, resentment of palpation
Inflammatory phase of injury - CS
*Lameness
*Pain on palpation
*Heat
*Swelling
How long does the inflammatory phase after injury last?
- days
Inflammatory phase of injury - pathology
*Haemorrhage
*Inflammation
*neutrophils
*macrophages and monocytes
*increased blood flow
*oedema
*proteolytic enzymes
Core lesion will be filled with haemorrhage in the acute phase, which quickly then organises itself by using inflammatory mediators into a fairly solid fibrin kind of clot. In this whole process have proteolytic enzymes piling in. Macrophages come in to chew up all the denatured proteins. Can get worsening of the lesion in the very acute phase if let inflammation run away. So definitely want anti-inflammatories.
Reparative/proliferative phase of injury - CS
*Reduction or absence of lameness BUT DOES NOT mean the horse is good to return to work
*Resolution of signs of inflammation
*Tendon still palpably enlarged and soft
*Signs of re-injury if exercised too early
How long does the reparative/proliferative phase after injury last?
- weeks
Reparative/proliferative phase of injury - pathology
*Angiogenesis
*Fibroplasia
*++ fibroblasts
*collagen III
*small collagen fibrils formed
How long does the remodelling/maturation phase after injury last?
- months-years
Remodelling/maturation phase of injury - CS
*Tendon size decreases
*Tendon less pliable
*Reduced fetlock extension
*Contractures
Remodelling/maturation phase of injury - pathology
*Collagen transformation from III to I
*Cross-linking
*Thicker collagen fibrils
How does a tendon with a mature core lesion behave when stress is applied?
- Elongation of the normal fibre
- Solid knot in middle isn’t very compliant
- Maximum stress in this is just above and just below the lump of scar tissue
- Tends to be how these injuries will propagate over time i.e. rehab a horse, year later gets injured again, generally will see old lesion looks good, going to have a new one just above or below it.
- Do get some spread laterally, medially, dorsally, palmar aspect but that’s only because of the cross links and they’re fairly weak in generally
- So generally these are going to be extending proximally and distally
