Distal soft tissue injuries Flashcards
Safety factor of equine soft tissues
the amount of stress that a structure can withstand before failure.
Many equine soft tissues have safety factors less than 1.5 and some are as low as 1.2
Factors affecting structural properties of tendons
Crimp
Glycosaminoglycans (GAG)
Cartilage oligometric 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
Glycosaminoglycans (GAGs)
Important components of the extracellular matrix
Cartilage Oligometric Matrix Peptide (COMP)
Correlates with elasticity of tendon
Increased COMP, more elastic
Tendon change with age
COMP and crimp reduce with age– tendons become less elastic
Affects injury rates
Blood supply of distal tendons
poor – particularly within sheaths and bursae
Poor recruitment of inflammatory cells
Collagen deposition in 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
Collagen deposition in the suspensory 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!
Pathophysiology of SDFT injuries
The vast majority of SDFT injuries/pathology occur in the mid metacarpal region of the forelimb
(Occasionally hindlimb pathology is seen, and occasionally disease of the branches close to the insertion onto second phalanx)
Pathophysiology of DDFT injuries
The vast majority of DDFT injuries/pathology occur within the digital flexor tendon sheath, pastern or within the hoof.
(Occasionally seen in the mid-metacarpal region in the forelimb alongside severe check ligament injury)
Pathophysiology of suspensory ligament injuries
The majority of SL injuries/pathology occur at the proximal origin or at the branches of insertion onto the proximal sesamoid bones.
(Occasionally lesions in the suspensory body are seen but rarely as solitary lesions)
Pathophysiology of check ligament injuries
Check ligament injuries are easily palpated in the proximal third of the forelimb metacarpus, usually larger on the lateral side.
(Hind limb injuries are VERY rare, and some horses don’t have a hindlimb check ligament at all!)
Pathophysiology of stifle soft tissue injuries
Stifle soft tissues including the cruciate ligaments and medial meniscus are a common site of pathology, usually accompany effusion
(Patellar ligaments can also be injured, and very occasionally the lateral meniscus)
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
Causes of microdamage of distal soft tissues
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…………….
Prevention of microdamage in the distal soft issues
A competitive horse is going to be working above thresholds for microdamage and degeneration, so how can we adapt a training program
Solid boots reduce risk of direct trauma
BUT – consider the implications these might have for the physiological heating effect!!
Consider track surfaces
SDFT damage
An easy diagnosis by palpation/visual inspection
Characteristic “palmar bow” seen to the profile of the tendon
Heat, pain, swelling, resentment of palpation
Clinical signs of the inflammatory phase of SDFT injury
Lameness,
pain on palpation,
heat,
swelling
Pathology of the inflammatory phase of SDFT injury
Haemorrhage,
inflammation,
neutrophils,
macrophages and monocytes,
increased blood flow,
oedema,
proteolytic enzymes
Clinical signs of the reparative/proliferative phase (fibrosis) phase of SDFT injuries
Reduction or absence of lameness,
resolution of signs of inflammation,
tendon still palpably enlarged and soft,
signs of re-injury if exercised too early
Pathology of the reparative/proliferative phase of SDFT injuries
Angiogenesis,
fibroplasia,
++ fibroblasts,
collagen III,
small collagen fibrils formed
Clinical signs of the remodelling/maturation phase of SDFT injuries
Tendon size decreases,
tendon less pliable,
reduced fetlock extension,
contractures
Pathology of the remodelling/maturation phase of SDFT injuries
Collagen transformation from III to I,
cross-linking,
thicker collagen fibrils
