Distal soft tissue injuries Flashcards

1
Q

Safety factor of equine soft tissues

A

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

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2
Q

Factors affecting structural properties of tendons

A

Crimp

Glycosaminoglycans (GAG)

Cartilage oligometric matrix peptide (COMP)

Collagen

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3
Q

Crimp

A

Straightens out in the initial phase of tendon loading

Distributed differently over the cross section of the tendon in older horses

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4
Q

Glycosaminoglycans (GAGs)

A

Important components of the extracellular matrix

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5
Q

Cartilage Oligometric Matrix Peptide (COMP)

A

Correlates with elasticity of tendon

Increased COMP, more elastic

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6
Q

Tendon change with age

A

COMP and crimp reduce with age– tendons become less elastic

Affects injury rates

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7
Q

Blood supply of distal tendons

A

poor – particularly within sheaths and bursae

Poor recruitment of inflammatory cells

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8
Q

Collagen deposition in DDFT

A

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

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9
Q

Collagen deposition in the suspensory ligament

A

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!

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10
Q

Pathophysiology of SDFT injuries

A

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)

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11
Q

Pathophysiology of DDFT injuries

A

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)

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12
Q

Pathophysiology of suspensory ligament injuries

A

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)

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13
Q

Pathophysiology of check ligament injuries

A

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!)

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14
Q

Pathophysiology of stifle soft tissue injuries

A

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)

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15
Q

Interference/overreach injuries:

A

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

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16
Q

Causes of microdamage of distal soft tissues

A

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…………….

17
Q

Prevention of microdamage in the distal soft issues

A

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

18
Q

SDFT damage

A

An easy diagnosis by palpation/visual inspection

Characteristic “palmar bow” seen to the profile of the tendon

Heat, pain, swelling, resentment of palpation

19
Q

Clinical signs of the inflammatory phase of SDFT injury

A

Lameness,

pain on palpation,

heat,

swelling

20
Q

Pathology of the inflammatory phase of SDFT injury

A

Haemorrhage,

inflammation,

neutrophils,

macrophages and monocytes,

increased blood flow,

oedema,

proteolytic enzymes

21
Q

Clinical signs of the reparative/proliferative phase (fibrosis) phase of SDFT injuries

A

Reduction or absence of lameness,

resolution of signs of inflammation,

tendon still palpably enlarged and soft,

signs of re-injury if exercised too early

22
Q

Pathology of the reparative/proliferative phase of SDFT injuries

A

Angiogenesis,

fibroplasia,

++ fibroblasts,

collagen III,

small collagen fibrils formed

23
Q

Clinical signs of the remodelling/maturation phase of SDFT injuries

A

Tendon size decreases,

tendon less pliable,

reduced fetlock extension,

contractures

24
Q

Pathology of the remodelling/maturation phase of SDFT injuries

A

Collagen transformation from III to I,

cross-linking,

thicker collagen fibrils

25
Q

How does scar tissue behave in tendons?

A

Core lesions -> fibrotic scar tissue -> non-compliant area in centre of tendon

Fibrotic lesion – less compliant than the tendon around it. Adds stress to surrounding tendon. Usually means that lesions propagate in a proximo-distal direction.

26
Q

The main structures in the digital flexor tendon sheath

A

Superficial digital flexor tendon
Deep digital flexor tendon
Manica flexoria
Palmar/Plantar annular ligament

27
Q

Manica Flexoria injuries

A

Often diagnosed with US but contrast tenography is more sensitive.

MRI struggles!

Definitive diagnostics and therapy:
- Tenoscopy and removal of the torn manica

28
Q

PAL Syndrome (Palmar/plantar annular ligament syndrome)

A

A compartment syndrome-like disease - inflammation of the sheath causes constriction of the ligament which causes further inflammation etc.