Tendons, ligaments and muscle

what is the role of tendons?

• passively transfer force generated by muscle to bony attachments - leads to movement

• supports joints

• store energy

what is the role of ligaments?

• attach bone to bone and stabilise joints - e.g. cruciate ligaments, collateral ligaments

• protect tendons

• proprioception

what are tenocytes and ligamentocytes responsible for?

synthesis, maintenance and degradation of ECM

what collagen types are tendons composed of?

• 95% collagen type I

• 1-5% type III

what collagen types are ligaments composed of?

• 90% collagen type I

• 10% type III

what types of injury do we get to tendons and ligaments?

• extrinsic - external trauma e.g. laceration

• intrinsic - overload / degenerative

what do we need to consider about the location and type of tendon or ligament injuries?

• intrasynovial / extrasynovial

• origin / insertion / mid-body / avulsion fracture

• extensor versus flexor tendon

what history is important for us to collect for diagnosis of a tendon/ligament injury?

• age, previous injury, type of injury

• recent exercise - e.g. lame after a jump, chasing a ball and twisted limb

• wound / laceration - but remember injury to tendon may be at different position to the wound due to recoil

what do we need to assess during clinical examination, for diagnosis of tendon / ligament injuries?

• stance / gait

• palpation

  • swelling, pain, oedema, effusion

  • range of motion, stability

what diagnostic imaging can help with diagnosis of tendon / ligament injuries?

• ultrasound

• radiography - good for luxation / avulstion fractures

• MRI - for more complicated or deeper structures

what would indicate a peroneus tertius rupture in a horse?

the ability to extend the tarsus while the stifle is flexed

—> functional stay apparatus makes tarsus and stifle flex and extend together

what features of tendon / ligament would we assess on ultrasound?

• change in cross sectional area

• fibre echogenicity

  • anechoic (black areas)

  • hypoechoic (lower echogenicity - darker)

  • hyperechoic (whiter areas)

  • mineralised

• margination

• position - e.g. rupture

• focal lesion vs generalised changes

• acute (hypoechoic or anechoic) vs chronic changes (hyperechoic or mineralised)

• blood flow to assess neovascularisation - doppler US

why do intrinsic injuries occur?

loss of strain energy as heat (hysteresis) - 43-45 degrees at gallop

—> protein uncoupling

what are the 3 phases of repair of tendon / ligament injuries?

1. inflammatory phase (hours to days)

2. proliferative phase (days to weeks)

3. tissue remodelling phase (weeks to months)

what are clinical signs of acute inflammatory phase?

• lameness

• pain on palpation

• heat

• swelling

what is the pathology of acute inflammatory phase?

• haemorrhage

• inflammation

  • neutrophils, macrophages and monocytes

  • increased blood flow + oedema

  • proteolytic enzymes

what treatment would we provide during acute inflammatory phase?

• limit inflammation - by cold therapy or NSAIDs

• protect limb / reduce further damage - support bandage + rest

what are clinical signs of the reparative / proliferative phase?

• reduction or absence of lameness

• resolution of signs of inflammation

• tendon still palpably enlarged and soft

• signs of re-injury is exercised too early

what is the pathology of the proliferative phase?

• angiogenesis

• fibroplasia

  • fibroblasts

  • collagen III

  • small collagen fibrils formed

what treatment would we provide during proliferative phase?

• promote angiogenesis - tendon splitting, stem cells / platelet rich plasma

• minimise formation of excessive scar tissue - stem cells, platelet rich plasma, physio, US therapy

• early exercise (if lesion resolved on US) - positive effect on collagen orientation

what are clinical signs of tissue modelling phase?

stiffer / thicker tendon

what is the pathology of the tissue modelling phase?

• fibrosis

• gradual change from collagen III to I

what treatment would we provide for the tissue modelling phase?

• increased loading and exercise programme

• improve fitness

• monitor progress by repeat US exam

how can we surgically manage a laceration injury?

• repair ends if feasible

• cast

how can we surgically manage avulsion fracture injuries?

• re-attach avulsed bone fragment

• arthrodese joint

• cast

how can we surgically manage intra-synovial tendon / ligament tear?

debride torn tendon / ligament fibres

how can we surgically manage joint instability injuries?

e.g. cruciate rupture in stifle - TPLO (Tibial Plateau Leveling Osteotomy)

what would cause carpus to be knuckling in a horse?

rupture / laceration in extensor carpi radialis

what would cause fetlock of horse to be dropped (hyperextended)?

rupture / laceration to suspensory ligament

what would cause horse’s toe to be elevated?

rupture / laceration to deep digital flexor tendon

what would cause fetlock of horse to be knuckled and horse keeps clipping toes when walking?

rupture / laceration to common digital extensor tendon

what is the function of skeletal muscle?

maintaining posture and allowing movement

what do skeletal myopathies cause?

weakness or spasm

what history is important for diagnosis of muscle conditions?

• injury / trauma

• breed

• feeding management

• single animal vs herd

• frequency / severity of exercise

what would we see during clinical examination with acute muscle injuries?

• swelling

• pain

what would we see during clinical examination with chronic muscle injuries?

• stiffness

• cramping

• pain

• fasciculations

• weakness

• atrophy

• fibrosis / calcification

what diagnostic tests can we do for muscle conditions?

• biochemistry - serum muscle enzymes (CK, AST, LDH), urine sample (myoglobin)

• ultrasound

  • haematoma —> acute

  • fibrosis / calcification —> chronic

• muscle biopsy

• post-mortem

what is atrophy?

reduction in size of muscle

is atrophy reversible?

• disuse atrophy - reversible if function restored

• denervation atrophy - irreversible when cells degenerate or de-differentiate

  • reinnervation if nerve sheath intact

what can cause denervation atrophy?

• trauma - e.g. laryngeal hemiplegia, brachial plexus avulsion due to RTA, disc protrusions due to metastatic tumours in spine

• myaesthenia gravis - defect at neuromuscular junction

when do we see net withdrawal of muscle protein?

• pregnancy

• rapid tumour formation

what is hypertrophy?

increased muscle bulk due to larger fibres as a result of increased work load (also in compensatory hypertrophy)

what are the three types of degeneration?

1. cellular swelling

   • minor chemical imbalances within muscle e.g. Na+/K+ or ATP exhaustion —> Ca2+ overload

   • moderate swelling but nuclei remain normal

2. hyaline degeneration

   • affects sarcoplasm but spares sarcolemma - often seen with nutritional myopathies

3. granular degeneration

   • severe damage with large basophilic granules of coagulated protein

   • stain positive for calcium

   • fibrosis or fat replacement

when do we see regeneration and repair?

• usually if less severe degeneration

• involves reconstitution of normal function. tothe fibre without complication

when do we see calcification?

with irreversibly-damaged tissue

when do we see ossification?

when damaged tissue undergoes metaplasia to bone

how do we get circulatory disturbances to muslce?

• normally collateral circulatory supply readily compensates in local injuries

• blockage of main arteries / veins can be serious - >6hr leads to loss of regenerative ability

  • arterial - partial blockage of distal aorta/iliacs can cause ischaemic paralysis

  • venous - blockage of large veins leads to congestion with leakage of blood to muscles —> muscle necrosis and fibrosis

what might cause a venous circulatory disturbance?

prolonged recumbency in large animals

what might cause an arterial circulatory distrubance?

• aortic-iliac thrombosis in horses

• saddle thrombi in cats with left sided cardiomyopathy

nutritional

nutritional clinical signs

nutritional treatment

stiff lamb disease

acute exertional rhabdomyolysis

what do we see with chronic exertional rhabdomyolysis?

• poor performance

• stiffness

• cramps

how do we diagnose chronic exertional rhabdomyolysis?

• history

• muscle enzymes

• muscle biopsy

how do we treat chronic exertional rhabdomyolysis?

• ensure warm up before races

• avoid stress

• avoid high energy feeds

polysaccharide storage myopathy

what breeds are affected by eosinophilic myositis (inflammatory response)?

large breed dogs e.g. german shepherds

what does eosinophilic myositis cause?

• acute recurrent pain and mandibular immobility

• bilaterally enlarged temporal / masticatory muscles —> atrophy/fibrosis, third eyelid protrusions and exophthalmos

what do we see with eosinophilic myositis?

• high percentage of eosinophils in the blood

• histology - central necrotic area with dead eosinophils and sarcoplasmic clumping, numerous eosinophils in periphery, some giant cells and inwardly radiating fibroblasts

what is the treatment of eosinophilic myositis?

corticosteroids

what bacterial conditions can affect muscles?

• Blackleg - Cl. chauvoei, pseudoanthrax, gangrenous myositis

• Malignant oedema - Cl. septicum, Cl. novyi, Cl. perfringens

what parasitic conditions can affect muscle?

• Trichonellosis - Trichenella spiralis in pigs

• Cysticercosis - C. ovis in sheep

• Toxoplasmal myositis

• Sarcocysts - Sarcocytis tenella in sheep

what toxic condition can affect muscle?

Atypical myoglobinuria in horses

what is atypical myoglobinuria associated with?

• horses at pasture are affected

• unknown cause - possibly sycamore seedlings involved

• associated with sudden change in weather conitions - spring or autumn

what are clinical signs of atypical myoglobinuria?

• acute onset, rapid and frequently fatal

• muscle weakness and recumbency

• increased CK/AST and myoglobinuria

• post-mortem - widespread myonecrosis (skeletal and cardiac muscle)

what treatment would we give for atypical myoglobinuria?

supportive therapy if the animals survive