Equine Myopathies

Question 1

1. Define myopathy.
2. Define rhabdomyolysis.
3. Exertional, exercise-induced, exercise-associated.

Answer 1

1. General term used to describe a disorder/pathology of muscles.
2. Term used to describe rapid breakdown of skeletal muscle cells.
3. Used interchangeably e.g. exertional rhabdomyolysis or exercise-induced myopathy.

Question 2

Presentation of 2 main muscle conditions in equine practice (may be emergency).

Answer 2

Atypical myopathy.
- typically presents as muscle weakness leading to recumbency, in pastured horses.
Sporadic exertional
rhabdomyolysis (exercise-induced myopathy, tying up, azoturia).
- typically presents as reluctance to move due to muscle ‘cramping’, stiffness and pain, associated w/ exercise.

Question 3

1. Atrophy.
2. Myalgia.

Answer 3

1. Decrease in muscle mass.
   e.g. neurogenic atrophy (rapid), disuse atrophy (slower).
2. Muscle pain. can e generalised or localised.
   e.g. localised pain in back musculature from poor fitting saddle, or delayed onset muscle soreness 24-48hrs after over-exertion.

Question 4

1. Muscle fasciculations.
2. Abnormal gait.
3. Reluctance to exercise and exercise intolerance.

Answer 4

1. Fine tremors.
   e.g. can occur w/ muscle weakness, EPM, EMND.
2. Lameness more commonly due to joint, tendon or ligament pathology. Muscle fibrosis (scarring) can cause mechanical gait abnormalities. e.g. fibrotic myopathy.
3. A wide range of conditions can present in this way not just muscle disease. e.g. reluctant to jump due to muscle strain.

Question 5

Main diagnostic techniques for investigating muscle diseases?

Answer 5

CK (creatine kinase) and AST (aspartate aminotransferase).
CK is muscle specific, peaks 4-6hrs, rises higher.
AST peaks 24hrs, can take couple weeks to return to normal.

Question 6

Single vs dynamic sampling of CK and AST.

Answer 6

Single: single sample at time of exam (most common practice).
Dynamic: before and after (4-6hrs) an exercise test (CK at 4hrs should not be more than double baseline value).
*Some clinicians take 3rd sample 24hrs later.

Question 7

Myoglobinuria and myopathy.

Answer 7

Myoglobin released from muscle cells as they break down.
Myoglobin excreted in the urine.
- dark coloured urine.
Myoglobin is nephrotoxic and can cause ARF.
Typically only seen in more severe rhabdomyolysis.

Question 8

Muscle biopsy.

Answer 8

Contact lab ahead of procedure as sample must be dealt w/ immediately on arrival.
Can use biopsy (e.g. Bergstrom) needle or open method.
- use clinically affected muscle.
- for exertional rhabdomyolysis, typically semimembranosus used.
- for EMND, use sacrocaudalis dorsalis (craniolateral to tail head).

Question 9

Exercise-induced myopathies.

Answer 9

Sporadic exertional rhabdomyolysis/azoturia/’tying up’.
- one-off or unusual occurrence.
Recurrent exertional rhabdomyolysis.
- frequently results from underlying heritable conditions incl. PSSM and RER.
Polysaccharide storage myopathy.

Question 10

Other myopathies.

Answer 10

Atypical myopathy.

Question 11

Sporadic exertional rhabdomyolysis.

Answer 11

Occurs during or after exercise.
Reluctance to move.
Typically affects hindlimb muscles.
Stiff, short striding hindlimb gait.

Question 12

SER clinical exam.

Answer 12

Muscles may be hard, painful or swollen.
May appear distressed (severe cases high HR, RR, sweating, muscle tremors, pawing ground, can mimic ‘colic’ signs).
Owners think of it as ‘muscle cramp’.

Question 13

SER dx.

Answer 13

Initial assumption based on clinical signs.
Confirmation by measuring CK and AST.
For a first/occasiona; episode, usually no need to undertake further dx tests.

Question 14

SER aetiopathogenesis.

Answer 14

Exact aetiopathogenesis not well understood.
Can be triggered after a rest period (w/o reduction in feed).
Overexertion above level of fitness.
Other proposed causes include dietary deficiencies of electrolytes, vit E and selenium, or exercise in conjunction w/ herpes or influenza virus infections.
Can occur on competition days, risk factors incl. overexertion, lack of appropriate warm up or cool down, hot, humid days may increase risk due to high body temps, loss of fluid and electrolytes in sweat, and depletion of muscle energy stores.

Question 15

SER tx and mx.

Answer 15

Rest.
NSAIDs (typically single IV dose to manage acute pain).
IV fluids if severe (and myoglobinuria present).

Prevention:
- improved mx, regular turn out / exercise, warm up and cool down, don’t exert, reduce feed when exercise drops, provide salt lick / electrolyte supplement, may consider vit E/selenium supplement.
Care excessive exercising in heat, care exercising if suspect respiratory infection.
If horse has ‘tied up’ once, may be more likely to do it again, so appropriate mx important.

Question 16

Which blood tube would you use if only measuring CK and AST?

Answer 16

Lithium heparin anticoagulant (green top).
Plain tube (red top).

Question 17

When can an owner ride/exercise their horse again following an episode of ‘tying up’?

Answer 17

When the horse is no longer showing signs of pain.
Potentially wait for CK/AST to return to normal.
- suggest turning out for a few days before re-introducing work and re-introduce work gradually.

Question 18

Recurrent exertional rhabdomyolysis.

Answer 18

Seen in thoroughbreds.
Tying up episodes (same as sporadic form) but can occur repeatedly in susceptible horses.
Typically develop clinical signs when they are fit.
Can be triggered by exercise at any pace (not just gallop).

Question 19

CE and Dx of RER.

Answer 19

CS same as SER but episodes can happen repeatedly.
Measure CK and AST.
When recurrent, consider measuring electrolytes.
Further dx tests such as muscle biopsies may be performed in difficult to manage cases, but of little practical benefit in most TBs.

Question 20

RER aetiopathogenesis.

Answer 20

Abnormality in IM calcium regulation.
More commonly seen in TBs w/ a nervous or excitable temperament.
More commonly seen in fillies and mares.
5-10% TBs affected in a racing season.

Question 21

RER tx and mx.

Answer 21

Acute episode - same as for sporadic.
- often returned to exercise quite quickly – as soon as comfortable, no need to wait for normal CK/AST.
Prevention:
- diet – change to high fat low starch (may not be able to completely replace starch in diet, as can be difficult to maintain body condition during racing).
- exercise/turn out daily.
- Dantrolene (muscle relaxant).
High fat appears to decrease muscle damage by reducing anxiety / excitability.
Effect of RER on racing performance thought to be minimal in most cases.

Question 22

Polysaccharide Storage Myopathy (PSSM).

Answer 22

PSSM seen in many breeds - esp. draught horses, quarter horses and warmbloods.
Present same as sporadic form i.e. can have acute episodes of ‘tying up’ during/after exercise, but can also have more subtly signs e.g.:
- more difficult to ride (unable to collect /extend).
- poor technique over fences.
- difficulty lifting limbs.

Question 22

PSSM CE.

Answer 22

Same as sporadic form i.e. can have acute episodes of ‘tying up’.
Other findings of clinical exam may include:
- painful firm back and hindquarter muscles.
- gait abnormalities.
- muscle atrophy.
- difficulty lifting limbs.

Question 23

PSSM Dx.

Answer 23

Measure CK and AST.
Muscle biopsy to identify abnormal glycogen accumulation.
Genetic testing to identify GYS1 mutation.

Question 24

PSSM aetiopathogenesis.

Answer 24

Glycogen storage disorder.
Results in increased skeletal muscle glycogen concentrations and the accumulation of abnormal amylase resistant polysaccharide in type 2 muscle fibres.
The glycogen accumulation is not related to an inability to metabolise glycogen but is due to enhance insulin sensitivity.
Mutation in glycogen synthase enzyme has been identified, leading to enhanced glycogen synthase activity (type 1 PSSM).
Horses (w/ abnormal muscle glycogen on biopsy) w/o GYS1 mutation are termed type 2 PSSM.
Type 1 v common in EU draft horses and uncommon in British draft horses.

Question 25

Tx and m of PSSM.

Answer 25

Initial tx for acute episode same.
Diet changes and mx key.
Establish routine for feeding and exercise!
Diet - high fat low starch.
– less glucose uptake into muscle cells and provision of more plasma free fatty acids for use in muscle fibres during aerobic exercise.

Question 26

Dietary mx.

Answer 26

Provision of high fat diets.
Veg oils highly unsaturated, v digestible, v energy dense, can be added to feed.
- BUT unpalatable to many, prone to rancidity in warm temps and difficult to feed large amounts (should also supplement vit E at 100IU per 100g added oil).
Several commercially prepared high fat balanced feeds which are more convenient and more palatable.
Both PSSM and RER managed w/ high fat low starch diets, but efficacy appears to be through different mechanisms.

Question 27

Atypical myopathy.

Answer 27

Recumbent or sudden death in field.
Not associated with exercise.
More than one horse may be affected.
Typically young.
Most common in autumn.
Fatal in approx. 75% of affected horses.

Question 28

CS and Dx of AM.

Answer 28

Sudden onset muscle weakness, leading to recumbency.
Appear depressed (low hanging head/neck).
Muscle trembling.
Usually afebrile w/ normal appetite.
May have dysphagia due to weakness of masticatory muscles or oesophageal muscles.
May show resp. difficulty.
May have cardiac arrhythmias.
Brown or dark red urine due to myoglobinuria.
Dx by CS, CK and AST, myoglobin in urine.

Question 29

Aetiopathogenesis of PSSM.

Answer 29

Hypoglycin A toxin from seeds and leaves of Sycamore tree (acer pseudoplatanus).
Hypoglycin A inhibits acetyl-CoA dehydrogenase, which is involved in metabolism of fatty acids to form ATP.
- normal energy supply to muscle cells is impaired.
Most common in winter and adverse weather conditions trigger disease.
- many cases after sharp decline in temp./high winds/excessive rainfall which cause Sycamore seeds and leaves to fall onto pasture, where they are ingested.
Can occur in spring by ingestion of new shoots.

Question 30

Tx of PSSM.

Answer 30

Discuss risk of fatality.
If standing and appropriate, consider transport to clinic/hospital but discuss risks of recumbency in horse box.
Consider challenges of managing a recumbent horse at owner’s premises.
Intensive care and nursing - regular turning if recumbent, monitor UOP.
IV fluids (supplementary calcium).
Analgesics.

Question 31

Preventing PSSM.

Answer 31

Critical to provide advice to owners.
Avoid affected fields.
Fence off around trees.
Pick up seeds/leaves.
Amount of toxin can vary - can measure Hypoglycin A in plant samples.
Limit grazing time to a few hrs/day.
(most affected horses graze >6hrs/day).
Ensure plenty of grass and supplementary feed.
Feed horses before letting them out to pasture.
Do not put hay on ground (in affected fields).