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In
association with Mark Andrews, BVM&S
CertEP MRCVS, of Equine Science Update we are pleased to
provide the latest Equine Veterinary Information
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Equine Rhabdomyolysis
Syndrome
Equine Rhabdomyolysis Syndrome (ERS) is also known as
Monday morning disease, setfast, azoturia, tying-up and exertional
rhabdomyolysis. The condition is characterised by damage ("lysis")
of striated muscle fibres (especially type II muscle fibres). Recent
surveys have shown that, in the UK, about 7% of flat racing
Thoroughbred horses, polo horses and competition horses
are affected.
The signs vary in degree from a mild
abnormality of gait to recumbency. ERS may cause behavioural
problems during backing.
Measurement of “muscle enzymes” in the
blood can give a guide to the severity of the muscle damage. The
most specific indicator of muscle damage is creatine kinase (CK) .
Levels in the blood increase rapidly after the onset of ERS. Values
above 20,000iu/l are not uncommon in severe cases. Aspartate
aminotransferase (AST) is less specific for muscle damage, and can
be increased as a result of other conditions such as liver problems.
It reaches peak levels more slowly than CK and persists
longer.
Mild cases of ERS can be detected by using an exercise test in which blood levels of the muscle enzyme
CK are checked before, and four hours after, 20 minutes of trotting
exercise. An increase of more than twice pre-exercise values,
confirms that the horse has ERS.
Our understanding of ERS has grown in the
last few years. Specific causes of the syndrome have been
identified, and the factors influencing the occurrence of the
disease have been further investigated.
Equine rhabdomyolysis syndrome appears in two forms:
sporadic and recurrent. It is important to differentiate the
sporadic cases from the acute recurrent episodes because the
management of each differs. Various causes of the sporadic form have
been described - such as carbohydrate overload, viral myositis,
vitamin E / Selenium deficiency and exertional
myopathy. These factors may also act as triggers for the recurrent
form.
Two specific causes of recurrent ERS have
been identified so far. Equine polysaccharide storage myopathy, and
a calcium channel disorder.
Equine polysaccharide storage myopathy (EPSM) was
first seen in Quarter horses in the USA, but has since been recorded
in other breeds - including draft horses and draft horse crosses,
and warmbloods. The diagnosis is confirmed using a muscle biopsy, which shows characteristic accumulation of abnormal
levels of polysaccharides (glycogen) in the muscle. Researchers at
Cornell University in the USA suggest that 50% of draft horses and
draft cross horses are affected to some extent.
Recent work shows that EPSM definitely
occurs in the UK. (1) It has been found in samples
of muscle taken from clinical cases and accounts for about 25% of
cases of ERS. A random sample of horses at abattoirs showed that 5
-10% of horses were affected. The cause of EPSM is unknown. Affected
horses have high resting glycogen levels in the muscle. But this is
not because they are unable to break the glycogen down - rather it
appears that they manufacture more of it.
The calcium channel disorder is a defect
in calcium metabolism within the muscle cell that interferes with
normal control of muscle contractions. This form is found in
Thoroughbreds and appears to be inherited.
Trigger factors depend on the horse and
the type of work it does. For example, in Thoroughbred horses in the
UK, nervous two-year old fillies are most likely to be affected. In
one study, ERS recurred within a season in most of the affected
horses, and 70% of affected horses were unable to race that season.
So it is debateable whether it is actually worth trying to train
these horses. Interestingly, diet and previous lameness have only
been associated with an increased risk of ERS in the USA, but not in
the UK.
In contrast to the situation in
Thoroughbreds, in eventing horses the only factor that has been
shown to affect the risk of the disease is turnout time.
The major trigger factor in polo horses
is lack of fitness. ERS tends to be seen early in the season; after
a rest period prior to exercise and if the horse has had more
strenuous exercise than normal. Horses with an excitable temperament
are more likely to be affected. Typically the signs of ERS in polo
horses are severe. (2)
Management of horses affected with ERS plays an
important role in reducing the risk of recurrence. The carbohydrate
content of the diet should be reduced as much as possible and
replaced by oil. To replace 20% of the caloric intake with oil would
require about 500ml for a 500kg horse. Oil should be added to the
diet even if the horse is turned out and only eating roughage. This
lowers the muscle glycogen and is unlikely to adversely affect
performance. Horses should receive a daily minimum roughage intake
of 1% of body weight .
Attention should be given to vitamin and
mineral levels. This is especially so if large amounts of oil are
added to the diet (in which case the requirements for vitamin E and
selenium may be increased).
It
is important to resume exercise early. According to Dr Cathy
McGowan, formerly of the Royal Veterinary College, it is not
necessary to wait until the muscle enzymes return to normal before
starting work again."If your horse is walking freely I`m happy for
you to exercise it."
She
advises that warm-up work should be relaxed rather than too
collected. It is also best to have regular exercise with no days
off. Horses should be turned out as much as possible without
exposing them to too much rich pasture.
Dantrolene, a drug that decreases the
release of calcium within the muscle, is sometimes helpful,
especially in Thoroughbreds, to allow the horse to get back to
regular work.
References
1. Four cases of equine
polysaccharide storage myopathy in the United Kingdom
McGowan CM, Menzies-Gow NJ, McDiarmid AM,
Patterson-Kane.JC. Veterinary Record (2003) 152, 109 -
112
2. Incidence of
exertional rhabdomyolysis in polo horses in the USA and the
United Kingdom in the 1999/2000 season.
McGowan CM, Posner RE, Christley
RM. Veterinary Record (2002) 150, 535 -
537
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