Cairo university

Faculty of veterinary medicine

Department of Internal medicine

Enzootic Ataxia

Prepared by: Aliaa Hany Mohamed Abo El-Rous.

Yasmeen Ali Mohamed Kashef.
Abd El-Monaem Mohamed El-saedy.
Under supervision of: Prof. Dr. Osama Abdo.
Content:

Other names of the disease. (3)

Definition of the disease. (3)
Incidence. (3)
Causes. (4)
Signs. (4)
Prognosis. (6)
How can I help my horse till veterinarian arrive. (6)
Diagnosis. (7)
Prevention and control. (8)
Treatment. (8)
Case. (9)
References. (18)
Other names of the disease:

1. Azoturia.
2. Exertional rhabdomyolysis syndrome (ERS).
3. Set-fast.
4. Tying-up syndrome.
5. Monday morning disease.
6. Equine paralytic myoglobinuria.

Definition of the disease:

Is a disturbance of the normal functioning of the muscles
in the horse that causes painful cramps and muscle
damage.
ERM is most often seen when there is an imbalance
between exercise and feeding, for example maintaining a
high energy diet while suddenly reducing the exercise
levels.

Incidence:
1. It can occur in horses and ponies of all types and ages
and can appear at any stage in their life, while fillies and
mares seem to be more prone than geldings.
2. The disease affects mostly draft (draught) horses, but
racehorses are sporadically affected.

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3. The disease occurs during exercise after a period of at
least 2 days of complete rest on a full working ration.

Causes:
1. Imbalance between exercise and feeding, for example
maintaining a high energy diet while suddenly reducing
the exercise levels.
2. In some cases, it is caused by a genetic disease:
polysaccharide storage myopathy (PSSM).
3. Overexertion.
4. Muscle trauma.
5. Nutritional or electrolyte imbalances and extreme
fatigue.
6. General anesthetic agents and overdosage with CNS
depressants drugs, such as narcotics, cyclic
antidepressants, benzodiazepines, antihistamines and
barbiturates.
7. Metabolic and genetic deficiencies that may cause
rhabdomyolysis include the following: Glycogen
phosphorylase deficiency.

Signs:

1. The horse is unwilling to move, may take short steps

and feel unsteady or stiff on his back legs.
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2. The muscles of the hindquarters feel hot and hard.
3. The horse is likely to appear distressed and may sweat
heavily.
4. There may be frequent attempts to urinate, although the
horse may struggle to take the normal stance to stale.
5. Tachycardia and tachypnea.
6. A slight increase in temperature.
7. Urine may be a red brown to dark chocolate in color
due to the release of myoglobin, a muscle breakdown
product.
8. Serum enzyme (creatine phosphokinase, lactic
dehydrogenase, and aspartate aminotransferase) levels are
elevated.
9. Histologically, there can be severe necrosis of the
skeletal muscles. Severely affected patients can die of
acute renal failure resulting from blockage of the renal
tubules by myoglobin casts.

In extreme cases the horse will be unable to move and

may collapse. the patient may be in extreme pain, which
can be confused with colic.
severe rhabdomyolysis can lead to renal compromise due
to ischemia and the combined nephrotoxic effects of
myoglobinuria, dehydration, and NSAID therapy.

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Prognosis:
severely affected patients can develop kidney failure,
leading to collapse and death.

How can l help my horse till veterinary arrive?

1. If you suspect your horse may be suffering from

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azoturia you should keep him still, cover his loins and
quarters a rug or blanket.
2. Try to encourage the horse to drink, if possible. Fluids
will help flush out the kidneys and reduce the problems
associated with muscle breakdown.
3. Also monitor if the horse can urinate normally and
catch a sample of any urine.
4. Offer the horse hay to eat to help reduce its stress
levels.

Diagnosis:
diagnosis of ERM may be suspected based on clinical
signs but can be confirmed with a blood sample.
Moderate to marked increased levels of three muscle
enzymes abbreviated as CK, AST and LDH are
consistent with a diagnosis of ERM.
The blood results can also indicate the degree of muscle
damage.
In severe cases kidney function should also be assessed
and monitored using repeat blood samples.
If the condition has occurred previously, a muscle biopsy
can be done to identify an underlying cause.
In severely affected animals, regular monitoring of BUN
and/or serum creatinine is advised to assess the extent of
renal damage.

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Prevention and control:

Prevention of further episodes of rhabdomyolysis requires

a very gradual increase in the amount of daily exercise
horses experience. Minimizing stress, providing regular
routines and daily exercise are highly beneficial.

Treatment:
This will depend on the disease severity, but will usually
involve:
1. Anti pain and anti-inflammatory as phenylbutazone
(bute), flunixin or similar potent anti-inflammatory
painkillers.
2. Fluid therapy and electrolytes (oral \ IV according to
severity of the disease) to restore fluid balance in the
patient and protecting the kidneys.
3. Keep the horse still to reduce further muscle damage.
4. Provide the horse with water and encourage it to drink.
5. If the horse is in severe pain or too excitable, use a
sedative/ painkiller combination.
6. Box rest the patient, followed by small paddock turnout
or short duration hand walking, until the blood enzyme
levels return to normal.

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Note:
Diuretics are contraindicated in the absence of IV fluid
therapy and are indicated if the horse is in oliguric renal
failure.

Case:

History:

A four-year-old Standardbred filly, purchased six months

before presentation, was in training and was stabled at the
home track. She was fed a diet of 0.8 kg of oats mixed
with sweet feed and 2 kg of alfalfa twice daily, plus 1.5
kg of bran mash in the evening.

The filly experienced her first tying-up episode after

heavy exercise one year before presentation to the Ontario
Veterinary College. There had been four to six additional
episodes of tying-up during the year, even with rest after
each episode.

Clinical signs common after exercise were reluctance to

move; profuse sweating; and hard, tense gluteal muscles.

Clinical Findings:

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Detailed physical examination on admission revealed no
abnormalities in the patient. Blood samples were collected
for hematologic and biochemical determinations. An
elevated aspartate aminotransferase value, probably
resulting from the tying-up episode the filly experienced
two weeks earlier, was noted.

Pre-exercise muscle biopsies of the superficial gluteal and

semi-tendinous muscles were taken. The horse was
exercised by trotting for approximately one and one-half
miles. After one mile, she demonstrated reluctance to
move, evidenced by a gradual reduction of stride in
both hind-limbs. The skeletal muscles were firm and
tense on palpation, and the filly sweated profusely.

At predetermined times, post-exercise urine and blood

samples were taken. The creatine phosphokinase level
peaked nine hours postexercise at 247,566 M/L (normal is
100 to 500 M/L), and the aspartate aminotransferase
peaked 24 hours postexercise at 31,822 M/L. (normal is
120 to 160 M/ L). The patient was estimated to be 4% to
6% clinically dehydrated, and urine sampled
immediately postexercise indicated myoglobin.
Metabolic acidosis was never observed in the filly.

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Skeletal muscle biopsies were taken immediately post-
exercise. Because of the myoglobinuria and the elevated
packed cell volume (52%), the patient was treated with
lactated Ringer's solution (20 L) to achieve diuresis of
the kidneys. Myoglobin was detectable in the urine up to
24 hours postexercise. Markedly elevated creatine
phosphokinase and aspartate aminotransferase levels
were detected in the serum up to seven days postexercise.

The pre-exercise muscle biopsies (Figure 5) showed signs

of regeneration of muscle fibers, possibly from previous
episodes of tying up; the postexercise biopsies indicated
extensive skeletal muscle destruction.

The acute degenerative changes were characterized by

contraction bands, discontinuity of myofibrillar
masses, pooling of glycogen (Figure 6) and sarcoplasm
in otherwise empty muscle sheaths and marked swelling
of muscle fibers (Figures 7).

Most of the acutely degenerative fibers were type II

(glycolytic-last), as determined by adenosine
triphosphatase histochemical staining at pH 9.5.

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Discussion:

This condition is reported more often in heavily muscled

horses and is frequently observed in fillies and mares.
The severe form of the condition usually occurs within a
few minutes of the commencement of exercise; the horse
exhibits pain, muscular stiffness, sweating, tachycardia,
tachypnea, and tremors in palpably hard skeletal muscles.
Myoglobinuria can be present, and serum enzyme
(creatine phosphokinase, lactic dehydrogenase, and
aspartate aminotransferase) levels are elevated.

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Histologically, there can be severe necrosis of the
skeletal muscles. Severely affected patients can die of
acute renal failure resulting from blockage of the renal
tubules by myoglobin casts.

It also is reported in endurance horses. Shortly after

exercise, the patients are reluctant to move. The hindlimb
muscles become hard and painful. Serum enzymes are
elevated, but not to the levels found in azoturia. In tying
up, the urine does not appear pigmented because
myoglobin is released in small quantities.

Endurance horses that tie up during or after exercise are

reported to have metabolic alkalosis rather than acidosis.
this alkalosis might be secondary to hypochloremia, a
sequence which is reported to result from sweat loss
during endurance rides. Endurance horses usually travel at
130 to 200 m/min; thus, acidosis is highly unlikely. At
slower speeds, the animals should sustain aerobic
metabolism for hours.

The fact that endurance horses traveling relatively slowly

nevertheless present with signs of exertional myopathies
reveals that the mechanisms of the disease are not well
understood Because the endurance horses had not
exercised strenuously and thus imposed lactic acid
anaerobic demands, the enhanced glycogen breakdown
in their diseased muscles must have resulted from another
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cause. Detective skeletal muscle metabolism. such as an
uncoupling of oxidative phosphorylation in the muscles
during exercise, might cause acute rhabdomyolysis in
horses, as it is believed to do in humans.

Equine investigations suggest a derangement of

carbohydrate metabolism, possibly caused by local
hypoxia.

The clinical signs of exertional rhabdomyolysis are

believed to result from excess production of lactic acid
as the patient reverts to anaerobic metabolism.
Mechanisms postulated to cause this lactic acid buildup
include oxygen debt, malonic acid production,
thiamine deficiency, low levels of ionized calcium,
potassium deficiency at the muscle level, and glycogen
buildup in the skeletal muscles during rest.

A rest period allows glycogen accumulation in the

skeletal muscles. Sudden exercise causes glycogen
breakdown and a subsequent increase in lactic acid. The
excess lactic acid is believed to cause muscle cell
breakdown, and this in turn might trigger a rise in the
serum enzymes, myoglobin release, pain, and stiffness.
Local accumulation of lactate might directly denature the
contractile proteins, or the lactate accumulation might
reveal a temporary insufficiency of the oxygen supply to
the muscle.
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Another theory is that the accumulated lactate causes
spasmodic contraction of the muscle that reduces the
free flow of blood; this would induce a still greater
oxygen shortage, and as the cramped or spasmodically
contracted muscle continued to work, the oxygen deficit
would increase. There is little doubt that ischemia often
contributes to the development of severe lesions.

The released myoglobin might cause myoglobinuria,

which might lead to renal tubular degeneration
resulting from the precipitation of myoglobin in the
tubules. The more severe the muscle damage, the greater
the frequency of myoglobinuria. Although myoglobin
might be excreted into the urine at a concentration that
does not result in visible brownish discoloration, the renal
tubular epithelium nevertheless might be injured by
myoglobin. (Myoglobin has a low renal threshold
because of its low molecular weight of 17,000; it is easily
filtered through the glomerulus.) Dark urine caused by
myoglobin derived from damaged muscles is reported
when myoglobin concentrations exceed 40 mg/dl of
urine. Brown urine color is therefore a sign of significant
muscle disease.

A new theory regarding exertional rhabdomyolysis asserts

that the condition might be secondary to
hypothyroidism. Low resting thyroxine (Ty) levels have
been identified in half of the myopathy cases examined.
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Summary:

Case clearly portrays the range of signs that can be

present in equine exertional rhabdomyolysis. The clinical
signs, the serum enzyme values, and the muscle biopsy
results can be so varied that prognoses and suitable
treatments sometimes are difficult to determine. This case
often are hard to classify as mild or severe exertional
rhabdomyolysis. More research into the etiology,
treatment, and prevention of this disease complex is
needed.

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References:
1. Mimi Arighi, John D Baird, TJ Hulland Compend
Contin Educ Pract Vet 6 (12), S726-S732, 1984.
2. Mimi Arighi, DVM John D. Baird, BVSc, PhI
Department of Clinical Studies T. J. Hulland, DVM, PhD
Department of Pathology Ontario Veterinary College
University of Guelph Guelph, Ontario, Canada.
3. Carol Phillips 9 December, 2019 13:25.
4. By Stephanie J. Valberg , DVM, PhD, DACVIM-
LAIM, DACVSMR, Department of Large Animal
Clinical Sciences, College of Veterinary Medicine,
Michigan State University Reviewed/Revised May 2022 |
Modified Oct 2022.

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