Medicine Lecture 5th Stage 28-11-2017 Dr.Osamah Muwafk
1
AZOTURIA, TYING-UP
Sporadic Acute Exertional Rhabdomyolysis In Horses
It is a complex syndrome that likely has numerous causes, probably it is
the most common muscle disorder and it is a frequent cause of poor
performance in horse.
Etiology:
1- The most common cause is performing exercise of unaccustomed
intensity or duration, which can result in metabolic exhaustion and
hyperthermia.
2- in young horses occur as a result of vitamin E and selenium
deficiency.
3- Other suggested causes include:
a- Hypothyroidism.
b- Sodium or potassium deficiency.
c- Viral infection.
d- High carbohydrate diets.
e- Abnormalities in metabolic function.
Pathogenesis:
1. during exercise or inadequate antioxidant activity.
2. Increased oxidant formation lead to oxidant injury to cells.
3. Accumulation of calcium in intracellular fluids secondary to deranged
energy and/or membrane function.
4. Dysfunction and death of myocytes.
5. Subsequent release of cellular constituents, including the enzymes
creatine kinase, aspartate aminotransferase and carbonic anhydrase,
and myoglobin.
6. Necrosis of myocytes caused pain and inflammation in the muscle,
with infiltration of inflammatory cells.
Medicine Lecture 5th Stage 28-11-2017 Dr.Osamah Muwafk
2
7. Release of cellular constituents results in electrolyte abnormalities,
primarily a hypochloremic metabolic alkalosis, a systemic
inflammatory response, and pigmenturia.
8. acute renal failure can develop as a result of myoglobinuric nephrosis.
Clinical Findings:
1- Signs can be mild and resolve spontaneously within 24 h or be severe
and progressive.
2- Horse that does not perform to expectation and displays a stiff or short
stepping gait that may be mistaken for lower leg lameness.
3- Reluctant to move when placed in its stall.
4- Apprehensive and anorexia, paw, and frequently shift its weight.
5- More severely affected have hard and painful muscles (usually gluteal
muscles).
6- Sweat excessively.
7- Tremble or have widespread muscle fasciculations.
8- Elevated heart and respiratory rates.
9- Deep red urine (myoglobinuria) occurs but is not a consistent finding.
10-
Severely affected horses may be recumbent.
Clinical Pathology:
1- Mildly or inapparently affected horses have moderate increases in
serum creatine kinase (CK) (20 000-5 0 000 IU/L), aspartate
aminotransferase (AST), and lactate dehydrogenase (LDH) activity.
2- Severely affected horses have large increases in CK (>100 000 IU/L)
and other muscle-derived enzymes.
3- Serum myoglobin concentrations increase markedly during exercise in
affected horses, and decline within 24-48 h.
4- Severely affected horses are often hyponatremic, hyperkalemic,
hypochloremic and azotemic.
5- Myoglobinuria is detectable either grossly or on chemical analysis.
6- Muscle biopsy.
Medicine Lecture 5th Stage 28-11-2017 Dr.Osamah Muwafk
3
Differential diagnosis:
1- Polysaccharide storage myopathy of Quarter horses
2- lonophore intoxication (monensin, salinomycin).
3- Equine lower motor neurone disease.
4- Hyperkalemic periodic paralysis.
5- Laminitis.
6- Colic.
7- Pleuritis.
8- Aorto-iliac thrombosis.
Treatment:
1- Rest.
2- correction of dehydration and electrolyte abnormalities.
3- prevention of complications including nephrosis and laminitis.
4- provision of analgesia ketoprofen (2.2 mg/kg N every 12 h).
========================================================================
To study the phenomena of disease without books is to sail
an unchartered sea, while to study books without patients is
not to go to sea at all.
##########################################################################