Page 418 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Musculoskeletal system: 1.9 Muscle disorders of the horse 393

VetBooks.ir thereby inhibiting acetyl-CoA dehydrogenases. mitochondrial function and provide analgesia. These
include:
This blocks energy metabolism, particularly from
fat, in type 1 (oxidative) muscle fibres. These are
most prevalent in the postural muscles, and hence • Fluid therapy. In the face of pigmenturia or
these muscle groups are the most severely affected. marked hypovolaemia, intravenous fluids are
preferred. Crystalloids such as compound
Clinical presentation sodium lactate are recommended. In less severe
Horses affected with AM usually present following a cases and with the absence of myoglobinuria,
history of recent turnout. Signs are often acute, with oral fluid may suffice.
weakness and stiffness and a lowered head carriage. • Glucose can be added to the fluids to provide
Horses may appear painful, depressed, trembling and energy. Up to 20 litres of a 5% glucose solution
sweating, and have firm muscles on palpation. They can be safely administered to a 500 kg horse
may be recumbent or reluctant to move. Darkened (i.e. 500 ml of a 50% glucose solution in a 5-litre
urine is often seen due to the presence of myoglo- bag of crystalloids). Plasma glucose should be
binuria. Physical examination may reveal congested monitored as these patients can frequently
mucous membranes and increased respiratory rate be hyperglycaemic. Should glucose increase above
and effort. Rectal examination may reveal a distended 10 mmol/L, insulin therapy may be required.
bladder. Some cases may be found dead at pasture. A bolus of 0.01–0.4 IU/kg or a constant rate of
infusion of 0.01–0.07 IU/kg/hr has been suggested.
Differential diagnosis • If toxin ingestion has occurred within the last
Horses can easily be mistaken for cases of colic, due 4–6 hours, administering laxatives or binding
to the similar clinical presentation. Rectal examina- agents may be of value, but frequently the time
tion and abdominal ultrasonography are, however, of ingestion is unknown.
unremarkable in AM. Other causes of weakness and • Vitamin E (5000 IU D-α-tocopherol) and
recumbency such as orthopaedic injury or botulism selenium (1 mg/kg) may be useful as free radical
should be excluded. Other causes of sudden death. scavengers.
• Riboflavin or vitamin B increases FAD
2
Diagnosis availability. This is found in many multivitamin
High muscle enzyme activity in a horse without a preparations.
recent history of exercise and with the above clini- • NSAIDs such as a meloxicam, flunixin
cal signs should prompt a high index of suspicion of meglumine or phenylbutazone are useful
AM, particularly where Acer trees are present on the analgesics. Care must be taken in the
pasture. Blood samples will reveal evidence of severe hypovolaemic patient to avoid renal injury.
muscle damage, hypocalcaemia, hyperglycaemia and • Supportive care is very important in horses
variable haematology results. Analysis of blood acyl- with AM. Horses should be kept warm and if
carnitines or urinary organic acids can confirm the recumbent, care must be taken to minimise
diagnosis, although this is only available at specific secondary complications such as pressure sores
laboratories and may take several days. Alternatively, or pneumonia. Supporting the head on bales of
skeletal muscle biopsy, of a muscle rich in type 1 hay or straw can prevent oedema developing.
muscle fibres, such as the masseter or intercostal Catheterisation of the bladder may also be
muscles, can be evaluated for the presence of abnor- necessary.
mal lipid staining.
Prognosis
Management The prognosis for horses with AM is guarded to
The aim of treatment is to correct dehydration and poor, with mortality rates of up to 85% reported.
any other electrolyte abnormalities, provide energy, Some horses, if identified early with AM, can make a
eliminate the toxin or its metabolites, support full recovery with appropriate supportive care.