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EQUINE CLINICAL PATHOLOGY - Rossdale & Partners

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G u i d e t o e q u i n e c l i n i c a l p a t h o l o g y<br />

about liver function. The liver has a large<br />

functional reserve and compensatory<br />

capacity. Liver enzyme rises suggest<br />

hepatopathy which can be differentiated<br />

to a degree into acute, chronic, biliary<br />

obstructive or mixed pathology, but bile<br />

acid assays and bromsulphalein clearance<br />

test results reveal either adequate (normal<br />

levels) or impaired (high levels) functional<br />

compensation. Impaired hepatic function<br />

suggests a guarded prognosis. Liver biopsy<br />

and ultrasound examinations are required<br />

to confirm an etiologic diagnosis and to<br />

refine prognosis.<br />

Amylase<br />

Elevations occur in the presence of<br />

pancreatitis, but this condition is rarely<br />

diagnosed in the horse.<br />

Glucose<br />

Other than for oral glucose and xylose<br />

absorption tests, useful for the diagnosis<br />

and evaluation of intestinal malabsorption<br />

cases, the value of this assay in adult<br />

horses is limited to cases of pituitary<br />

pars intermedia dysfunction (equine<br />

Cushing’s syndrome) which are frequently<br />

hyperglycaemic. Measurement of blood<br />

glucose is invaluable in the management of<br />

critically ill foals as profound hypoglycaemia<br />

is often seen in neonatal septicaemia.<br />

Samples for glucose assay must be taken<br />

into fluoride anticoagulant or must reach<br />

the laboratory within hours of collection.<br />

Oral Glucose Absorption Test<br />

The horse to be tested should be fasted<br />

for 18-24 hours. 1 g glucose per kg body<br />

weight is administered by stomach tube.<br />

Blood samples are collected into fluoride<br />

anticoagulant at times 0, 30, 60, 90, 120,<br />

150, 180, 210 and 240 mins. Glucose<br />

levels should peak at double resting (0<br />

mins) levels at 60-120 mins and return to<br />

resting levels by 240 mins.<br />

Cholesterol and Triglycerides<br />

Elevations are seen in the presence<br />

of abnormal lipid metabolism and<br />

hyperlipidaemia. These conditions are<br />

typically seen in the Shetland and other<br />

small ponies, donkeys and occasionally as<br />

a secondary complication in horses that<br />

are anorexic or unable to eat. Pregnant<br />

Shetland pony mares appear particularly<br />

susceptible following a managemental and<br />

nutritional change/challenge.<br />

Urea<br />

Urea is produced in the liver from the<br />

metabolism of ammonia. Elevations are<br />

seen in the presence of abnormal renal<br />

function. Urea levels may also rise in<br />

the haemoconcentrated and ‘over-trained’<br />

horse, associated with fluid balance shifts<br />

rather than renal disease. Many cases<br />

of equine dysautonomia (‘grass sickness’)<br />

have a degree of uraemia but this is<br />

usually caused by catabolism. A period<br />

of anorexia can have a similar result.<br />

29

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