APPLIED MEDICINE: CLINICAL PATHOLOGY AND DERMATOLOGY


first 2 to 3 weeks of life.4–6 Bilirubin concentration is highest in young foals and reduces to normal adult horse ranges by 7 to 14 days of age.5,6 Both total and unconjugated bilirubin concentrations in foals are increased over adult values from birth through 7 to 14 days postpartum.6 Neonatal hyperbiliru- binemia may be the result of immature hepatic func- tion or hemolysis of fetal erythrocytes.3,4,6 The ability of the fetal liver to excrete bilirubin is mini- mal, and bilirubin must be excreted across the pla- centa by the fetus.6 Foals less than 5 days of age have less hepatic glucuronyl transferase activity than adults and therefore a slower rate of bilirubin uptake and conjugation.4 Increased direct biliru- bin concentration in foals 2 days of age or less may be due to a lack of bilirubin transport proteins.3 Serum bile acid concentration is highest at birth


diagnostic use to identify hepatic disease.2 Al- though mare colostrum contains a low amount of GGT, postsuckle GGT activity in foals is not associ- ated with serum immunoglobulin G concentration10 and cannot be used to determine colostrum intake.11 Hepatic GGT activity is increased in young animals and may account for some of the increased GGT activity in foals.2,10 Neonatal hyperbilirubinemia is normal during the


and gradually declines for at least 6 weeks postpar- tum.5 Serum bile acid concentration in foals may be elevated because of increased hepatic production, decreased excretion, differences in gastrointestinal flora, or enhanced intestinal absorption. Hepatic uptake of serum bile acid and excretion into bile require active transport, which may not be fully functional in foals. Triglyceride concentration in foals tends to be highest during the first 2 weeks of life and moder- ately increased for up to 6 weeks of age.5,6 Triglyc- eride concentrations in foals may decrease as hepatic function matures and triglycerides are used to synthesize other lipoproteins.6 Triglycerides can be very elevated in foals that have recently nursed, as the result of digestion of fat in mare’s milk.


3. Renal Function


Increased creatinine concentration in newborn foals is usually caused by placental pathology and/or fetal stress rather than renal disease.1 Placental pa- thology appears to affect serum blood urea nitrogen (BUN) concentration less than creatinine, probably because urea is a smaller and more diffusible molecule. Spurious hypercreatininemia in foals 2 days of


age is defined by serum creatinine concentration 5 mg/dL, and creatinine concentration decreases by 50% in the first 24 hours of treatment and each day until it is within normal range by 72 hours.12 Serum creatinine concentration in foals with spuri- ous hypercreatininemia normalizes regardless of fluid administration, including foals that are only nursing free-choice. Seventy-one percent of foals affected by spurious hypercreatininemia were also


diagnosed with neonatal encephalopathy in one re- port.12 It is unknown if placental abnormalities predispose newborn foals to spurious hypercreati- ninemia. Blood urea nitrogen concentration is near normal


adult ranges at birth, declines during the first 48 hours of life, and remains low until 1 to 18 weeks of age.4,7,13 Very young foals may be azotemic, but renal indices and plasma osmolality should decrease as the foal nurses and fluid intake expands plasma volume and stimulates diuresis.13 Increased BUN concentration often occurs when foals are in a cata- bolic state and using endogenous protein as an en- ergy source.1 Deamination of protein results in increased urea production and excretion. Low BUN concentration in growing foals may be the re- sult of increased amino acid utilization for protein synthesis.3


4. Electrolytes


from birth until at least 18 weeks of age.7 Schmitz et al4 found that serum inorganic phosphorus con- centration was initially slightly higher than ex- pected adult ranges and peaked between 2 to 3 weeks of age. Serum inorganic phosphorous con- centration then gradually decreased but remained above normal adult ranges at 6 months of age. Hyperphosphatemia is apparently related to skele- tal ossification and osteoblastic activity.4,13


At birth, both total and ionized calcium concentra- tions are 25% to 30% higher than in adult horses.1 Hours after birth, blood calcium concentration is approximately 20% lower than in adults and then gradually returns to normal limits in the first few days of life. Edwards et al13 reported that serum calcium concentration decreased significantly dur- ing the first 48 hours of age and returned to normal ranges by 7 days. Inorganic phosphorous concentration is elevated


5. Conclusions


Interpretation of serum chemistry values in neona- tal foals can be complicated when normal ranges from adult horses are used. Comparison of refer- ence ranges from textbooks and between different laboratories and serum chemistry analyzers is not always reliable. Ideally, the normal expected ranges used in foals are stratified by age and are based on a large sample of healthy foals. However, this is often not possible, and knowing the inherent differences in serum chemistry values between foals and adult horses helps to determine if an abnormal- ity is significant.


References


1. Axon JE, Palmer JF. Clinical pathology of the foal. Vet Clin Equine 2008;24:357–385.


2. Gossett KA, French DD. Effect of age on liver enzyme ac- tivities in serum of healthy Quarter Horses. Am J Vet Res 1984;45:354–356.


3. Bauer JE, Harvey JW, Asquith RL, et al. Clinical chemistry reference values of foals during the first year of life. Equine Vet J 1984;16:361–363.


AAEP PROCEEDINGS  Vol. 59  2013 499


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