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Review of Serum Chemistry Interpretation in Neonatal Foals

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Review of Serum Chemistry Interpretation in Neonatal Foals APPLIED MEDICINE: CLINICAL PATHOLOGY AND DERMATOLOGY Review of Serum Chemistry Interpretation in Neonatal Foals Bryan M. Waldridge, DVM, MS, Dipomate ABVP (Equine Practice), Diplomate ACVIM Interpretation of serum chemistry results in foals can be very confusing because reference ranges are usually based on adult samples, and many values are increased in foals compared with adults. Un- derstanding the expected differences in serum chemistry results between foals and adult horses improves the recognition of abnormalities and facilitates making an accurate diagnosis. Author’s address: PO Box 1843, Georgetown, KY 40324; e-mail: [email protected]. © 2013 AAEP. 1. Introduction Serum alkaline phosphatase (ALP) activity is 2,3,6,7 Reference ranges for many serum chemistry values highest during the first 2 to 8 weeks of life and 7 6 in adult horses cannot reliably diagnose disease in remains elevated for 8 weeks to at least 90 days. foals.1–4 Placental abnormalities may influence There is a wide individual variation and large stan- dard deviation of ALP activity in foals, which limits clinicopathologic results in neonates during the first 2 1 its effectiveness to diagnose hepatobiliary disease. few days of life. Most hepatic indices in foals are 8 significantly different from adult horses, especially Hank et al measured activity of specific ALP during the neonatal period. Ideally, age-specific isoenzymes and determined that 80% to 92% of total ALP activity is from bone. However, Dumas and reference ranges should be used in foals, but it is 9 difficult to sample a large enough population of clin- Spano reported that increased ALP activity in foals ically normal foals and few laboratories are able to is mainly of hepatic origin. Although the contribu- generate age-specific references. Whenever possi- tion of the various ALP isoenzymes to total ALP ble, the reference ranges in this report have been activity remains unclear, most of the increased ALP obtained from clinically healthy foals. activity in foals is attributed to increased osteoblas- tic activity and bone formation in young, growing animals.2,4,6,8 2. Hepatic Indices Gamma glutamyltransferase (GGT) activity in Sorbitol dehydrogenase and aspartate transaminase foals ranges from 1.5 to 3 times normal adult values are reliable indicators of hepatocellular disease in for the first 3 to 4 weeks of life.2,10 Gamma glutam- foals.2,5 Sorbitol dehydrogenase and aspartate yltransferase activity in foals is most increased from transaminase have more narrow standard devia- adult horses at 7 to 21 days of age.6 Similar to ALP tions in foals, and their normal reference ranges are activity, there is a normal wide individual variation closer to those of adults. in GGT activity between foals, which restricts its NOTES 498 2013 ր Vol. 59 ր AAEP PROCEEDINGS APPLIED MEDICINE: CLINICAL PATHOLOGY AND DERMATOLOGY diagnostic use to identify hepatic disease.2 Al- diagnosed with neonatal encephalopathy in one re- though mare colostrum contains a low amount of port.12 It is unknown if placental abnormalities GGT, postsuckle GGT activity in foals is not associ- predispose newborn foals to spurious hypercreati- ated with serum immunoglobulin G concentration10 ninemia. and cannot be used to determine colostrum intake.11 Blood urea nitrogen concentration is near normal Hepatic GGT activity is increased in young animals adult ranges at birth, declines during the first 48 and may account for some of the increased GGT hours of life, and remains low until 1 to 18 weeks of activity in foals.2,10 age.4,7,13 Very young foals may be azotemic, but Neonatal hyperbilirubinemia is normal during the renal indices and plasma osmolality should decrease first 2 to 3 weeks of life.4–6 Bilirubin concentration as the foal nurses and fluid intake expands plasma is highest in young foals and reduces to normal adult volume and stimulates diuresis.13 Increased BUN horse ranges by 7 to 14 days of age.5,6 Both total concentration often occurs when foals are in a cata- and unconjugated bilirubin concentrations in foals bolic state and using endogenous protein as an en- are increased over adult values from birth through 7 ergy source.1 Deamination of protein results in to 14 days postpartum.6 Neonatal hyperbiliru- increased urea production and excretion. Low binemia may be the result of immature hepatic func- BUN concentration in growing foals may be the re- tion or hemolysis of fetal erythrocytes.3,4,6 The sult of increased amino acid utilization for protein ability of the fetal liver to excrete bilirubin is mini- synthesis.3 mal, and bilirubin must be excreted across the pla- centa by the fetus.6 Foals less than 5 days of age 4. Electrolytes have less hepatic glucuronyl transferase activity At birth, both total and ionized calcium concentra- 1 than adults and therefore a slower rate of bilirubin tions are 25% to 30% higher than in adult horses. uptake and conjugation.4 Increased direct biliru- Hours after birth, blood calcium concentration is bin concentration in foals 2 days of age or less may approximately 20% lower than in adults and then be due to a lack of bilirubin transport proteins.3 gradually returns to normal limits in the first few 13 Serum bile acid concentration is highest at birth days of life. Edwards et al reported that serum and gradually declines for at least 6 weeks postpar- calcium concentration decreased significantly dur- tum.5 Serum bile acid concentration in foals may ing the first 48 hours of age and returned to normal be elevated because of increased hepatic production, ranges by 7 days. decreased excretion, differences in gastrointestinal Inorganic phosphorous concentration is elevated 7 flora, or enhanced intestinal absorption. Hepatic from birth until at least 18 weeks of age. Schmitz 4 uptake of serum bile acid and excretion into bile et al found that serum inorganic phosphorus con- require active transport, which may not be fully centration was initially slightly higher than ex- functional in foals. pected adult ranges and peaked between 2 to 3 Triglyceride concentration in foals tends to be weeks of age. Serum inorganic phosphorous con- highest during the first 2 weeks of life and moder- centration then gradually decreased but remained ately increased for up to 6 weeks of age.5,6 Triglyc- above normal adult ranges at 6 months of age. eride concentrations in foals may decrease as Hyperphosphatemia is apparently related to skele- 4,13 hepatic function matures and triglycerides are used tal ossification and osteoblastic activity. 6 to synthesize other lipoproteins. Triglycerides can 5. Conclusions be very elevated in foals that have recently nursed, as the result of digestion of fat in mare’s milk. Interpretation of serum chemistry values in neona- tal foals can be complicated when normal ranges 3. Renal Function from adult horses are used. Comparison of refer- Increased creatinine concentration in newborn foals ence ranges from textbooks and between different is usually caused by placental pathology and/or fetal laboratories and serum chemistry analyzers is not stress rather than renal disease.1 Placental pa- always reliable. Ideally, the normal expected thology appears to affect serum blood urea nitrogen ranges used in foals are stratified by age and are (BUN) concentration less than creatinine, probably based on a large sample of healthy foals. However, because urea is a smaller and more diffusible this is often not possible, and knowing the inherent molecule. differences in serum chemistry values between foals Spurious hypercreatininemia in foals Ͻ2 days of and adult horses helps to determine if an abnormal- age is defined by serum creatinine concentration Ͼ5 ity is significant. mg/dL, and creatinine concentration decreases by References Ն 50% in the first 24 hours of treatment and each 1. Axon JE, Palmer JF. Clinical pathology of the foal. Vet 12 day until it is within normal range by 72 hours. Clin Equine 2008;24:357–385. Serum creatinine concentration in foals with spuri- 2. Gossett KA, French DD. Effect of age on liver enzyme ac- ous hypercreatininemia normalizes regardless of tivities in serum of healthy Quarter Horses. Am J Vet Res 1984;45:354–356. fluid administration, including foals that are only 3. Bauer JE, Harvey JW, Asquith RL, et al. Clinical chemistry nursing free-choice. Seventy-one percent of foals reference values of foals during the first year of life. Equine affected by spurious hypercreatininemia were also Vet J 1984;16:361–363. AAEP PROCEEDINGS ր Vol. 59 ր 2013 499 APPLIED MEDICINE: CLINICAL PATHOLOGY AND DERMATOLOGY 4. Schmitz DG, Joyce JR, Reagor JC. Serum biochemical val- phosphatase isoenzymes based on their electrophoretic mo- ues in Quarter Horse foals in the first 6 months of bility by polyacrylamide gel disc electrophoresis. Am J Vet life. Equine Pract 1982;4:24–30. Res 1980;41:2076–2081. 5. Barton MH, LeRoy BE. Serum bile acids concentrations in 10. Patterson WH, Brown CM. Increase of serum ␥-glutamyl- healthy and clinically ill neonatal foals. J Vet Intern Med transferase in neonatal Standardbred foals. Am J Vet Res 2007;21:508–513. 1986;47:2461–2463. 6. Bauer JE, Asquith RL, Kivipelto J. Serum biochemical in- 11. Braun JP, Tainturier D, Be´zille P, et al. Transfer of gamma- dicators of liver function in neonatal foals. Am J Vet Res glutamyltransferase from mother colostrum to newborn goat 1989;50:2037–2041. and foal. Enzyme 1984;31:193–196. 7. Rumbaugh GE, Adamson PJW. Automated serum chemical 12. Chaney KP, Holcombe SJ, Schott HC, et al. Spurious hy- analysis in the foal. J Am Vet Med Assoc 1983;183:769–772. percreatininemia: 28 neonatal foals. J Vet Emerg Crit 8. Hank AM, Hoffman WE, Sanecki RK, et al. Quantitative Care 2010;20:244–249.
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