Texas Equine Veterinary Association

www.texasequineva.com • 10 SERUM CHEMISTRY Muscle enzymes, such as creatine kinase (CK) and aspartate aminotransferase (AST), can be elevated at birth if trauma during parturition or white muscle disease is present, or within the first week of life due to increased exercise. Alkaline phosphatase is elevated in the first month of life due to increased osteoblastic activity and intestinal development. Aer the first month, ALP will start to decrease to adult values. Gamma glutamyltransferase (GGT) will be elevated from five to 14 days of age and is assumed to be due to hepatocellular maturation. Sorbitol dehydrogenase (SDH) has similar values in adults and foals, therefore being a better indication of hepatocellular disease as compared to other liver enzymes. Unconjugated bilirubin (UB) is elevated for the first week of life and is most likely due to decreased hepatic function in younger foals and turnover of fetal RBCs. Severe hyperbilirubinemia can occur with neonatal isoerythrolysis (NI), sepsis, hypoxemic ischemic enceophalopathy, hepatobiliary congenital abnormalities, infectious/inflammatory hepatobiliary conditions, meconium impaction, or iron toxicity. When evaluating hepatic function in neonates compared to adults, it's important to recognize higher serum bile acid (SBA) levels in foals in the first six weeks of life and low-level production of ammonia in the foal's colon. Significant elevations of both SBA and ammonia without concurrent changes in hepatocellular enzymes may indicate a portosystemic shunt. Electrolyte disturbances are seen in a number of conditions observed in neonatal foals, including uroperitoneum, renal disease, sepsis, diarrhea (infectious, osmotic, etc), and hypoxic ischemic encephalopathy (HIE) as well as iatrogenic due to fluid therapy. At birth, sodium is on the high end of normal adult RR and will decrease with fluid shis within the first few days of life. Hyponatremia and hypochloridemia along with hypo-/hyperkalemia can occur due to gastrointestinal, renal, or severe placental disease. In uroperitoneum, classically hyponatremia, hypochloridemia and hyperkalemia are seen; however, these electrolyte disturbances may be masked by concurrent intravenous fluid therapy with polyionic fluids. Hypercalcemia (total and ionized calcium) is noted at birth with a rapid drop within hours. Phosphorus at birth is similar to adult horses and will increase within the first few months of life and may continue to be elevated for several months due to bone metabolism. Severe rhabdomyolysis due to selenium deficiency will cause electrolyte disturbances similar to uroperitoneum along with elevations in muscle enzymes. Glucose will be approximately 50–60% of maternal glucose of birth and will decrease over the next two hours. Over the next one to two days, glucose will increase and is higher in foals than adults. Spurious hypercreatinemia as a result of placental dysfunction can be seen from birth up to 36 hours of age with substantial drop in creatinine within hours of birth. If no change or slow decreases of creatinine are seen, renal or post-renal causes of hypercreatinemia should be considered. Foal's creatinine will drop below adult RR in the first few months of life due to their high fluid volume diet. e first urination is hypersthenuric, with urine specific gravity >1.030, aer which normal foal urine should be hyposthenuric Continues on page 12

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