Newborn Liver Functions as an Adjunct Biomarker in Timing Fetal Neurologic Injury

Abstract

Background: We hypothesized that in the presence of an intrapartum hypoxic ischemic insult, redistribution of cardiac output away from the hepatic circulation will result in unique patterns of hepatic dysfunction dependent on the degree and duration of the hypoxic ischemic insult. We evaluated the rise and clearance of Aspartate Aminotransferase (AST) and Alanine Aminotransferase (ALT) in term newborns with three common patterns of hypoxic ischemic encephalopathy as an adjunct biomarker in timing of fetal neurologic injury. Methods: We identified 230 term newborns with image proven hypoxic ischemic encephalopathy with profound neurologic impairment over a 30 year period from multiple institutions. Eighty four had liver transaminases in the first 72 hours of life to evaluate patterns of rise and clearance. Results: A total of 215 AST, 220 ALT and 204 NRBC values were collected. Similar to NRBC’s, the general trend was the more chronic asphyxia, the more elevated transaminases are shortly after birth with delayed clearance often beyond 48 hours of life. In acute profound intrapartum injury, liver transaminases demonstrated minimal rise with rapid normalization. There was no difference between groups regarding gender, gestational age and birthweight. Conclusion: No single proven biomarker is diagnostic of neonatal encephalopathy but newborn AST/ALT measured shortly after birth and daily for three days can provide additional evidence based medicine to confirm or refute allegation of acute intrapartum asphyxia.