Dysnatremia in extremely low birth weight infants is associated with multiple adverse outcomes.

OBJECTIVE: The objective of this study is to discern patterns of serum sodium in a broad cohort of extremely low birth weight (ELBW) infants and associate those patterns with hospital outcomes. STUDY DESIGN: Retrospective cohort study of ELBW infants from 323 neonatal intensive care units (NICUs) discharged from 2004 to 2014. We included patients who survived at least 7 days and had daily sodium levels available, and categorized infants by their minimum and maximum sodium levels. RESULTS: We identified 26,871 infants of whom 12,428 met inclusion criteria. Only 1964 (15.8%) maintained eunatremia for the first week. We found most dysnatremias to be associated with increased overall mortality compared with eunatremic patients including moderate hyponatremia (12.9% vs. 8.6%, p < 0.05) and severe hypernatremia (34.8% vs. 8.6%, p < 0.001). Most of these associations were maintained after regression modeling for mortality. CONCLUSION: Sodium fluctuations occurring within the first week of life are associated with increased mortality.

Mouse model of heterotaxy with single ventricle spectrum of cardiac anomalies.

Heterotaxy arises from a failure of the embryo to establish normal left-right asymmetry and is known to affect 3% of infants with congenital heart disease. A recessive mutation causing heterotaxy was recovered in a mouse mutagenesis screen focused on congenital heart defects. Homozygote mutants exhibit abnormal situs in the thoracic and abdominal cavities. Dextrocardia, levocardia, or mesocardia was seen together with right pulmonary isomerism and complex structural heart defects in the single ventricle spectrum. A dominant chamber of left ventricular morphology positioned on the left or right is seen together with transposition of the great arteries. Right atrial isomerism with or without total anomalous pulmonary venous connection was observed in half of the mutants. Because ciliary motion at the embryonic node is required for the specification of laterality, we examined the tracheal epithelia of newborn mice as a proxy for the nodal cilia. However, videomicroscopy showed no defect in ciliary motion. Genome scanning using polymorphic microsatellite markers mapped the mutation to a 3.3 Mb interval on mouse chromosome 7. None of the genes previously described for familial heterotaxy were found in this interval, indicating a novel mutation in this mouse model of heterotaxy.