Case Report-Severe Hyponatremia at Birth in a Premature Infant.

Abstract

Given the role of the placenta in maintaining maternal-fetal equilibrium, changes in maternal sodium levels affect the fetus. Clinicians must also account for the direct impact of maternal conditions and medications on the neonate. Gestational hyponatremia develops in approximately one-third of mothers with preeclampsia with severe features. Additionally, the use of selective antidiuretic (V2 receptor) agonist 1-deamino-8-D-arginine-vasopressin, commonly known as DDAVP, during pregnancy leads to maternal hyponatremia by inhibiting maternal diuresis. We present a case of severe hyponatremia in a premature infant born to a mother with preeclampsia with severe features who was taking DDAVP for von Willebrand Disease (VWD). A preterm female infant was born at 34 weeks gestation to a mother with pre-eclampsia with severe features treated with magnesium sulfate, and the use of DDAVP for VWD was found to have severe hyponatremia (122 mmol/L). Causes of hyponatremia were explored, such as mineralocorticoid deficiency, renal tubular dysfunction, inappropriate secretion of antidiuretic hormone (SIADH), and renal failure. Initial investigation of the neonatal hyponatremia prompted obtaining a maternal serum sodium level, which also demonstrated severe hyponatremia (122 mmol/L), identical to the infant's serum sodium level. The infant was managed with fluid restriction and close monitoring of serial serum and urine chemistries. Gradually, serum sodium levels increased and normalized by day 4 of life. We speculate that severe maternal hyponatremia induced by preeclampsia with severe features, along with the use of DDAVP during pregnancy, led to fetal and neonatal hyponatremia. DDAVP during pregnancy to treat VWD is associated with maternal hyponatremia and subsequent neonatal hyponatremia. It is important to monitor electrolytes in neonates born to mothers treated with DDAVP to promptly correct electrolyte abnormalities.