Maternal Over-Hydration in Labor can Cause Dilutional Hyponatremia in Neonates

Abstract

A term baby was born by semi-elective cesarean section for maternal prolonged rupture of membranes and nonprogression of labor. His mother had received 2 L of intravenous fluids prior to delivery. The baby was well at birth and establishing breast feeds. He underwent blood investigations for risk of sepsis and intravenous antibiotics were started. At 4 h of age, the baby developed brief (<2 min) seizures, and was admitted to the neonatal unit. Cerebral function monitoring did not reveal any abnormality. Blood glucose was normal, while the blood investigations conducted previously, revealed serum sodium of 124 mmol/L (normal range 135–145 mmol/L), with other electrolytes and inflammatory markers being normal. He was successfully treated with a bolus of 3 % sodium chloride and no further seizures were noted. Further history revealed that his mother had ingested 2.5 L of water during the 8 h prior to delivery, which had not been recorded in obstetric charts. A diagnosis of dilutional hyponatremia secondary to maternal overhydration was made. Pediatricians should consider potential mechanisms and differential diagnoses in newborn babies presenting with hyponatremia within the first 24 h of life.Most cases in neonates will be of dilutional hyponatremia, with imbalance between fluid intake and urine output, and low levels of urine sodium. Oliguria with a risk of dilutional hyponatremia can occur in the syndrome of inappropriate antidiuretic hormone secretion (SIADH) which is typically associated with infection e.g., congenital pneumonia, in birth asphyxia (with hypoxic renal injury) and in preterm infants who have impaired ability to concentrate urine [1–4]. Dilutional hyponatremia with apparently normal urine output occurs with excess administration of hypotonic fluids to an infant (as revealed by assessing fluid balance, input/output charts and weight). Situations where that administration has occurred in utero as a result of maternal over-hydration, it may not be evident immediately [3]. It is worth noting that these conditions may co-exist, such as an infant with disrupted tubular function due to birth asphyxia will be more vulnerable to incautious intravenous fluid management. Non-dilutional hyponatremia is most typically associated with renal salt-wasting, for example in congenital adrenal hyperplasia (CAH). The source of sodium loss can be confirmed by an inappropriately high urinary sodium in the presence of low serum sodium, and other clinical and biochemical abnormalities may be evident (e.g., hyperkalemia, poor glycemic control and ambiguous genitalia in CAH). There are multiple reports of dilutional hyponatremia in infants due to maternal water intoxication [5]. It occurs due to excess transfer of free water across the placenta following excessive administration of fluids to the mother in labor [4, 5]. Pregnant women have lower serum sodium (by ~3–5 mmol/L) than non-pregnant women, while the sodium concentration in the fetus is about 3 mmol/L lower than that of the mother [5]. Thus, maternal hyponatremia (due to iatrogenic fluid overload and/or drinking hypotonic fluids), results in the fetus becoming hyponatremic [3]. Anti-diuretic hormone (ADH) levels in the fetus rise before the onset of labor and remain elevated. High ADH and limited renal capacity in neonates makes them vulnerable to water overload causing hyponatremia [5]. S. P. Paul (*) Department of Pediatric Gastroenterology, Bristol Royal Hospital for Children, Paul O’Gorman Building, Upper Maudlin Street, Bristol BS2 8BJ, UK e-mail: siba@doctors.org.uk