• hyponatraemia
• preterm

The need for a conservative approach to hyponatraemia in preterm neonates was emphasised by Manzer.¹ Chasing hyponatraemia (serum sodium: 124 mmol/l) during hyperglycaemia requiring insulin infusion in a 1060 g neonate was associated with fluid retention and patent ductus arteriosus (PDA). The maximum serum sodium levels achieved were 136 mmol/l (maximum sodium supplements: 15 mmol/day). However, spurious hyponatraemia is well known during hyperglycaemia and hypertriglyceridaemia.²

Elevation of serum glucose levels induces a translocation of water from the intracellular fluid to the extracellular compartment sufficient to reduce serum sodium.² Correction factor of Katz states that the serum sodium level decreases by 1.6 mmol/l for each 5.6 mmol/l increase in glucose level.² Hyponatraemia during hypertriglyceridaemia is a method dependent artifactual reduction of serum sodium concentration resulting from displacement of a portion of a water phase of the plasma by lipid. This problem (which may be observed with flame emission spectrometry) can be avoided by using a sodium selective electrode without dilution.² Hyperglycaemia and hypertriglyceridaemia are common in extremely low birth weight (ELBW) neonates—the group at highest risk for chronic lung disease (CLD) and symptomatic PDA.³ The incidence of hyperglycaemia in very premature neonates ranges from 20% to 86% and is at least 18 times greater in ELBW neonates. The consequences of chasing such spurious hyponatraemia in neonates at risk for CLD and PDA cannot be overemphasised.