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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.
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