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Editor—In a recent issue, Hartnollet al 1 2 described the effect of postnatal sodium supplementation on oxygen dependency, body weight, and body composition of preterm infants. According to them, an overzealous approach to correcting hyponatraemia in preterm infants is not scientific. In the same context, I would like to describe a case of a preterm infant who developed symptomatic patent ductus arteriosus after supplementation with sodium.
The infant was a 1060 g baby boy born at 29 weeks of gestation with no significant antenatal history. The first five days were unremarkable. On day 6 of life, he was noted to have hyperglycaemia, which persisted, requiring an insulin drip. At the same time, his hyponatraemia was corrected with extra sodium supplementation. On day 11, he was noted to have a murmur, which later was confirmed by echocardiography as patent ductus arteriosus. Table 1 summarises the events.
The case clearly indicates a need for a conservative approach to hyponatraemia in preterm infants, as “chasing” it may lead to fluid retention and development of patent ductus arteriosus.
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