Arch Dis Child Fetal Neonatal Ed 85:F29-F32 doi:10.1136/fn.85.1.F29
  • Original article

Randomised controlled trial of postnatal sodium supplementation in infants of 25–30 weeks gestational age: effects on cardiopulmonary adaptation

  1. G Hartnoll,
  2. P Bétrémieux,
  3. N Modi
  1. Department of Paediatrics and Neonatal Medicine, Imperial College School of Medicine, Hammersmith Campus, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
  1. Dr Modin.modi{at}
  • Accepted 21 February 2001


BACKGROUND It has previously been shown that, in preterm babies, routine sodium supplementation from 24 hours after birth is associated with increased risk of oxygen dependency and persistent expansion of the extracellular compartment.

OBJECTIVE To explore whether this is mediated by a delayed fall in pulmonary artery pressure (PAP). Postnatal changes in PAP, estimated as the ratio of time to peak velocity to right ventricular ejection time, corrected for heart rate (TPV:RVET(c)), were compared in preterm infants who received routine sodium supplements that were either early or delayed.

METHODS Infants were randomised, stratified according to sex and gestation, to receive a sodium intake of 4 mmol/kg/day starting either from 24 hours after birth or when a weight loss of 6% of birth weight was achieved. Echocardiographic assessment was made on the day of delivery (day 0), and on days 1, 2, 7, and 14. Babies with congenital heart disease were excluded.

RESULTS There was no difference between the two groups in TPV:RVET(c) measured sequentially after birth. On within group testing, when compared with values at birth, the ratio was higher by day 3 in the early supplemented group, suggesting a more rapid fall in PAP compared with the late supplemented group, in whom a significant fall did not occur until day 14.

CONCLUSIONS The timing of sodium supplementation after preterm birth does not appear to affect the rate of fall in PAP as measured by the TPV:RVET(c) ratio. The previous observation linking routine sodium supplementation from 24 hours after birth with increased risk of continuing oxygen requirement therefore does not appear to be mediated by a delayed fall in PAP. Instead, the increased risk of continuing oxygen requirement is likely to be a direct consequence of persistent expansion of the extracellular compartment and increased pulmonary interstitial fluid, resulting from a sodium intake that exceeded sodium excretory capacity. This adds further weight to the view that clinical management, in this case the timing of routine sodium supplementation, should be individually tailored and delayed until the onset of postnatal extracellular volume contraction, marked clinically by weight loss.

  • Delaying routine sodium supplementation until after the onset of postnatal weight loss has a beneficial effect on oxygen requirement after preterm birth

  • The adverse effect of routine sodium supplementation is not mediated by alterations in pulmonary artery pressure but by impaired loss of extracellular fluid from the pulmonary interstitium


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