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

Background-It has previously been shown that, in preterm babies, routine so dium supplementation from 24 hours after birth is associated with increased risk of oxygen dependency and persistent expansion of the extracellular co mpartment. Objective-To explore whether this is mediated by a delayed fall in pulmonar y artery pressure (PAP). Postnatal changes in PAP, estimated as the ratio o f time to peak velocity to right ventricular ejection time, corrected for h eart rate (TPV:RVET(c)), were compared in preterm infants who received rout ine 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. Echo cardiographic assessment was made on the day of delivery (day 0), and on da ys 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) measu red sequentially after birth. On within group testing, when compared with v alues at birth, the ratio was higher by day 3 in the early supplemented gro up, 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 n ot 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 dire ct consequence of persistent expansion of the extracellular compartment and increased pulmonary interstitial fluid. resulting from a sodium intake tha t exceeded sodium excretory capacity. This adds further weight to the view that clinical management, in this case the timing of routine sodium supplem entation, should be individually tailored and delayed until the onset of po stnatal extracellular volume contraction, marked clinically by weight loss.