G Hartnoll1, P Bétrémieux, 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.
Abstract
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.
RCT Entities:
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.
Authors: A Kitabatake; M Inoue; M Asao; T Masuyama; J Tanouchi; T Morita; M Mishima; M Uematsu; T Shimazu; M Hori; H Abe Journal: Circulation Date: 1983-08 Impact factor: 29.690
Authors: Liset E Elstgeest; Shirley E Martens; Enrico Lopriore; Frans J Walther; Arjan B te Pas Journal: PLoS One Date: 2010-02-03 Impact factor: 3.240