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Tolerance to early intravenous lipid in the sick very low birth weight infant (VLBW)
128 1 Boyd, R.D.H., Glazier, J.D., Sibley, C.P. and Ward, B.S. (1989): Am. J. Physiol., in press. 2 Sibley, C.P., Ward, B.S., Glazier, J.D., Moore, W.M.O. and Boyd, R.D.H. (1986): Am. J. Physiol. 250, R414-R484.
Surf&ant apoprotein A @P-A) in infants with and without RDS. Stephanie Bartholain, Barbara Schadow, Evelyn WaiP, Marius Bartsch and Paul Stevens, Department of Neonatology, UKRV Charlottenburg, Heubnerweg 6, 1000 Berlin 19, West-Berlin, Germany.
The aims of our ongoing study are: (1) to improve on the clinical diagnosis of respiratory distress syndrome of the newborn (RDS) by adding biochemical criteria and (2) to study the influence of surfactant substitution and artificial ventilatoin on the surfactant metabolism. Tracheal aspirates were collected from 46 infants (gestational age ranging from 26 to 40 weeks) with (n = 29) and without (n = 17) RDS. Stomach contents were aspirated at birth in 10 healthy term infants. SP-A content of these samples was determined by ELISA. Protein (Prot) and phospholipid (PL) content was measured and phospholipid thin-layer chromatography performed.
Preterm RDS SP-A pg/ml) day 1 0.20 + 0.07 (20) day 5 3.19 f 2.08 (20)
Preterm non-RDS
Term
SP-A/Prot Ccg/ml)
SP-A pg/ml)
SP-A/Prot .ug/ml)
SP-A Ccg/ml)
SP-A/Prot pgjml)
0.41 + 0.13 (20) 4.22 2 1.28 (10)
10.59 f 4.18 (13) 1.77 + 0.76 (10)
8.42 f 3.25 (11) 7.31 + 5.84 (10)
11.74 f 2.82 (10
2.03 + 0.44 (10)
In infants with RDS, SP-A (P < 0.0005) and SP-A/Prot ratio (P < 0.01) increased from day 1 to day 5. Infants without RDS on day 1 as well as term infants at birth had significantly higher SP-A (P < 0.05) and SP-A/Prot (P < 0.005) values than infants with RDS. On day 5, no differences betweeng groups were found. However, several non-RDS infants had lower SP-A value on day 5 than on day 1, corresponding to a clinical deterioration of their pulmonary status. A combination of surfactant protein and phospholipid parameters should allow a better prediction and diagnosis of RDS. It might also shed new light on the course of respiratory disease and the effects of artificial ventilation in newborns. Hallman, M., Arjomaa, P., Mizumoto, M. and Akino, T. (1988): Am. J. Obstet. Gynecol., 158, 531-535. Chida, S., Phelps, D., Cordle, C., Soil, R., Floros, J. and Teusch, H.W. (1988) Am. Rev. Respir. Dis., 137,943-947.
Tolerance to early
intravenous lipid in the sick very low birth weight infant (VLBW). N.J. Gilbertson”, L.M. Croweb, D.J. Coxb, T.N. Palme? and I.Z. Kovar’, Departments of “Child Health and bBiochemistry, Charing Cross and Westminster Medical School, London W6 SRF, U.K.
Parenteral nutrition (PN) is often necessary in the sick preterm infant. These babies have a minimal nonprotein energy requirement in the region of 70 kcal/kg/day to permit growth and nitrogen retention. This energy can be provided either as intravenous glucose or lipid (containing triglyceride). Common practice is to initially offer glucose alone and to delay the introduction of lipid. This approach is questioned; the
129 liver may have a mandatory requirement for fatty acids (derived from triglyceride) to permit hepatic gluconeogenesis to facilitate normoglycaemia [l]. The aim of this study is to assess whether VLBW infants tolerate early intravenous lipid (Intralipid) and whether it is clinically beneficial to introduce this into the PN regimen from the first day oflife in the sick ventilator dependent infant (< 32 wks gestation); the specific issue being the impact of intravenous lipid on blood metabolite profiles. Sixteen infants (with Bwt < 1500 g) were entered sequentially on admission into one of two groups. Vamin Infant R, dextrose and electrolyte mixtures were given to both groups with Intralipid added on the first day of life for study group infants (n = 9) or on the eighth day for control group infants (n = 7). Regimens for both groups were isocaloric and isovolumetric throughout. Early introduction of Intralipid had no adverse effects on glycaemia or on blood fatty acid, ketone body, lactate, pyruvate or alanine concentrations compared with those in the control group. The inverse relationship between glucose and FFA, which would be expected if the glucose-fatty acid cycle is operational, was not found. Major metabolic disturbances were seen in both groups within the first few hours of life. These included hyperglycaemia in approximately 20% of infants, accompanied by elevation in blood lactate and alanine. No significant hypertriglyceridaemia was observed in either group and no adverse clinical effects of lipid administration were detected. Conclusion. VLBW infants tolerate Intralipid from day 1 of life. Sick preterm infants show transient disturbances in glucose homeostasis independent of intravenous lipid. 1 Girard, J. (1986) Biol. Neonate, 50,237-258.
Slow infusion of indomethacin reduces cerebral blood flow in sick preterm infants. A.D. Edwards, J.S. Wyatt, C. Richardson, M. Cope, D.T. Delpy and E.O.R. Reynolds, Departments of Paediatrics, and Medical Physics and Bioengineering, University College and Middlesex School of Medicine, London, U.K.
We have shown previously, using near infrared spectroscopy (NIRS), that rapid infusion of indomethacin (0.1-0.2 mg’kg-*) causes a marked reduction in cerebral blood flow (CBF) [l]. The purpose of the present investigation was to assess the effects of a slow infusion on CBF, cerebral oxygen delivery (COD), cerebral blood volume (CBV) and CBV response to changes in arterial carbon dioxide tension (CVR). Methods. 6 infants admitted to the Neonatal Unit of University College Hospital were studied. Their median gestation was 27 (range 23-29) weeks, birthweight 0.81 (0.66-l .40) kg and age at study 15 (827) days. Indomethacin (0.1-0.2 mg’kg-I) was infused over 20-30 minutes. Measurements were made for a median of 113 (range 60-185) minutes before and 65 (50-l 18) minutes after infusion. CBF, CBV and CVR were quantified using NIRS methods that have been previously described [2,3]. COD was calculated from CBF and arterial oxygen saturation. Results. In every infant CBF, COD, CBV and CVR fell after indomethacin. For the group median CBF fell from 22 to 12 ml.100 g-I’min-‘; COD from 2.44 to 1.47 ml’100 g-“min-I; CBV from 1.75 to 1.41 m1’100 g-’ and CVR from 0.13 to 0.06 ml.100 g-I’kPa-‘. These results were all significant at the 5% level using the Wilcoxon rank sum test. Conclusion. Slow infusion of indomethacin reduced cerebral blood flow, cerebral oxygen delivery, cerebral blood volume and the response of cerebral blood volume to changes in arterial carbon dioxide tension. The reductions were similar in magnitude to those previously observed following rapid infusion [ 11.
1 2 3
Edwards, A.D. et al. (1989): Early Hum. Dev., 19,69. Wyatt, J.S. et al. (1986): Lancet, ii, 1063-1066. Edwards, A.D. et al. (1988): Lancet, ii, 770-771.
Surf&ant apoprotein A @P-A) in infants with and without RDS. Stephanie Bartholain, Barbara Schadow, Evelyn WaiP, Marius Bartsch and Paul Stevens, Department of Neonatology, UKRV Charlottenburg, Heubnerweg 6, 1000 Berlin 19, West-Berlin, Germany.
The aims of our ongoing study are: (1) to improve on the clinical diagnosis of respiratory distress syndrome of the newborn (RDS) by adding biochemical criteria and (2) to study the influence of surfactant substitution and artificial ventilatoin on the surfactant metabolism. Tracheal aspirates were collected from 46 infants (gestational age ranging from 26 to 40 weeks) with (n = 29) and without (n = 17) RDS. Stomach contents were aspirated at birth in 10 healthy term infants. SP-A content of these samples was determined by ELISA. Protein (Prot) and phospholipid (PL) content was measured and phospholipid thin-layer chromatography performed.
Preterm RDS SP-A pg/ml) day 1 0.20 + 0.07 (20) day 5 3.19 f 2.08 (20)
Preterm non-RDS
Term
SP-A/Prot Ccg/ml)
SP-A pg/ml)
SP-A/Prot .ug/ml)
SP-A Ccg/ml)
SP-A/Prot pgjml)
0.41 + 0.13 (20) 4.22 2 1.28 (10)
10.59 f 4.18 (13) 1.77 + 0.76 (10)
8.42 f 3.25 (11) 7.31 + 5.84 (10)
11.74 f 2.82 (10
2.03 + 0.44 (10)
In infants with RDS, SP-A (P < 0.0005) and SP-A/Prot ratio (P < 0.01) increased from day 1 to day 5. Infants without RDS on day 1 as well as term infants at birth had significantly higher SP-A (P < 0.05) and SP-A/Prot (P < 0.005) values than infants with RDS. On day 5, no differences betweeng groups were found. However, several non-RDS infants had lower SP-A value on day 5 than on day 1, corresponding to a clinical deterioration of their pulmonary status. A combination of surfactant protein and phospholipid parameters should allow a better prediction and diagnosis of RDS. It might also shed new light on the course of respiratory disease and the effects of artificial ventilation in newborns. Hallman, M., Arjomaa, P., Mizumoto, M. and Akino, T. (1988): Am. J. Obstet. Gynecol., 158, 531-535. Chida, S., Phelps, D., Cordle, C., Soil, R., Floros, J. and Teusch, H.W. (1988) Am. Rev. Respir. Dis., 137,943-947.
Tolerance to early
intravenous lipid in the sick very low birth weight infant (VLBW). N.J. Gilbertson”, L.M. Croweb, D.J. Coxb, T.N. Palme? and I.Z. Kovar’, Departments of “Child Health and bBiochemistry, Charing Cross and Westminster Medical School, London W6 SRF, U.K.
Parenteral nutrition (PN) is often necessary in the sick preterm infant. These babies have a minimal nonprotein energy requirement in the region of 70 kcal/kg/day to permit growth and nitrogen retention. This energy can be provided either as intravenous glucose or lipid (containing triglyceride). Common practice is to initially offer glucose alone and to delay the introduction of lipid. This approach is questioned; the
129 liver may have a mandatory requirement for fatty acids (derived from triglyceride) to permit hepatic gluconeogenesis to facilitate normoglycaemia [l]. The aim of this study is to assess whether VLBW infants tolerate early intravenous lipid (Intralipid) and whether it is clinically beneficial to introduce this into the PN regimen from the first day oflife in the sick ventilator dependent infant (< 32 wks gestation); the specific issue being the impact of intravenous lipid on blood metabolite profiles. Sixteen infants (with Bwt < 1500 g) were entered sequentially on admission into one of two groups. Vamin Infant R, dextrose and electrolyte mixtures were given to both groups with Intralipid added on the first day of life for study group infants (n = 9) or on the eighth day for control group infants (n = 7). Regimens for both groups were isocaloric and isovolumetric throughout. Early introduction of Intralipid had no adverse effects on glycaemia or on blood fatty acid, ketone body, lactate, pyruvate or alanine concentrations compared with those in the control group. The inverse relationship between glucose and FFA, which would be expected if the glucose-fatty acid cycle is operational, was not found. Major metabolic disturbances were seen in both groups within the first few hours of life. These included hyperglycaemia in approximately 20% of infants, accompanied by elevation in blood lactate and alanine. No significant hypertriglyceridaemia was observed in either group and no adverse clinical effects of lipid administration were detected. Conclusion. VLBW infants tolerate Intralipid from day 1 of life. Sick preterm infants show transient disturbances in glucose homeostasis independent of intravenous lipid. 1 Girard, J. (1986) Biol. Neonate, 50,237-258.
Slow infusion of indomethacin reduces cerebral blood flow in sick preterm infants. A.D. Edwards, J.S. Wyatt, C. Richardson, M. Cope, D.T. Delpy and E.O.R. Reynolds, Departments of Paediatrics, and Medical Physics and Bioengineering, University College and Middlesex School of Medicine, London, U.K.
We have shown previously, using near infrared spectroscopy (NIRS), that rapid infusion of indomethacin (0.1-0.2 mg’kg-*) causes a marked reduction in cerebral blood flow (CBF) [l]. The purpose of the present investigation was to assess the effects of a slow infusion on CBF, cerebral oxygen delivery (COD), cerebral blood volume (CBV) and CBV response to changes in arterial carbon dioxide tension (CVR). Methods. 6 infants admitted to the Neonatal Unit of University College Hospital were studied. Their median gestation was 27 (range 23-29) weeks, birthweight 0.81 (0.66-l .40) kg and age at study 15 (827) days. Indomethacin (0.1-0.2 mg’kg-I) was infused over 20-30 minutes. Measurements were made for a median of 113 (range 60-185) minutes before and 65 (50-l 18) minutes after infusion. CBF, CBV and CVR were quantified using NIRS methods that have been previously described [2,3]. COD was calculated from CBF and arterial oxygen saturation. Results. In every infant CBF, COD, CBV and CVR fell after indomethacin. For the group median CBF fell from 22 to 12 ml.100 g-I’min-‘; COD from 2.44 to 1.47 ml’100 g-“min-I; CBV from 1.75 to 1.41 m1’100 g-’ and CVR from 0.13 to 0.06 ml.100 g-I’kPa-‘. These results were all significant at the 5% level using the Wilcoxon rank sum test. Conclusion. Slow infusion of indomethacin reduced cerebral blood flow, cerebral oxygen delivery, cerebral blood volume and the response of cerebral blood volume to changes in arterial carbon dioxide tension. The reductions were similar in magnitude to those previously observed following rapid infusion [ 11.
1 2 3
Edwards, A.D. et al. (1989): Early Hum. Dev., 19,69. Wyatt, J.S. et al. (1986): Lancet, ii, 1063-1066. Edwards, A.D. et al. (1988): Lancet, ii, 770-771.