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Background. Inhaled nitric oxide (INO) might favour the prevention of bronchopulmonary dysplasia (BPD) in preterm infants through its anti-inflammatory action, regulatory effect in pulmonary angiogenesis, and minimising lung injury through a reduction in oxygen and ventilatory requirements.

BACKGROUND: PDA is a common complication of prematurity that frequently requires surgical or medical treatment. The most widely employed medical therapy for closure of PDA is indomethacin followed by intravenous ibuprofen. Oral ibuprofen has recently been investigated as an effective and safe alternative for PDA closure.

Background: Intraventricular hemorrhage (IVH) remains a frequent complication in preterm infants and this point is crucial because the most severe IVH are related to a high risk of neurodevelopmental handicaps. Ibuprofen enhances cerebral blood flow autoregulation and has been shown to protect neurological functions following oxidative stresses in an animal model. For these reasons we hypothesized that the prophylactic use of ibuprofen would reduce the occurrence of IVH.

Objectives. To evaluate the effect of 2 cord-care regimens (salicylic sugar powder vs chlorhexidine as a 4% detergent water solution) on cord separation time and other outcomes in preterm infants.Methods. A prospective, randomized, controlled trial was conducted on 244 preterm newborns with a gestational age of Results. The cord separation time was significantly lower in infants who were treated with salicylic sugar powder (6 ± 2 days) than in infants who were treated with chlorhexidine (9 ± 2 days). The programmed cord-care regimen was changed in a significantly higher number of newborns in the chlorhexidine group (17) than in the salicylic sugar group (3). None of the newborns died, and we found only sporadic cases of sepsis (1 patient in each group) and omphalitis (1 patient in the chlorhexidine group). A significantly higher percentage of nurses were satisfied with the salicylic sugar powder treatment (98%) than with the chlorhexidine treatment (67%), notwithstanding a more frequent occurrence of slight cord scar bleeding in the salicylic sugar group (7.8%) than in the chlorhexidine group (4%). The rate of negative umbilical swabs was significantly higher in infants treated with salicylic sugar powder (73.1%) than with chlorhexidine (53%).Conclusions. In neonatal intensive care units and neonatal special care units of developed countries, salicylic sugar powder can be used effectively and safely for UC care of preterm infants.

Objective. The purpose of this study was to evaluate the development of significant hyperbilirubinemia in a large unselected newborn population in a metropolitan area with particular attention to the relationship between type of feeding and incidence of neonatal jaundice in the first week of life. Study Design. A population of 2174 infants with gestational age ≥37 weeks was prospectively investigated during the first days of life. Total serum bilirubin determinations were performed on infants with jaundice. The following variables were studied: type of feeding, method of delivery, weight loss after birth in relationship to the type of feeding, and maternal and neonatal risk factors for jaundice. Statistical analyses were performed using thez test for parametric variables and the ttest for nonparametric variables. In addition, the multiple logistic regression allows for the estimation of the role of the individual characteristics in the development of hyperbilirubinemia. Data concerning serum bilirubin peak distribution in jaundiced newborns were analyzed using a single and a double Gaussian best fit at least squares. The t test was performed to compare 2 values (high and low) of the serum bilirubin peak in breastfed and supplementary-fed infants with those in bottle-fed infants. Results. The maximal serum bilirubin concentration exceeded 12.9 mg/dL (221 μmol/L) in 112 infants (5.1%). The study demonstrated a statistically significant positive correlation between patients with a total serum bilirubin concentration >12.9 mg/dL (221 μmol/L) and supplementary feeding; oppositely, breastfed neonates did not present a higher frequency of significant hyperbilirubinemia in the first days of life. However, best Gaussian fitting of our data suggests that a small subpopulation of breastfed infants have a higher serum bilirubin peak than do bottle-fed infants. Newborns with significant hyperbilirubinemia underwent a greater weight loss after birth compared with the overall studied population, and infants given mixed feeding lost more weight than breastfed and formula-fed newborns, indicating that formula has been administered in neonates who had a weight loss beyond a predetermined percentage of birth weight. Significant hyperbilirubinemia was also strongly associated with delivery by vacuum extractor, some perinatal complications (cephalohematoma, positive Coombs' test, and blood group systems of A, AB, B, and O [ABO] incompatibility) and Asian origin. Multiple logistic regression analysis shows that supplementary feeding, weight loss percentage, ABO incompatibility, and vacuum extraction significantly increase the risk of jaundice, while only cesarean section decreases the risk. Conclusion. The present study confirms the important role of fasting in the pathogenesis of neonatal hyperbilirubinemia, although breastfeeding per se does not seem related to the increased frequency of neonatal jaundice but to the higher bilirubin level in a very small subpopulation of infants with jaundice. In fact, in the breastfed infants, there is a small subpopulation with higher serum bilirubin levels. These infants, when starved and/or dehydrated, could probably be at high risk of bilirubin encephalopathy.

Background and Objective.Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is frequently associated with neonatal hyperbilirubinemia, which in severe cases may cause kernicterus and death. Because G-6-PD-deficient individuals frequently undergo acute, trigger-induced hemolytic episodes, increased hemolysis has frequently been implied in the pathogenesis of this neonatal hyperbilirubinemia. However, in Sephardic Jewish G-6-PD-deficient neonates, the rate of hemolysis, reflected by blood carboxyhemoglobin values corrected for inspired carbon monoxide, has been shown to be elevated, not only in those who developed hyperbilirubinemia, but also, to a similar extent, in those who remained only moderately jaundiced. Because at any point, serum total bilirubin values reflect a balance between bilirubin production on the one hand and bilirubin conjugation and elimination on the other, we suspected bilirubin conjugation to be a key factor in the pathogenesis of the hyperbilirubinemia. Physiologically, a fraction of conjugated bilirubin refluxes from the hepatocyte to the serum, and accurate determination of serum conjugated bilirubin fractions can be used to mirror intrahepatocytic bilirubin. Using this principle, we previously demonstrated a decreased diconjugated bilirubin fraction in hyperbilirubinemic G-6-PD-deficient neonates compared with hyperbilirubinemic G-6-PD-normal controls, suggesting diminished bilirubin conjugation. This conjugated bilirubin pattern probably reflects the recently described interaction between G-6-PD deficiency and the variant promoter for the gene encoding the bilirubin conjugating enzyme UDP glucuronosyltransferase, as seen in Gilbert's syndrome. Therefore, we postulated that efficiency of bilirubin conjugation is a crucial factor in the development of hyperbilirubinemia in G-6-PD-deficient neonates. We hypothesized that those G-6-PD-deficient neonates who develop hyperbilirubinemia would have decreased bilirubin conjugation ability, whereas those with a more efficient conjugating system would have a lesser degree of bilirubinemia.Methods.Term, healthy, male, G-6-PD-deficient neonates with no other obvious predisposing cause for hyperbilirubinemia were selected at random when their serum diazo total bilirubin values ranged from 171 to 254 μmol/L (10–14.9 mg/dL). At this point, simultaneous with the diazo bilirubin determination, serum was collected and frozen for high-performance liquid chromatography (HPLC) measurement of serum bilirubin fractions. The infants were followed clinically and with serum diazo bilirubin determinations until they either did not exceed a serum diazo bilirubin value of 254 μmol/L (14.9 mg/dL) (nonhyperbilirubinemic) or until bilirubin values rose above this level (hyperbilirubinemic), by a process of self-selection. A method of alkaline methanolysis, followed by reverse-phase HPLC, was used to measure unconjugated bilirubin and the mono- and diconjugated fractions of serum conjugated bilirubin. Total HPLC bilirubin and total conjugated bilirubin values were calculated from these measured bilirubin fractions. Patients also were classified according to the serum total conjugated bilirubin value as low bilirubin conjugators (serum total conjugated bilirubin less than median) or as high bilirubin conjugators (serum total conjugated bilirubin greater than median). The data were analyzed by comparing serum conjugated bilirubin fractions between the hyperbilirubinemic and nonhyperbilirubinemic groups and the risk of developing hyperbilirubinemia in the low bilirubin conjugators, relative to that of the high bilirubin conjugators.Results.Neonates were sampled at 53 ± 12 and 58 ± 12 hours for the subsequently hyperbilirubinemic and nonhyperbilirubinemic groups, respectively (NS). Initial (ie, at the time of sampling) serum total diazo bilirubin values (mean ± SD) were almost identical for the subsequently hyperbilirubinemic and nonhyperbilirubinemic groups (214 ± 27 μmol/L [12.5 ± 1.6 mg/dL] vs 212 ± 19 μmol/L [12.4 ± 1.1 mg/dL], respectively, NS), as were the HPLC-determined serum total bilirubin values (162 ± 32 μmol/[9.5 ± 1.9 mg/dL] vs 160 ± 16 μmol/L [9.4 ± 0.9 mg/dL, respectively, NS). However, despite similarity in the simultaneously drawn serum diazo bilirubin values, HPLC-determined conjugated bilirubin fractions (mean [range]), measured from the same serum samples, were lower in those infants who ultimately became hyperbilirubinemic than in those who remained nonhyperbilirubinemic: total conjugated bilirubin 0.82 (0–2.07) μmol/L vs 1.24 (0.6–11.0) μmol/L,; monoconjugated bilirubin 0.80 (0–2.07) μmol/L vs 1.24 (0.60–1.23) μmol/L; and diconjugated bilirubin 0.00 (0.00–0.42) μmol/L vs 0.11 (0–1.78) μmol/L. The diconjugated bilirubin fraction was especially affected; 18 (69%) neonates in the subsequently hyperbilirubinemic group had no detectable diconjugate compared with 8 (36%) in the nonhyperbilirubinemic neonates. Conversely, more of those neonates with serum total conjugated bilirubin fraction less than the median value of 1.06 μmol/L (0.06 mg/dL) developed hyperbilirubinemia than those with greater than the median (17/24 [71%] vs 9/24 [37.5%]), respectively (relative risk: 1.89; 95% confidence interval: 1.06–3.36).Conclusions.Although serum total bilirubin levels at the time of sampling were virtually identical, those neonates who subsequently developed hyperbilirubinemia had significantly lower serum conjugated bilirubin fractions than those who remained within the nonhyperbilirubinemic range. The diconjugated bilirubin fraction was especially affected. Those infants with serum total conjugated bilirubin fraction less than the median had a greater risk of developing hyperbilirubinemia than those with greater than the median. These findings reflect inefficient bilirubin conjugation ability in G-6-PD-deficient neonates who develop hyperbilirubinemia. We believe that the current findings are the functional manifestation of the interaction previously reported between G-6-PD deficiency and the variant gene promoter, as seen in Gilbert's syndrome. Diminished bilirubin conjugation ability appears to be a determining factor in the pathogenesis of G-6-PD deficiency associated neonatal hyperbilirubinemia.

Does early closure of PDA with ibuprofen reduce the severity of RDS in premature infants? † 1736

Introduction. Partial liquid ventilation (PLV) is emerging as an alternative strategy of ventilation in neonatal acute respiratory failure. The literature reports the treatment with PLV of infants ventilated with conventional mandatory ventilation only: we describe a case of an infant treated with PLV during HFOV and chest drainage of Pnx. Case. An AGA male infant born at 40 weeks' gestation developed progressive respiratory failure and on the 2nd day of life was intubated and mechanically ventilated with SIMV. On the 3rd day he required drainage of a left hemothorax and suffered a pulmonary hypertension without response to iNO that successively normalized. On the 8th day a chest radiograph showed a persistent interstitial pulmonary emphysema (PIPE). At the beginning of the 4th week of life the infant developed a bilateral pneumothorax and, after pleural drainage, he was treated with HFOV (Babylog 8000®, Drager,). The HFOV setting was gradually increased until a MAP of 25 cmH2O with a FiO2 of 100%, but after a further episode of desaturation we were not able to increase the SaO2 over the 50% and to normalize the gas exchange; we decided, after parental informed consent, to perform PLV as compassionate treatment. From the side port of the tracheal tube we instilled 15 ml/Kg of PFC (Rimar 101®,Miteni,Italy) at a rate of 3 ml/min, maintaining HFOV at the same setting and keeping continuous pleural drainage(-10 cmH2O), until a column of PFC welled up in the endotracheal tube during transient disconnection from the ventilator and replaced the PFC loss through evaporation (about 5 ml/Kg) every hour. After 1 hour of PLV we observed an increase of SaO2 over 90% and a decrease of MAP from 25 to 21 cmH2O, an increase of OI from 60 to 25 and of PaCO2 from 68 to 55 mmHg. We stopped PLV at the end of a 48 hour period when the SaO2 was 93%, the MAP 20 cmH2O, the OI 25 and the PaCO2 58 mmHg, without deterioration of the respiratory function. Successively, due to the persistence of Pnx, a thoracotomy was performed and bilateral broncho-pleural fistulas were successfully treated; the middle lobe, because entirely dysplastic, was resected and the lung hystology confirmed the diagnosis of PIPE in association with pulmonary dysplasia. Finally, the infant, due to intractable respiratory failure, joined a lung transplantation program and is now waiting for donor organs. Conclusion. This case suggests that PLV can be safe and beneficial also during HFOV and pleural drainage and that it may be useful in the treatment of acute worsening of chronic lung injuries.

Objective: It has not been determined whether phototherapy (PT) has any effect on the induction of bilirubin conjugation. Serum conjugated bilirubin fractions were measured as an index of hepatic bilirubin conjugation to determine any effect of PT on bilirubin conjugation. Methods: Serum was sampled from 21 jaundiced (serum diazo bilirubin ≥274 μmol/L) term neonates prior to PT, and after 24 hours of PT. Unconjugated bilirubin(UCB), and mono- (MCB) and diconjugated (DCB) fractions of total conjugated bilirubin (TCB) were determined by alkaline methanolysis and reverse phase HPLC (results may be lower than diazo methods). Serum total bilirubin (STB), and MCB and DCB as%TCB, were calculated. Values [median (25-75% range)] we compared pre-PT to those at 24 hours by one way repeated measures analysis of variance on ranks. Significance was defined as p

The incidence of respiratory disorders in Italian neonates was studied prospectively from 1st February to 30th April 1995. All the newborns in 45 maternity wards, which were representative of all the various national regions, were investigated for RDS, transient tachypnea, meconium aspiration syndrome, persistent fetal circulation, pulmonary infection, and other miscellaneous disorders. The total number of the studied infants was 17,290. The incidence of respiratory disorders in neonates was 2.94%, in LBW (< 2500 gm) was 15.76%, in VLBW (< 1500 gm) 47.75%, and in ELBW (< 1000 gm) 48.75%. A striking difference in the survival of LBW infants was found between the northern, the central and the southern part of Italy (mortality rates for respiratory disorders were 0.79%, 0.57%, 1.3% respectively). The overall mortality due to the aforementioned disorders was 0.43%. The percentage of infants under 34 weeks of gestational age who received antenatal corticosteroid treatment was 40.9%, whereas 5.4% received antenatal ambroxol. The incidence of RDS in the former group was 36.6%, in the latter group was 23.1% and 33.7% in infants who did not receive any antenatal treatment.