Transcatheter closure has become a common treatment method for patent ductus arteriosus in premature infants at many centres; however, many remain uncertain about the ability to perform the procedure in the catheterisation laboratory for infants requiring high-frequency ventilation. This study presents our centre’s experience following the implementation of neonatal ventilatory guidelines, which resulted in 100% procedural success without any procedural or respiratory adverse events.

Necrotising enterocolitis (NEC) is one of the most frequent and fatal intestinal disorders in preterm infants and has very limited treatment options. Breast-fed infants are at a 6–10-fold lower NEC risk than formula-fed infants, and we have previously shown that human milk oligosaccharides (HMO) improved survival and reduced pathology in a rat NEC model. The HMO disialyllacto-N-tetraose (DSLNT) was most effective, and sialylation was shown to be essential for its protective effect. Galacto-oligosaccharides (GOS), currently added to some infant formula, but not containing sialic acid, had no effect. In addition to DSLNT, our previous work also showed that the neutral HMO fraction, which contains high concentrations of 2′-fucosyllactose (2′FL), slightly improved pathology scores. Here, we assessed the in vivo efficacy of 2′FL, as well as of GOS that we enzymatically sialylated (Sia-GOS). Neonatal rats were randomised into the following study groups – dam-fed (DF), formula-fed (FF), FF containing pooled HMO (10 mg/ml), GOS (8 mg/ml), Sia-GOS (500 µm) or 2′FL (2 mg/ml) – and subjected to the established NEC protocol. The DF and HMO groups had the lowest pathology scores with mean values of 0·67 (sd 0·34) and 0·90 (sd 0·47), respectively. The FF group had significantly elevated pathology scores of 2·02 (sd 0·63). Although the addition of GOS to the formula had no protective effect and generated scores of 2·00 (sd 0·63), the addition of Sia-GOS or 2′FL significantly lowered pathology scores to 1·32 (sd 0·56) (P<0·0034) and 1·43 (sd 0·51) (P<0·0040), respectively. The results warrant further studies to investigate the underlying mechanisms and to assess safety and efficacy in human neonates.

Objective: To assess myocardial function in preterm infants with different degrees of ductal patency in the first week of life using tissue Doppler imaging. Study design: Infants <30 weeks of gestation underwent echocardiography on day 3. A total of 72 infants were recruited into the study and categorised into three groups (i) haemodyamically significant ductus arteriosus, (ii) patent ductus arteriosus and (iii) no patent ductus arteriosus. Those with haemodynamically significant ductus arteriosus were treated with indometacin and echocardiography was repeated after 48–72 hours following treatment. Peak systolic and diastolic myocardial velocities were obtained using tissue Doppler imaging, and myocardial performance index was calculated. Results: Initial myocardial velocities were significantly lower and myocardial performance index significantly higher in the haemodynamically significant ductus arteriosus group compared with other groups. For the haemodynamically significant ductus arteriosus group, post-treatment myocardial velocities were higher and myocardial performance index lower than pre-treatment. Conclusion: Preterm infants with haemodynamically significant ductus arteriosus had lower myocardial velocities and higher myocardial performance index, suggesting relative systolic and diastolic myocardial dysfunction. Babies whose patent ductus arteriosus remained open despite indometacin had lower pre-treatment myocardial velocities and higher myocardial performance index than those babies whose patent ductus arteriosus closed, suggesting worse myocardial function in this group. Measurement of myocardial function using tissue Doppler imaging in preterm infants is feasible and may prove to be helpful in the management of babies with patent ductus arteriosus.

Premature infants constitute a risk group for thiamin deficiency but only little is known about their thiamin status. The aim of the present study was to investigate the thiamin status of premature infants by determination of thiamin diphosphate (TDP) and to identify risk factors for low TDP concentrations. In a prospective, longitudinal study TDP was determined by HPLC in whole blood in the first days of life and approximately every 2 weeks. Demographical data, weight gain, type of nutrition and thiamin intake were recorded. A total of 111 premature infants were included at the Children's Hospital of the University of Cologne, Germany from May 2009 until December 2010 and 222 blood samples were analysed. TDP concentrations showed an age-dependent decline (age 0–10 d, mean TDP = 110·6 ng/ml; age 11–20 d, mean TDP = 95·4 ng/ml; age 21–103 d, mean TDP = 33·6 ng/ml). There was no significant difference between males and females. Young gestational age and low birth weight were associated with low TDP concentrations. No infant was diagnosed with thiamin deficiency. The current nutritional regimen in our hospital did not lead to thiamin deficiency in the study cohort. Further research is required to evaluate how TDP concentrations are regulated in premature infants.

As gut immaturity precludes full enteral feeding, very low birth weight (VLBW) preterm infants receive parenteral nutrition (PN) during the first few weeks of life. Weaning VLBW infants off PN, however, is a top priority since PN is associated with a high risk of complications. The decision making is purely empirical, as there is currently no suitable index of gastrointestinal (GI) maturity. Plasma citrulline concentration is considered an index of GI function in conditions such as short-bowel syndrome and coeliac disease in adults. To identify the factors determining urinary citrulline excretion, and determine whether urinary citrulline excretion could be used as a non-invasive index of GI tolerance to enteral feeding, nutritional intake and urinary citrulline were monitored bi-weekly in forty-seven preterm infants < 1500 g (interquartiles 880–1320 g), during their stay in the Neonatology unit. Median urinary citrulline was 24·7 μmol/mmol creatinine (14·5–38·6 μmol/mmol creatinine). No relationship was observed with the percentage of energy tolerated enterally. In multivariate regression analysis, weak correlations were found with post-conceptional age (P = 0·001), parenteral amino acid supply (P = 0·001) and the daily volume of enteral mixture administered (P = 0·043). A significant correlation was found with urinary nitrite+nitrate excretion (r 0·47; P < 0·001). We conclude that in preterm infants: (1) one of the major determinants of urinary citrulline may be the biosynthesis of citrulline from arginine by NO-synthase; (2) urinary citrulline cannot be used to predict GI tolerance. This is consistent with the observations that, in neonatal gut, citrulline is converted to arginine in situ rather than exported towards the kidneys as observed in adults.

Glutamate toxicity from hypoxia-ischaemia during the perinatal period causes white matter injury that can result in long-term motor and intellectual disability. Blocking ionotropic glutamate receptors (GluRs) has been shown to inhibit oligodendrocyte injury in vitro, but GluR antagonists have not yet proven helpful in clinical studies. The opposite approach of activating GluRs on developing oligodendrocytes shows promise in experimental studies on rodents as reported by Jartzie et al., in this issue. Group I metabotropic glutamate receptors (mGluRs) are expressed transiently on developing oligodendrocytes in humans during the perinatal period, and the blood–brain-barrier permeable agonist of group I mGluRs, 1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD), reduces white matter damage significantly in a rat model of perinatal hypoxia-ischaemia. The results suggest drugs activating this class of GluRs could provide a new therapeutic approach for preventing cerebral palsy and other neurological consequences of diffuse white matter injury in premature infants.

Aims: Measurement of electrocardiographic intervals to assess dispersion in ventricular repolarization may be helpful in the assessment of the risk of ventricular arrhythmia. We measured QTc, QT dispersion, and T wave intervals in premature infants before and while on treatment with the IKr blocker cisapride as markers for dispersion in ventricular repolarization. Methods and Results: We enrolled 15 non-ventilated premature infants with a mean gestational age of 30.5 weeks, ranging from 26.5 to 33.5 weeks, and mean postnatal age of 24 days, with a range from 5 to 51 days. A digital 12 lead electrocardiogram was recorded prior to and 3 days after administering cisapride at a dose of 0.8mg/kg/day. Serum electrolytes were simultaneously measured. Electrocardiographic measurements before and after included: QT, QTc Bazett, QT dispersion, R–R, T wave interval peak to end, T wave interval peak to end/onset Q to T wave peak, T wave axis, T wave maximum voltage and QRS–T angle. A paired t test and analysis of variance was used to compare the variables before and during treatment. The QTc, T wave interval peak to end and the ratio T wave interval peak to end/onset Q to T peak increased significantly following treatment with cisapride. Results expressed as before and during treatment were for QTc: 429 (65) ms versus 454 (29) ms p < 0.02; for T wave interval peak to end: 65 (11) ms versus 103 (24) p < 0.01, for the ratio T wave interval peak to end/onset Q to T peak: 0.32 (0.06) versus 0.55 (0.16) p < 0.001. Treatment with the IKr blocker did not significantly alter the QT dispersion, T wave voltage, angle or QRS–T angle. Conclusion: The interval from the peak to the end of the T wave and the ratio of this value to the onset Q to T peak interval, represents regional dispersion of repolarization across the ventricular wall. This is a potentially useful clinical index in the assessment of arrhythmic risk in premature infants being treated by blockade of the IKr channels.

The gut of preterm neonates is colonised with a paucity of bacterial species originating more from the environment than from the mother. Furthermore, a delayed colonisation by bifidobacteria promotes colonisation by potentially pathogenic bacteria. This may contribute towards the development of neonatal necrotising enterocolitis (NEC). The physiopathology of NEC is still unclear but immaturity of the gut, enteral feeding and bacterial colonisation are all thought to be involved. None of the current preventive treatments are considered satisfactory. Modulating the autochthonous microflora by probiotics or prebiotics could be a more reliable approach to prevention. Using gnotobiotic quails as an experimental model of NEC we have shown that onset of intestinal lesions requires a combination of low endogenous lactase activity, lactose in diet, and colonisation by lactose-fermenting bacteria such as the clostridia. The protective role of bifidobacteria was demonstrated in this model through a decrease in clostridial populations and in butyric acid. Oligofructose dietary supplementation was shown to enhance this effect with an increase in the bifidobacterial level and consequently a greater decrease in clostridia. However, oligofructose was unable to promote a bifidobacterial acquisition when the microflora was initially deprived of this group. Nevertheless, oligofructose can act as an anti-infective agent and decrease the occurrence or severity of the lesions depending on the bacteria involved. According to these results and to the fact that oligosaccharides are a major component of breast milk, the addition of oligofructose in formula milks may be a nutritional approach to favouring colonisation by a beneficial flora.