Aim: To determine whether the addition of heparin to total parenteral nutrition (TPN) fluid would prevent blockage of peripherally inserted central catheters (PICCs) in neonates. Methods: This was a randomized, double‐blind, controlled study of 66 eligible neonates with PICCs inserted for the administration of TPN. Infants were randomized to receive TPN containing either 1 IU ml‐1 of heparin (n= 35) or no heparin (n= 31). Results: There was no significant difference in the incidence of blocked catheters between the two groups of infants (heparin: 14.3%; no‐heparin: 22.6%, p= 0.4). Although a higher percentage (62.9%) of infants in the heparin group received a complete course of TPN successfully via PICC than those in the no‐heparin group (48.4%), the difference was not statistically significant (p= 0.3). There were no significant differences in the incidence of catheter‐related sepsis, hypertriglyceridaemia, hyperbilirubinaemia, coagulopathy or intraventricular haemorrhage between the two groups. Conclusion: Addition of heparin to TPN fluid was not associated with a significant reduction in the incidence of blocked PICCs. However, the sample size of this study was too small to exclude even rather marked differences between the groups.

Aim A collaborative study was conducted between two Southeast Asian university hospitals to compare the nutritional intervention and growth outcomes and evaluate the extent of post‐natal growth faltering (PNGF) among very low birthweight (VLBW) infants. Methods Data of all infants admitted during the 2011–2012 period to the two hospitals at Singapore (SG) and Malaysia (MY) were pooled and analysed. Results Of the 236 infants, SG infants received lower total protein and energy intake than MY infants (2.69 vs. 3.54 g/kg/day and 92.4 vs. 128.9 kcal/kg/day respectively; P < 0.001) in enteral feeds, with Singaporean infants predominantly fed fortified breast milk than Malaysian infants (45/48 vs. 10/41; P < 0.01). The mean weight z‐score from birth to 36 weeks corrected age was significantly different (SG,−2.2 (0.9) vs. MY, −1.4 (0.7); P = 0.001). More SG than MY extremely low birthweight (ELBW) infants had severe PNGF >−2 SDS (55 vs. 16%; P = 0.001). The greater use of a diuretic in SG to treat haemodynamically significant patent ductus arteriosus (hsPDA) may have contributed to the higher PNGF rate. Mean growth velocity of at least 15 g/kg/day was attained by VLBW infants only from Day 14 and by ELBW infants only from Day 28 post‐natally. Overall, severe PNGF rates (z‐score change >−2 SDS at 36 weeks' corrected age) were 28.8 and 36.5% for VLBW and ELBW infants, respectively. Conclusions Being very preterm, ELBW with hsPDA and receiving insufficient protein and energy were risk factors for severe PNGF. Increasing protein and energy content, augmenting fortification of breast milk and concentrating feed volumes, especially if there is an hsPDA, may curb severe PNGF among these infants.

Background:Gardnerella vaginalis (GV) is most frequently associated with bacterial vaginosis and is the second most common etiology causing intrauterine infection after Ureaplasma urealyticum. Intrauterine GV infection adversely affects pregnancy outcomes, resulting in preterm birth, fetal growth restriction, and neonatal pneumonia. The knowledge of how GV exerts its effects is limited. We developed an in vivo animal model to study its effects on fetal development.Materials and Methods: A survival mini-laparotomy was conducted on New Zealand rabbits on gestational day 21 (28 weeks of human pregnancy). In each dam, fetuses in the right uterine horn received intra-amniotic 0.5 × 102 colony-forming units of GV injections each, while their littermate controls in the left horn received sterile saline injections. A second laparotomy was performed seven days later. Assessment of the fetal pups, histopathology of the placenta and histomorphometric examination of the fetal lung tissues was done.Results: Three dams with a combined total of 12 fetuses were exposed to intra-amniotic GV, and 9 fetuses were unexposed. The weights of fetuses, placenta, and fetal lung were significantly lower in the GV group than the saline-inoculated control group [mean gross weight, GV (19.8 ± 3.8 g) vs. control (27.9 ± 1.7 g), p &lt; 0.001; mean placenta weight, GV (5.5 ± 1.0 g) vs. control (6.5 ± 0.7 g), p = 0.027; mean fetal lung weight, GV (0.59 ± 0.11 g) vs. control (0.91 ± 0.08 g), p = 0.002. There was a two-fold increase in the multinucleated syncytiotrophoblasts in the placenta of the GV group than their littermate controls (82.9 ± 14.9 vs. 41.6 ± 13.4, p &lt; 0.001). The mean alveolar septae of GV fetuses was significantly thicker than the control (14.8 ± 2.8 μm vs. 12.4 ± 3.8 μm, p = 0.007). Correspondingly, the proliferative index in the interalveolar septum was 1.8-fold higher in the GV group than controls (24.9 ± 6.6% vs. 14.2 ± 2.9%, p = 0.011). The number of alveoli and alveolar surface area did not vary between groups.Discussion: Low-dose intra-amniotic GV injection induces fetal growth restriction, increased placental multinucleated syncytiotrophoblasts and fetal lung re-modeling characterized by alveolar septal hypertrophy with cellular proliferative changes.Conclusion: This intra-amniotic model could be utilized in future studies to elucidate the acute and chronic effects of GV intrauterine infections.

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