BackgroundNecrotizing enterocolitis (NEC) is a catastrophic disease of preterm infants, and microbial dysbiosis has been implicated in its pathogenesis. Studies evaluating the microbiome in NEC and preterm infants lack power and have reported inconsistent results.Methods and resultsOur objectives were to perform a systematic review and meta-analyses of stool microbiome profiles in preterm infants to discern and describe microbial dysbiosis prior to the onset of NEC and to explore heterogeneity among studies. We searched MEDLINE, PubMed, CINAHL, and conference abstracts from the proceedings of Pediatric Academic Societies and reference lists of relevant identified articles in April 2016. Studies comparing the intestinal microbiome in preterm infants who developed NEC to those of controls, using culture-independent molecular techniques and reported α and β-diversity metrics, and microbial profiles were included. In addition, 16S ribosomal ribonucleic acid (rRNA) sequence data with clinical meta-data were requested from the authors of included studies or searched in public data repositories. We reprocessed the 16S rRNA sequence data through a uniform analysis pipeline, which were then synthesized by meta-analysis.We included 14 studies in this review, and data from eight studies were available for quantitative synthesis (106 NEC cases, 278 controls, 2944 samples). The age of NEC onset was at a mean ± SD of 30.1 ± 2.4 weeks post-conception (n = 61). Fecal microbiome from preterm infants with NEC had increased relative abundances of Proteobacteria and decreased relative abundances of Firmicutes and Bacteroidetes prior to NEC onset. Alpha- or beta-diversity indices in preterm infants with NEC were not consistently different from controls, but we found differences in taxonomic profiles related to antibiotic exposure, formula feeding, and mode of delivery. Exploring heterogeneity revealed differences in microbial profiles by study and the target region of the 16S rRNA gene (V1-V3 or V3-V5).ConclusionsMicrobial dysbiosis preceding NEC in preterm infants is characterized by increased relative abundances of Proteobacteria and decreased relative abundances of Firmicutes and Bacteroidetes. Microbiome optimization may provide a novel strategy for preventing NEC.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-017-0248-8) contains supplementary material, which is available to authorized users.

We evaluated the outcome in infants with esophageal atresia (EA) treated in our department over the last two decades. The medical records of 147 infants treated from 1986 to 2005 were reviewed. Patient characteristics, associated anomalies, surgery and complications were recorded. We divided the material into two time-periods: 1986-1995 and 1996-2005; 125 patients or parents were interviewed regarding gastrointestinal function, respiratory symptoms and education. The incidence of major cardiac defects increased from 23 to 29% and the overall survival increased from 87 to 94%. Using Spitz' classification survival increased from 93.5 to 100% in group I and from 68.4 to 77.8% in group II. In group III, during the second time period, survival was 100% in three patients. The incidence of anastomotic leakage and recurrent fistula did not change over time. The rate of anastomotic strictures increased from 53 to 59% between the two time-periods. A primary anastomosis could be done in 85% of the patients during the second period versus 78% of the patients during the first period. Anti-reflux surgery was done in only 11 and 9%, respectively, during the two time-periods. In patients who were 16-20 years old, 40-50% had gastrointestinal and respiratory symptoms. Ninety percent of the patients attended normal school. The major difference between the periods 1986-1995 and 1996-2005 was an increased survival despite an increased incidence of major cardiac defects. Gastrointestinal and respiratory symptoms were frequent. Long-term follow-up and treatment of complications of esophageal atresia is important for this patient group.

BackgroundThe composition of the intestinal microbiota seems to be an important factor in determining the clinical outcome in children with short bowel syndrome (SBS). Alterations in the microbiota may result in serious complications such as small bowel bacterial overgrowth (SBBO) and intestinal mucosal inflammation that lead to prolonged parenteral nutrition (PN) dependency with subsequently increased risk of liver failure and sepsis. To date, there are no reported mappings of the intestinal microbiome in children with SBS. Here, we present the first report on the intestinal microbial community profile in children with SBS.FindingsThe study includes children diagnosed with SBS in the neonatal period. Healthy siblings served as controls. Fecal samples were collected, and microbial profiles were analyzed by using 16S rRNA gene sequencing on the Illumina MiSeq platform. We observed a pronounced microbial dysbiosis in children with SBS on PN treatment with an increased and totally dominating relative abundance of Enterobacteriacae in four out of five children compared to children with SBS weaned from PN and healthy siblings.ConclusionsThe overall decreased bacterial diversity in children with SBS is consistent with intestinal microbiome mappings in inflammatory bowel diseases such as Crohn’s disease and necrotizing enterocolitis in preterm infants. Our findings indicate that intestinal dysbiosis in children with SBS is associated with prolonged PN dependency.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-015-0084-7) contains supplementary material, which is available to authorized users.

No significant differences in the composition of intestinal microbiota of patients developing NEC were detected; however, some findings need to be scrutinized in subsequent studies.

Parenteral fish oil in combination with ω-6/9 lipid emulsions was associated with improved outcome in premature neonates with SBS. When used instead of traditional soybean-based emulsions, this mixed lipid emulsion may facilitate intestinal adaptation by increasing the IFALD-free period.

The incidence of adhesive small bowel obstruction after laparotomy in infants is high.

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Background: Surgery for total colonic aganglionosis (TCA) is designed to preserve continence and achieve satisfactory quality of life. This study evaluated a comprehensive group of clinical and social outcomes. Methods: An international multicentre study from eight Nordic hospitals involving examination of case records and a patient-reported questionnaire survey of all patients born with TCA between 1987 and 2006 was undertaken. Results: Of a total of 116 patients, five (4⋅3 per cent) had died and 102 were traced. Over a median follow-up of 12 (range 0⋅3-33) years, bowel continuity was established in 75 (73⋅5 per cent) at a median age of 11 (0⋅5-156) months. Mucosectomy with a short muscular cuff and straight ileoanal anastomosis (SIAA) (29 patients) or with a J pouch (JIAA) (26) were the most common reconstructions (55 of 72, 76 per cent). Major early postoperative complications requiring surgical intervention were observed in four (6 per cent) of the 72 patients. In 57 children aged over 4 years, long-term functional bowel symptoms after reconstruction included difficulties in holding back defaecation in 22 (39 per cent), more than one faecal accident per week in nine (16 per cent), increased frequency of defaecation in 51 (89 per cent), and social restrictions due to bowel symptoms in 35 (61 per cent). Enterocolitis occurred in 35 (47 per cent) of 72 patients. Supplementary enteral and/or parenteral nutrition was required by 51 (55 per cent) of 93 patients at any time during follow-up. Of 56 responders aged 2-20 years, true low BMI for age was found in 20 (36 per cent) and 13 (23 per cent) were short for age. Conclusion: Reconstruction for TCA was associated with persistent bowel symptoms, and enterocolitis remained common. Multidisciplinary follow-up, including continuity of care in adulthood, might improve care standards in patients with TCA.