Case report: Catastrophic event: neonatal gastric perforation and complication of capillary leak syndrome

Neonatal gastric perforation (NGP) is a rare, but life-threatening condition that can lead to serious conditions, such as capillary leak syndrome (CLS). Here, we present the case of a preterm male infant with NGP complicated by CLS after stomach repair. The patient was born at 33 2/7 weeks, weighed 1,770 g, and was diagnosed with respiratory distress syndrome. On the fourth day of life, the patient presented with distention and an unstable cardiovascular system. Routine blood tests revealed a white blood cell count of 2.4 × 109/L. Chest and abdominal radiography revealed a pneumoperitoneum, suggesting a gastrointestinal perforation. The patient was urgently transferred to a tertiary hospital for exploratory laparotomy, where a 2 cm diameter perforation was discovered in the stomach wall and subsequently repaired. Pathological findings indicated the absence of a muscular layer in the stomach wall. The patient unexpectedly developed CLS postoperatively, leading to multiorgan dysfunction and eventual death. The underlying pathological mechanism of NGP-induced CLS may be related to severe chemical peritonitis, sepsis, endothelial glycocalyx dysfunction, enhanced systemic inflammation, and translocation of the gut microbiota, causing endothelial hyperpermeability. Notablely, abdominal surgery itself can be a significant triggering factor for CLS occurrence. Complications of NGP and CLS are extremely dangerous. Investigating the mechanism by which NGP triggers CLS could potentially improve the prognosis. Conservative treatment for pneumoperitoneum secondary to gastric perforation may be a reasonable option, especially when the condition of the patient is unstable

Maternal separation leads to dynamic changes of visceral hypersensitivity and fecal metabolomics from childhood to adulthood

Abstract We assessed dynamic changes in visceral hypersensitivity and fecal metabolomics through a mouse model of irritable bowel syndrome (IBS) from childhood to adulthood. A mouse model of IBS was constructed with maternal separation (MS) in early life. Male mice aged 25, 40, and 70 days were used. Visceral sensitivity was assessed by recording the reaction between the abdominal withdrawal reflex and colorectal distension. Metabolomics was identified and quantified by liquid chromatography-tandem mass spectrometry. The visceral sensitivity of the MS group was significantly higher than that of the non-separation (NS) group in the three age groups. The top four fecal differential metabolites in the different age groups were lipids, lipid molecules, organic heterocyclic compounds, organic acids and derivatives, and benzenoids. Five identical differential metabolites were detected in the feces and ileal contents of the MS and NS groups at different ages, namely, benzamide, taurine, acetyl-L-carnitine, indole, and ethylbenzene. Taurine and hypotaurine metabolism were the most relevant pathways at P25, whereas histidine metabolism was the most relevant pathway at P40 and P70. Visceral hypersensitivity in the MS group lasted from childhood to adulthood. The different metabolites and metabolic pathways detected in MS groups of different ages provide a theoretical basis for IBS pathogenesis

Clusters of Human Infection and Human-to-Human Transmission of Avian Influenza A(H7N9) Virus, 2013–2017

To detect changes in human-to-human transmission of influenza A(H7N9) virus, we analyzed characteristics of 40 clusters of case-patients during 5 epidemics in China in 2013–2017. Similarities in number and size of clusters and proportion of clusters with probable human-to-human transmission across all epidemics suggest no change in human-to-human transmission risk