Objective: Enteral feeding tubes are used in neonatal intensive care units (NICU) to assess feeding tolerance by utilizing pre-prandial gastric residual aspiration. This study evaluates the effect of gastric residual aspiration on the preterm infant fecal microbiome and gastrointestinal inflammation. Study Design: Fifty-one very low birth weight (VLBW) infants (<32 weeks gestational age and <1250g) enrolled in a larger single-center randomized controlled trial evaluating the effects of routine and non-routine gastric residual aspiration were selected for further analysis. Of those infants, 30 infants had microbiome analysis performed on stools collected at 6 weeks by sequencing the bacterial V1-V3 variable regions of the genes encoding for 16S rRNA. In an additional 21 infants, stool samples collected at 3- and 6-weeks were analyzed for intestinal inflammation using a cytokine multiplex panel. Results: Microbial communities between groups were not distinct from each other and there was no difference in intestinal inflammation between groups. Analyses using gene expression packages DESeq2 and edgeR produced statistically significant differences in several taxa possibly indicating a more commensal intestinal microbiome in infants not undergoing gastric residual aspiration. Conclusion: Omission of routine gastric residual aspiration was not associated with intestinal dysbiosis or inflammation, providing additional evidence that monitoring pre-prandial gastric residuals is unnecessary.

Background: Infantile hypertrophic pyloric stenosis refractory to initial complete pyloromyotomy is extremely rare and distinguished from incomplete pyloromyotomy by a prolonged postoperative symptomatic improvement before symptom recurrence. The pathogenesis is uncertain but is theorized to be a continuation of the process that initially produces infantile hypertrophic pyloric stenosis (IHPS), which has been associated with chromosome region 9q duplications. Case Presentation: Here we present a case of a neonate presenting with respiratory distress syndrome, hydronephrosis, pulmonary valve stenosis, and hypotonia at birth. A microarray identified a deletion of the terminal region of chromosome 9q, consistent with Kleefstra syndrome. The infant was diagnosed with pyloric stenosis after abdominal ultrasound was ordered to investigate difficulties with feeding, vomiting, and poor weight gain. Following initial surgical repair at five weeks of age, the infant demonstrated consistent postoperative weight gain for six weeks and resolution of emesis. However, vomiting returned and weight gain halted during weeks eleven and twelve of life; a barium swallow series and repeat abdominal ultrasound demonstrated recurrent IHPS. The infant underwent repeat pyloromyotomy and with post-operative clinical improvement. Conclusions: We present the first known case of recurrent pyloric stenosis in a patient with Kleefstra syndrome, and which further supports the hypothesis of an association between chromosome 9 and pyloric stenosis, due to an increased incidence of pyloric stenosis in chromosome 9 pathologies such as Kleefstra Syndrome found in current literature.

A 6-year-old girl with chronic constipation was referred for intermittent mass per rectum. Colonoscopy was performed to exclude rectal polyp. Due to poor bowel preparation and looping of colonoscope in the redundant sigmoid colon, the visualization was poor as the scope was advanced through the colon and procedure was prolonged but successfully completed. On withdrawal of the colonoscope, 4 discreet vascular lesions were seen between splenic flexure and sigmoid colon (Fig. 1). The lesions were raised, purple in color, interspersed with normal colonic mucosa, and not actively bleeding. The findings were thought to represent angiodysplasia with concern for blue rubber bleb nevus syndrome (1). Coagulation studies, computerized tomography angiogram chest/abdomen, esophagogastroduodenoscopy, and capsule endoscopy were subsequently normal. Repeat flexible sigmoidoscopy 3 months later was normal; the previously visualized lesions were not seen. The vascular lesions were most likely intramural hematomas resulting from trauma secondary to looping of colonoscope and loop reduction maneuvers.Colonic intramural hematoma is an uncommon complication of diagnostic colonoscopy, with only a handful of reported cases (2-4). Colonic hematomas have been reported in children secondary to accidental and nonaccidental trauma, bleeding disorders, and anticoagulant therapy (5-8). This is one of the first reported case of colonic hematoma complicating diagnostic colonoscopy in a pediatric patient. No cases of colonic hematoma have been reported in the Pediatric Endoscopy Database System-Clinical Outcomes Research Initiative database (personal communication from Dr Douglas Fishman, June 15, 2021). In our case, the knowledge gap due to lack of reported cases and images of this complication led to an extensive evaluation for angiodysplasia, which could have been avoided if the hematoma had been correctly identified. The parents consented to publication of the details of this case.