The value of prophylactic chest tubes in tracheoesophageal fistula repair.

PURPOSE: Intraoperative chest tubes (IOCTs) can be placed during esophageal atresia/tracheoesophageal fistula (EA/TEF) repair to control pneumothoraces and detect esophageal leaks, potentially preventing the need for postoperative chest tubes (POCTs). However, data are lacking regarding IOCTs' effect. We hypothesized that IOCT placement would not reduce the risk of POCT placement and would increase hospital length of stay (LOS). METHODS: This was a single-center case-control study of type C EA/TEF patients repaired at a tertiary referral center between 2006 and 2017. Postoperative complications of patients who received IOCTs (n = 83) were compared to that of patients who did not receive IOCTs (n = 26). Patients were compared via propensity score matching. Additionally, sensitivity analyses excluding low birth weight (LBW) patients and patients undergoing delayed esophageal anastomosis were also performed. RESULTS: There was no significant difference in rates of pneumothoraces or esophageal leaks between the IOCT and no-IOCT groups, nor were either of these complications detected earlier in the IOCT group. Rates of POCT placement and mortality also did not differ between groups. IOCT patients were associated with increased hospital LOS (28 vs 15.5 days, p < 0.001) and esophageal strictures (30% vs 8%, p = 0.04) requiring a return to the operating room (RTOR). CONCLUSION: IOCTs did not improve outcomes in EA/TEF repair. IOCTs seem associated with increased LOS and ROTR for esophageal stricture, suggesting that IOCTs may not be beneficial after EA/TEF repair.

Ursodeoxycholic acid protects against intestinal barrier breakdown by promoting enterocyte migration via EGFR- and COX-2-dependent mechanisms.

The intestinal barrier is often disrupted in disease states, and intestinal barrier failure leads to sepsis. Ursodeoxycholic acid (UDCA) is a bile acid that may protect the intestinal barrier. We hypothesized that UDCA would protect the intestinal epithelium in injury models. To test this hypothesis, we utilized an in vitro wound-healing assay and a mouse model of intestinal barrier injury. We found that UDCA stimulates intestinal epithelial cell migration in vitro, and this migration was blocked by inhibition of cyclooxygenase 2 (COX-2), epidermal growth factor receptor (EGFR), or ERK. Furthermore, UDCA stimulated both COX-2 induction and EGFR phosphorylation. In vivo UDCA protected the intestinal barrier from LPS-induced injury as measured by FITC dextran leakage into the serum. Using 5-bromo-2'-deoxyuridine and 5-ethynyl-2'-deoxyuridine injections, we found that UDCA stimulated intestinal epithelial cell migration in these animals. These effects were blocked with either administration of Rofecoxib, a COX-2 inhibitor, or in EGFR-dominant negative Velvet mice, wherein UDCA had no effect on LPS-induced injury. Finally, we found increased COX-2 and phosphorylated ERK levels in LPS animals also treated with UDCA. Taken together, these data suggest that UDCA can stimulate intestinal epithelial cell migration and protect against acute intestinal injury via an EGFR- and COX-2-dependent mechanism. UDCA may be an effective treatment to prevent the early onset of gut-origin sepsis. NEW & NOTEWORTHY In this study, we show that the secondary bile acid ursodeoxycholic acid stimulates intestinal epithelial cell migration after cellular injury and also protects the intestinal barrier in an acute rodent injury model, neither of which has been previously reported. These effects are dependent on epidermal growth factor receptor activation and downstream cyclooxygenase 2 upregulation in the small intestine. This provides a potential treatment for acute, gut-origin sepsis as seen in diseases such as necrotizing enterocolitis.

Pilot Study of the Effect of Plant-Based Enteral Nutrition on the Gut Microbiota in Chronically Ill Tube-Fed Children.

BACKGROUND: Dietary intake sharply impacts the structure and function of the gut microbiota, which is important for childhood health. However, little is known about the microbiota of children who cannot eat by mouth. Standard enteral formulas for supplemental nutrition are low in fiber and high in processed sugars and are commonly associated with gastrointestinal side effects. In this pilot study, we examined the effects of plant-based enteral nutrition (PBEN) upon the gut bacteria of chronically ill children. METHODS: Ten children (median age 3.5 years, age range 2-8 years) dependent upon conventional enteral formula were transitioned to PBEN for 2 months. Microbial diversity within fecal samples collected before and after PBEN was assessed by 16S ribosomal RNA gene sequence analysis and was compared with rectal swabs from healthy children. Fecal short-chain fatty acids and bile acids were measured in parallel. RESULTS: Relative to control samples, fecal samples from study subjects were depleted of commensals (eg, Faecalibacterium) and enriched with pathogens (eg, Enterococcus). Postintervention samples from study subjects were more similar to healthy controls. Most subjects experienced PBEN-induced alterations in the gut microbiota, but these changes varied significantly across individuals. Clinical diaries indicated that PBEN was well tolerated, with improvement in symptoms noted in several subjects. CONCLUSION: Results from this pilot study suggest that PBEN is well tolerated and could improve the health of the microbiota in chronically ill children. This trial provides a rationale for systematic evaluation of PBEN in clinical trials of children who require supplemental nutrition.