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.

Inconsistency in Opioid Prescribing Practices After Pediatric Ambulatory Hernia Surgery.

INTRODUCTION: Nonmedical opioid use is a major public health problem. There is little standardization in opioid-prescribing practices for pediatric ambulatory surgery, which can result in patients being prescribed large quantities of opioids. We have evaluated the variability in postoperative pain medication given to pediatric patients following routine ambulatory pediatric surgical procedures. METHODS: Following IRB approval, pediatric patients undergoing umbilical hernia repair, inguinal hernia repair, hydrocelectomy, and orchiopexy from 2/1/2017 to 2/1/2018 at our tertiary care children's hospital were retrospectively reviewed. Data collected include operation, surgeon, resident or fellow involvement, utilization of preoperative analgesia, opioid prescription on discharge, and patient follow-up. RESULTS: Of 329 patients identified, opioids were prescribed on discharge to 37.4% of patients (66.3% of umbilical hernia repairs, 20.6% of laparoscopic inguinal hernia repairs, and 33.3% of open inguinal hernia repairs [including hydrocelectomies and orchiopexies]). For each procedure, there was large intrasurgeon and intersurgeon variability in the number of opioid doses prescribed. Opioid prescription ranged from 0 to 33 doses for umbilical hernia repairs, 0 to 24 doses for laparoscopic inguinal repairs, and 0 to 20 doses prescribed for open inguinal repairs, hydrocelectomies, and orchiopexies. Pediatric surgical fellows were less likely to discharge a patient with an opioid prescription than surgical resident prescribers (P < 0.01). In addition, surgical residents were more likely to prescribe more than twelve doses of opioids than pediatric surgical fellows (P < 0.01). Increasing patient age was associated with an increased likelihood of opioid prescription (P < 0.01). There were two phone calls and two clinic visits for pain control issues with equal numbers for those with and without opioid prescriptions. CONCLUSIONS: There is significant variation in opioid-prescribing practices after pediatric surgical procedures; increased awareness may help minimize this variability and reduce overprescribing. Training level has an impact on the frequency and quantity of opioids prescribed.

Closing gastroschisis: The good, the bad, and the not-so ugly.

PURPOSE: The diagnosis of "closing" or "closed gastroschisis" is made when bowel is incarcerated within a closed or nearly closed ring of fascia, usually with associated bowel atresia. It has been described as having a high morbidity and mortality. METHODS: A retrospective review of closing gastroschisis cases (n = 53) at six children's hospitals between 2000 and 2016 was completed after IRB approval. RESULTS: A new classification system for this disease was developed to represent the spectrum of the disease: Type A (15%): ischemic bowel that is constricted at the ring but without atresia; Type B (51%): intestinal atresia with a mass of ischemic, but viable, external bowel (owing to constriction at the ring); Type C (26%): closing ring with nonviable external bowel +/- atresia; and Type D (8%): completely closed defect with either a nubbin of exposed tissue or no external bowel. Overall, 87% of infants survived, and long-term data are provided for each type. CONCLUSIONS: This new classification system better captures the spectrum of disease and describes the expected long-term results for counseling. Unless the external bowel in a closing gastroschisis is clearly necrotic, it should be reduced and evaluated later. Survival was found to be much better than previously reported. TYPE OF STUDY: Retrospective case series with no comparison group. LEVEL OF EVIDENCE: Level IV.

Lactobacillus murinus HF12 colonizes neonatal gut and protects rats from necrotizing enterocolitis.

The use of lactobacilli in prevention of necrotizing enterocolitis (NEC) is hampered by insufficient knowledge about optimal species/strains and effects on intestinal bacterial populations. We therefore sought to identify lactobacilli naturally occurring in postnatal rats and examine their ability to colonize the neonatal intestine and protect from NEC. L. murinus, L. acidophilus, and L. johnsonii were found in 42, 20, and 1 out of 51 4-day old rats, respectively. Higher proportion of L. murinus in microbiota correlated with lower NEC scores. Inoculation with each of the three species during first feeding significantly augmented intestinal populations of lactobacilli four days later, indicating successful colonization. L. murinus, but not L. acidophilus or L. johnsonii, significantly protected against NEC. Thus, lactobacilli protect rats from NEC in a species- or strain-specific manner. Our results may help rationalizing probiotic therapy in NEC.

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.

Liver steatosis induced by small bowel resection is prevented by oral vancomycin.

BACKGROUND: Intestinal failure-associated liver disease causes significant mortality in patients with short bowel syndrome. Steatosis, a major component of intestinal failure-associated liver disease has been shown to persist even after weaning from parenteral nutrition. We sought to determine whether steatosis occurs in our murine model of short bowel syndrome and whether steatosis was affected by manipulation of the intestinal microbiome. METHODS: Male C57BL6 mice underwent 50% small bowel resection and orogastric gavage with vancomycin or vehicle for 10 weeks. DNA was extracted from stool samples then sequenced using 16s rRNA. Liver lipid content was analyzed. Bile acids were measured in liver and stool. RESULTS: Compared with unoperated mice, small bowel resection resulted in significant changes in the fecal microbiome and was associated with a >25-fold increase in steatosis. Oral vancomycin profoundly altered the gut microbiome and was associated with a 15-fold reduction in hepatic lipid content after resection. There was a 17-fold reduction in fecal secondary bile acids after vancomycin treatment. CONCLUSION: Massive small bowel resection in mice is associated with development of steatosis and prevented by oral vancomycin. These findings implicate a critical role for gut bacteria in intestinal failure-associated liver disease pathogenesis and illuminate a novel, operative model for future investigation into this important morbidity.

Heller Myotomy Is Superior to Balloon Dilatation or Botulinum Injection in Children with Achalasia: A Two-Center Review.

INTRODUCTION: Achalasia is an uncommon disorder in children. Currently, there is no consensus regarding the optimal treatment for achalasia. We investigate the effectiveness of symptom relief in patients who underwent endoscopic treatments versus Heller myotomy (HM). METHODS: We conducted a retrospective review of all children (age 0-18 years) treated for achalasia at two pediatric hospitals from 2004 to 2014. Demographics, presenting symptoms, outcomes, and complications were analyzed. RESULTS: Twenty-three patients (61% male) were identified with a mean age at diagnosis of 11.6 ± 5.0 years. About 47.8% of the cohort had no comorbidities. Common presenting symptoms included weight loss/failure to thrive (87.0%), emesis (69.6%), and dysphagia (69.6%). Mean time from symptom onset to diagnosis was 18 ± 18.9 months. Nine patients underwent laparoscopic HM as their primary treatment, whereas 14 received esophageal dilatation (ED) as their first-line therapy. Patients who underwent ED as their initial treatment were younger (9.92 versus 15.6 years, P = .047). Patients who underwent HM were more likely to attain symptom resolution compared to those managed with ED alone (P = .004). Of the 14 patients who underwent ED initially, 10 subsequently required HM due to persistent symptoms. None of the 4 patients who underwent ED alone achieved long-term symptom relief and, on the average, required an increased number of procedures compared to their HM counterparts (5.25 versus 2.47, P = .010). There was a trend toward increased intraoperative mucosal perforation in patients who underwent preoperative ED and botulinum injections. CONCLUSION: Our data suggest that HM is superior to balloon dilatation or botulinum injection in children with achalasia. We conclude that HM should be recommended for newly diagnosed children with achalasia as a first-line therapy.

Routine contrast enema is not required for all infants prior to ostomy reversal: A 10-year single-center experience.

INTRODUCTION: The incidence of intestinal stricture is low for most conditions requiring a primary small bowel stoma in infants. Routine performance of contrast enemas (CE) prior to stoma closure adds cost and radiation exposure. We hypothesized that routine CE prior to ostomy reversal is not necessary in all infants, and sought to identify a subset of patients who may benefit from preoperative CE. METHODS: Medical records of infants under age 1 (N=161) undergoing small bowel stoma reversal at a single institution between 2003 and 2013 were retrospectively reviewed. Student's T-test was used to compare groups. RESULTS: Contrast enemas were performed on 80% of all infants undergoing small bowel ostomy reversal during the study period. Infants with necrotizing enterocolitis (NEC) were more likely to have a CE than those with intestinal atresia (p=0.03) or those with all other diagnoses combined (p=0.03). Nine strictures were identified on CE. Of those, 8 (89%) were in patients with NEC, and only 4 were clinically significant and required operative resection. The overall relevant stricture rate was 2.5%. No patient that underwent ostomy takedown without CE had a stricture diagnosed intraoperatively or an unrecognized stricture that presented clinically after stoma takedown. CONCLUSIONS: Routine CE is not required prior to small bowel ostomy reversal in infants. We recommend judicious use of enema studies in patients with NEC and high likelihood of stricture.

Pathogenesis of neonatal necrotizing enterocolitis.

Although necrotizing enterocolitis (NEC) is the most lethal gastrointestinal disease in the neonatal population, its pathogenesis is poorly understood. Risk factors include prematurity, bacterial colonization, and formula feeding. This review examines how mucosal injury permits opportunistic pathogens to breach the gut barrier and incite an inflammatory response that leads to sustained overproduction of mediators such as nitric oxide and its potent adduct, peroxynitrite. These mediators not only exacerbate the initial mucosal injury, but they also suppress the intestinal repair mechanisms, which further compromises the gut barrier and culminates in bacterial translocation, sepsis, and full-blown NEC.