Urinary waste products (UWP) in the amniotic fluid have been held responsible for the intestinal damage (ID) in gastroschisis, based on the fact that the fetus urinates physiologically into the amniotic cavity. However, experimental and clinical evidence suggests that intrauterine defecation is a physiological event; thus gastrointestinal waste products (GWP) may also be responsible for ID in gastroschisis. An experimental study was performed to investigate the effects of intraperitoneal human neonatal urine and diluted meconium on rat intestines. Adult Wistar albino rats were used. Sterile urine and meconium were obtained from newborn humans and 5% meconium suspension was prepared. Histopathological features of the intestines of the rats injected with urine did not differ from the intestines of the untreated rats. The bowel in rats injected with a meconium suspension showed serosal thickening, inflammation, focal fibrin and collagen deposits. Histopathological changes in intestines induced by intraperitoneal diluted meconium were consistent with those described for human gastroschisis specimens. We conclude that GWP, rather than UWP, seems to be responsible for the ID in gastroschisis.

Objective: Experimental studies have shown that neural tissue damage in myelomeningocele (MMC) is acquired, resulting from exposure of neural tissue to amniotic fluid (AF). Similar to neural tissue damage in MMC, in gastroschisis, intestines exposed to AF are damaged. In gastroschisis, intestinal damage can be prevented by changing the composition of the AF with partial AF exchanges. An experimental study was performed to investigate whether the neural tissue damage in MMC can be prevented by AF exchange. Methods: Thirteen-day-old fertilized chick eggs were used. In group 1, the amnio-allantoic membrane was opened to create a common cavity, and MMC was created (MMC-only group). In group 2, after creation of MMC, amnio-allantoic fluid exchange was performed (MMC-plus-exchange group). Chicks were extirpated for histopathologic examination 5 days later. Results: While edema, focal calcification, fibrosis, capillary cell proliferation and scattered mononuclear cells were observed in the MMC-only group, histopathologic changes were mild in the exchange group. The number of neuron-specific enolase stainings (+) neural cell count was significantly higher in the exchange group compared to the MMC-only group (p < 0.01). Conclusion: Exposure of MMC to AF causes structural neural tissue damage that can be prevented by AF exchange. AF exchange is minimally invasive compared to open in utero surgery for the closure of MMC. By AF exchange, neural tissue damage that occurs during the gestational period may be prevented.

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Coin ingestion with subsequent esophageal coin impaction is common in children. Considerable debate surrounds the choice of technique for the removal of esophageal coins. This study demonstrates a minimally invasive technique for upper esophageal coin extraction. A retrospective review was conducted of 165 children who had upper esophageal coins extracted by using a Magill forceps. One hundred fifty-six coins (96.4%) were successfully removed without any complications. The average time taken to remove the coin was 33 seconds. Use of the Magill forceps technique minimizes instrumentation of the esophagus and is an easy, safe technique for removing coins from the upper end of the esophagus.

PurposeIt is common practice for premature infants undergoing elective inguinal hernia (IH) repair to be hospitalized for postoperative apnea monitoring. This study evaluated the risk of apnea after IH repair with regard to gestational age (GA) and postconceptional age (PCA) in formerly premature infants.MethodsFormerly premature infants who had undergone elective IH repair between 01/2000 and 12/2012 were reviewed retrospectively in terms of GA, PCA, body weight, and comorbidities. All postoperative apneas were evaluated.ResultsA total of 428 formerly premature infant charts were reviewed. Eleven babies had postoperative apnea. Infants younger than 45 weeks PCA were found more prone to develop postoperative apnea after IH repair. In older infants (PCA between 46 and 60 weeks), comorbidities create predisposition to apnea postoperatively. These comorbidities are bronchopulmonary dysplasia, necrotizing enterocolitis and former apnea episodes. Anemia and lower birth weight are also risk factors.ConclusionThis study suggests that low GA and PCA, low birth weight, anemia, and complicated past medical history affect respiratory complication rates, particularly apnea in formerly premature infants undergoing elective IH repair. Severe apneas occurred earlier than mild ones. Overnight monitoring is mandatory in small infants with low GA and PCA. Otherwise healthy, older infants may be operated on outpatient basis.