End-results of experimental gastroschisis created by abdominal wall versus umbilical cord defect

Abstract

An experimental study was conducted to determine the end-results of two different defects on the anterior abdominal wall: an abdominal wall defect (AWD) versus an umbilical cord defect (UCD) using chick embryos. The AWD was created by leaving an intact skin bridge between the defect and the umbilical cord in group 1; the UCD was created on the umbilical cord near the junction of the skin in group 2. At the end of incubation, the intestines appeared hemorrhagic in the AWD group, but not in the UCD group. During microscopic examination, hemorrhagic areas were observed in the bowel wall and mucosal villi in the AWD group but not in the UCD group. The end-result of the defect causing the physiological umbilical hernia resulted in bowel damage resembling the classic picture of gastroschisis (GS). We conclude that the site of the defect in GS is not the abdominal wall itself, but the physiological umbilical hernia.

The aetiology of gastroschisis

“…The suggestion that gastroschisis is caused by in utero rupture of the membrane covering a hernia of the umbilical cord, either between the 5th to 10th weeks or later if normal closure of the umbilical ring has failed to occur 9 , is supported by the association with intestinal nonrotation 10 and a case report of gastroschisis at 34 weeks of gestation in a fetus that seven weeks earlier had an umbilical hernia detected by ultrasound scan 11 . In a chick embryo model, an umbilical cord defect produced a result more closely resembling gastroschisis than an abdominal wall defect alongside the cord 12 . Nevertheless, the numerous epidemiological differences between gastroschisis and exomphalos 13,14 suggests a different aetiology from exomphalos.…”

To observe the intensity of the inflammatory reaction caused by neonatal urine and meconium on the intestinal wall of rats in order to understand etiology of intestinal damage in gastroschisis

“…Olguner et al .,[12] showed that intraamniotic neonatal human urine has no effect on intestines, while intraamniotic neonatal human diluted meconium causes intestinal damage in chick embryos that is identical to the histopathologic features of human gastroschisis specimens described by Amoury et al .,[13] and with the histopathologic features of chick gastroschisis specimens described by other investigators.…”

Reação inflamatória nas alças intestinais de ratos: pode a urina intraperitonial causar dano?

“…17 However, other substances that make up human amniotic fluid, including meconium, [2][3][4][14][15][16][24][25][26] may be responsible for the event. Innumerable experiments have demonstrated that intrauterine defecation can be considered physiological, 2,16,24,25,[27][28][29] and as such the differences that we did not find in our study could be related to a secondary role played by urine in the presence of an inflammatory effect by one of these other components which were not tested in the experiment.…”

“…Its etiology is unknown, although it is possible that it is part of a wide spectrum of fetal disorders that includes vascular factors, factors related to the position of the defect and the capacity of the fetus to heal. 26 The intensity of the inflammatory reaction present in the intestinal walls of these patients is a defining factor in their prognosis from which springs the importance of establishing its etiology and identifying factors which may be associated with worse progress. In our study the injection of neonatal urine was not capable of producing significant inflammatory reactions on the intestinal walls of rats when compared with animals in a control group submitted to just the paracentesis procedure.…”