Intestinal damage in gastroschisis is independent of the size of the abdominal defect

Abstract

The intestinal damage in gastroschisis (GS) has been attributed to a narrow abdominal wall defect (AWD), among other causes, but this causal effect is difficult to prove in humans. The present experimental study was done to ascertain the damaging effect of clinically extrapolable mild and moderate constriction at the AWD on the intestine of fetuses with GS. AWDs of two different sizes were carried out in the fetal rabbit model: small-ring GS (1.5x bowel diameter, SRG) and large-ring GS (3x bowel diameter, LRG); a group of unoperated littermates served as controls. Fetal body weight, intestinal length and weight, bowel diameter and wall thickness, and histology were checked 7 days later. No statistical difference was found in body weight and bowel diameter among the groups. Intestinal length, weight, and wall thickness were significantly different in the GS groups compared to the controls, but no difference was found between the GS groups. Histology did not show venous stasis, ischemic lesions, or differences in the degree of edema between groups SRG and LRG. Mesothelial hyperplasia was seen in both GS groups. The intestinal changes in length, weight, diameter, wall thickness, and histology in GS should thus not be attributed to the diameter of the AWD.

Maturity of the Myenteric Plexus Is Decreased in the Gastroschisis Rat Model

“…0.001). BW was not as altered in the subgroups (p = 0.793) as in the E18.5 and E19.5 groups (p = 0.271); these results are different from those of Albert et al [2] and FranchiTeixeira et al [27] who found a smaller BW in gastroschisis fetuses.…”

“…Experimental studies in which constriction of the vascular pedicle of the eviscerated bowel by a narrow AWD was analyzed to try to explain bowel thickening, edema and ischemic lesions have been made in chick embryo and lamb models, but their conclusions showed no relationship of intestinal changes with moderate or mild constriction at the site of the AWD [2] . These authors affirmed that there were no differences between constriction by an AWD 1.5 or 3 times the normal intestinal diameter.…”

“…These authors affirmed that there were no differences between constriction by an AWD 1.5 or 3 times the normal intestinal diameter. Despite chronic constriction of the bowel at the site of the AWD being an important contributing factor to the intestinal damage seen in gastroschisis, the effect of AF on the myenteric neurons (intrinsic nervous system) is present and could respond to transitory intestinal dysmotility in the postnatal period [2] .…”

Aminiotic Fluid and Intrauterine Growth Restriction in a Gastroschisis Fetal Rat Model

“…In subsequent studies it became clear that intestinal infl ammation was the consequence of several substances in the AF and not because of any ischemic injury [16,17] .…”

Congenital Abdominal Wall Defects: An Update

“…Histology did not show venous stasis, ischemic lesions, or differences in the degree of edema between groups with a 2.6-mm ring compared to a 4.8-mm abdominal ring in a rabbit model. The conclusion was that intestinal changes in the length, weight, diameter, wall thickness, and histology in gastroschisis should not be attributed to the diameter of the abdominal wall defect [21]. In the rat and chicken model, meconium within the amniotic fluid has been associated with bowel damage.…”