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Background/purpose: Prolonged exposure to amniotic fluid causes the intestinal changes such as serosal edema, thickening, fibrous coating, and adhesions in gastroschisis. The effect of amnio-allantoic fluid (AAF) pH on intestines was evaluated using a chick embryo gastroschisis model., Methods: Seventy fertile eggs were divided into 5 groups: preliminary study (PS, n = 20), AAF control (AAC, n = 10), just gastroschisis (JG, n = 10), gastroschisis pretreated with placebo (GPP, n = 15), and gastroschisis pretreated with sodium bicarbonate (GPS, n = 15). The PS group was also divided into 2 subgroups to determine the biochemical differences between the amniotic and the allantoic fluid. Gastroschisis was created surgically at the 14th day of incubation. In GPS group, 8.4% NaHCO(3) solution (0.1 mL/100 mg/d) was instilled into the AAF for 4 days., Results: A significant decrease in intestinal damage was observed both macroscopically and microscopically in the group GPS compared with the JG and GPP groups., Conclusions: Pretreatment with alkalization of AAF prevented intestinal damage because of gastroschisis. Alkalization could be a simple alternative for pretreatment with amniotic fluid exchange for human fetuses with gastroschisis., (Copyright 2001 by W.B. Saunders Company.)

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., (Copyright 2001 S. Karger AG, Basel.)

Experimental amnio-allantoic fluid (AAF) exchange has been shown to prevent intestinal damage in the chicken embryo gastroschisis model. AAF contains both urinary and gastrointestinal waste products (UWP and GIWP). An experimental study was performed to find the waste products responsible for this intestinal damage. Gastroschisis was created in 20 chick embryos. Half were treated with AAF exchange, the other half were not treated. AAF samples were obtained for biochemical determination of urea nitrogen and creatinine as UWP, bile acids and bilirubin as GIWP at the end of the incubation. Intestines were evaluated by light microscopy. While GIWP (Bile salts and bilirubin) were significantly removed from AAF by exchange, the levels of UWP (urea nitrogen and creatinine) were unaffected. Intestinal wall thickness was less in the exchange group compared to the untreated group. The unchanged levels of UWP after AAF exchange may be attributed to their relatively rapid production compared to GIWP. Dilution of GIWPs by AAF exchange results in prevention of the intestinal damage in gastroschisis.

The prevention of intestinal damage in gastroschisis was reported after amnio-allantoic fluid (AAF) exchange using serum saline. However it is not clear why AAF exchange prevents intestinal damage. Are some harmful chemicals withdrawn from AAF by exchange or sodium content of AAF is merely increased? A study was planned to find the end results of AAF exchange performed by using two different solutions in the chicken embryo gastroschisis model. After creation of gastroschisis, three groups were studied. In the first group AAF exchange was not performed. In the second group AAF exchange was performed using 0.075% NaCl solution (physiologic saline for chicken). In the third group AAF exchange was performed using 0.054% NaCl plus 1% dextrose solution. Exchange with two different solutions prevented cellular infiltration and fibrous peel formation in intestines which are observed in the non-treatment group. In the third group, intestinal edema was an additional pathologic finding. This study shows that in gastroschisis, the intestines outside the abdominal cavity are very sensitive to the quality of the fluid in which they are bathed. The intestinal damage resembling that encountered in human gastroschisis can be prevented by removing the harmful chemicals from AAF by exchange.

Background: Intestinal thickening in gastroschisis results from prolonged exposure to amniotic fluid (AF). Experimental AF exchange has been shown to prevent intestinal thickening in gastroschisis., Case: A 25-year-old primigravida was referred at 24 weeks' gestation with a prenatal diagnosis of gastroschisis. Transabdominal AF exchange was performed at 29 weeks. This pretreatment did not cause any complications and prevented intestinal thickening in our patient. Thus, we were able to perform primary fascial closure with an intra-abdominal pressure less than 5 mmHg. We began feeding the infant on the 5th day and discharged her on the 8th day., Conclusion: Evidence obtained from this initial case seems promising for the further application of the AF exchange for prevention of intestinal thickening in gastroschisis.

In gastroschisis, the protruding intestine is usually shortened, thickened, and covered with a fibrous peel. Urine components, which are increased in the amniotic fluid with the onset of renal function, are responsible for these changes. In the chick embryo model of gastroschisis, the authors performed amnio-allantoic fluid exchange to reduce the effect of urinary products. There were three study groups: control, gastroschisis only, and gastroschisis plus exchange. There was a significant decrease in creatinine (P < .05) and a slight decrease in urea concentrations in the gastroschisis-plus-exchange group compared with the gastroschisis-only group. Whereas macroscopic and microscopic studies showed severe fibrosis and bowel-wall thickening in the latter group, the bowel was normal or slightly oedematous in the former. On the basis of this study, the authors suggest that antenatal amniotic fluid exchange might reduce the bowel damage in human foetuses.