Akademik Veri Yönetim Sistemi
Pediatrik Cerrahi Dergisi, cilt.14, sa.3, ss.101-106, 2000 (Scopus)
Amniotic fluid (AF) does not cause adverse effects on the skin and gastrointestinal mucosa of the fetus. However AF exerts harmful effects on tissues that do not anatomically contact with AF during normal fetal development. Intestinal damage encountered in gastroschisis and neural tissue injury in myelomeningocele are examples. Fetal urine had been held responsible for the intestinal damage in gastroschisis. However the results of studies on intestinal damage confirm that, intraamniotic meconium is responsible for intestinal damage in gastroschisis, rather than fetal urine. In gastroschisis the concentration of intraamniotic meconium has been shown to be the determining factor for the occurrence of intestinal damage. Intraamniotic meconium below certain concentration does not cause serosal inflammation. Above this threshold level, intestinal damage occurs. Far from being destructive, presence of urine in the AF is beneficial. Intraamniotic meconium to urine ratio plays an important role in determining the intestinal damage in gastroschisis. Intraamniotic meconium concentration can be lowered by three methods. In fetuses with oligohydramnios accompanying gastroschisis, amnioinfusion prevents intestinal damage by amniodilution. In gastroschisis cases with normal AF volume, AF exchange is the preferred method where AF is partially replaced by normal saline. Other than these two methods, intraamniotic diuretic injection seems to be a promising third method where the intraamniotic meconium is eliminated from the AF by natural ways. If the intraamniotic concentration of meconium can be held below this threshold level by prenatal treatment modalities, fetuses with gastroschisis or meningomyelocele may stay in AF, till the end of gestation without any damage.