morphine and Gastroschisis

Topics: Amniotic Fluid; Female; Gastroschisis; Humans; Infant, Newborn; Infant, Newborn, Diseases; Intestines; Meconium; Pregnancy

The aim of this study was to determine if meconium-stained amniotic fluid (MSAF) was associated with neonatal outcomes in gastroschisis.. A retrospective chart review of gastroschisis patients from 2000 to 2014 at a single, tertiary institution was performed. Statistical analysis was performed with Fisher exact test, Welch's t-test, logistic regression and/or linear regression with significance at p < 0.05.. Sixty-four of 135 (47.4%) gastroschisis patients had MSAF. On univariate analysis, patients with MSAF were more likely to require staged closure (30 (46.9%) vs. 18(25.4%), p = 0.012), had more ventilator days (8.9 ± 11.1 vs. 5.3 ± 6.3, p = 0.021) and longer times to commence enteral feeds (24.9 ± 21.7 vs. 18.5 ± 14.5, p = 0.045). However, multi-variate regression analysis controlling for the type of closure, showed that delayed closure, but not MSAF, was associated with worse outcomes.. In gastroschisis patients, MSAF is associated with delayed closure but is not associated with outcomes independent of closure type. This association may be because of the matting of the bowel or increased intestinal damage. The MSAF status will aid in setting expectations for parents during their initial NICU stay and further investigation is warranted.. Clinical Research Paper Level of evidence: III.

Topics: Amniotic Fluid; Female; Gastroschisis; Humans; Infant, Newborn; Linear Models; Logistic Models; Male; Meconium; Prognosis; Retrospective Studies

Intraamniotic meconium has been responsible for intestinal damage in gastroschisis and meconium-dependent intestinal ischemia has been proposed to induce additional intestinal damage in gastroschisis. This study is aimed to determine the effects of lipid and water-soluble meconium subfractions on the contractility of the superior mesenteric artery (SMA).. The study was conducted on 18-day fertilized chick embryos (Gallus Domesticus). Meconium is fractioned into water and lipid-soluble components. Only one SMA tissue was prepared from each embryo and suspended in the organ bath. Isometric contraction responses (ICR) were created in SMA tissues by one hour of incubation in Krebs-Henseleit solution for each group. Groups consisted of control, meconium, water-soluble meconium subfraction and lipid-soluble meconium subfraction. ICR of the SMA specimens were evaluated with a transducer-amplifier system on a computer. The data were expressed (mean±1SD) as milliNewton (mN).. The ICR of the meconium, water-soluble meconium subfraction and lipid-soluble meconium subfraction groups were significantly high when compared to the control group (p<0.01). The meconium and water-soluble meconium subfraction created more contraction response than the lipid-soluble meconium subfraction (p<0.01). The ICR of the meconium group was not different from the ICR of the water-soluble meconium subfraction group (p>0.05).. Water-soluble meconium subfraction has a profound vasoconstrictor effect on the SMA compared to the lipid-soluble meconium subfraction.

Topics: Animals; Chick Embryo; Gastroschisis; Glucose; Intestinal Diseases; Intestines; Lipids; Meconium; Mesenteric Artery, Superior; Tromethamine; Vasoconstriction; Water

To investigate the association between meconium staining and perinatal and neonatal outcomes in pregnancies with gastroschisis.. Retrospective analysis of infants with prenatally diagnosed gastroschisis born in two academic medical centers between 2008 and 2013. Neonatal outcomes of deliveries with and without meconium staining were compared. Primary outcome was defined as any of the following: neonatal sepsis, prolonged mechanical ventilation, bowel atresia or death. Secondary outcomes were preterm delivery, preterm-premature rupture of membranes (PPROM) and prolonged hospital length of stay.. One hundred and eight infants with gastroschisis were included of which 56 (52%) had meconium staining at delivery. Infants with meconium staining had a lower gestational age at delivery (36.3 (±1.4) versus 37.0 (±1.2) weeks, p = 0.007), and a higher rate of PPROM (25% versus 8%, p = 0.03) than infants without meconium. Meconium staining was not significantly associated with the primary composite outcome or with any of its components. After adjustments, meconium staining remained significantly associated with preterm delivery at <36 weeks [odds ratio OR = 4.0, 95% confidence intervals (CI): 1.5-11.4] and PPROM (OR = 3.8, 95%CI: 1.2-14.5).. Among infants with gastroschisis, meconium staining was associated with prematurity and PPROM. No significant increase in other adverse neonatal outcomes was seen among infants with meconium staining, suggesting a limited prognostic value of this finding.

Topics: Adult; Amniotic Fluid; Cohort Studies; Delivery, Obstetric; Female; Gastroschisis; Humans; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature; Length of Stay; Meconium; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Retrospective Studies; Staining and Labeling

It is unclear which substances in meconium are responsible for intestinal damage in gastroschisis. An experimental study was designed to investigate the effects of the lipid or water soluble subfractions of meconium on the intestines of gastroschisis in a chick model.. Meconium was pooled, homogenated, rota-evaporated dry and diluted. Meconium subfractions were obtained from water soluble and lipid soluble extracts of the meconium. Five days old fertilized chick embryos were used and divided into 5 groups: control, sham, water soluble meconium subfraction, lipid soluble meconium subfraction and whole meconium. All embryos were extirpated on the 18days and the intestines were harvested for histopathological examination. Serosal thickness was measured under light microscopy.. Serosal thickness of the meconium (36.36±2.8μm), the water soluble meconium (14.15±0.93μm) and the lipid soluble meconium (23.88±1.69μm) subfractions groups were significantly increased compared with the control (7.47±0.68μm) and the sham (7.48±0.71μm) groups (p<0.001). Serosal thickness of the lipid soluble meconium subfraction group was significantly increased compared with the water soluble meconium subfraction group (p<0.001). Serosal thickness of the meconium group was significantly increased compared to both the water and the lipid soluble meconium subfraction groups (p<0.001).. Lipid soluble meconium subfraction induces more intestinal damage compared to water soluble meconium subfraction.

Topics: Animals; Chick Embryo; Gastroschisis; Intestinal Diseases; Intestines; Lipids; Meconium; Solubility; Water

Intestinal damage has been shown to occur when intra-amniotic meconium concentration exceeds threshold level. However, the mechanism of the meconium-induced intestinal damage is still unclear. Intestinal ischemia can cause intestinal damage in gastroschisis. This study was aimed to determine the effects of intra-amniotic meconium on the contractility of superior mesenteric artery (SMA).. Eighteen-day-old fertilized chick embryos (Gallus Domesticus) were extirpated and intestines were harvested. The SMA specimens were prepared as 4 mm segments in the organ bath with Krebs-Henseleit buffer. The isometric contraction responses of the SMA specimens were evaluated with norepinephrine, different meconium concentrations, and clear amniotic fluid. Maximum isometric contractions responses (MICR) of the SMA specimens were recorded with an amplifier system on a computer.. In the norepinephrine group, MICR was found as 2.92 ± 0.57 mN. While MICR of the 1/100 meconium group (highest meconium concentration) was found as 1.56 ± 0.40 mN, MICR of the clear amniotic fluid group was 0.41 ± 0.07 mN. The MICR of the norepinephrine group was significantly increased compared with the 1/100 meconium and clear amniotic fluid groups. MICR of the 1/100 meconium group was also found to be significantly increased compared with clear amniotic fluid group. No statistically significant difference was found among the meconium subgroups.. Intra-amniotic meconium in fetuses with gastroschisis might cause ischemic intestinal damage by reducing the intestinal blood flow. Further studies are needed to show the outcomes of the vasoactive effect of meconium on the SMA blood flow.

Topics: Animals; Chick Embryo; Disease Models, Animal; Gastroschisis; Humans; In Vitro Techniques; Intestines; Ischemia; Isometric Contraction; Meconium; Mesenteric Artery, Superior; Norepinephrine; Vasoconstriction; Vasoconstrictor Agents

Intestinal damage causes intestinal dysmotility in gastroschisis. Urinary trypsin inhibitor (UTI) has been shown to prevent intestinal damage in chick embryos with gastroschisis. The effect of intra-amniotic administration of UTI on intestinal motility in gastroschisis has not been investigated.. Five-day-old fertilized chick embryos were used. Gastroschisis was created through the amniotic cavity without opening the allantoic cavity. There were six groups; control, gastroschisis only, gastroschisis plus meconium and three treatment groups. In the treatment groups, 100 IU/mL, 200 IU/mL and 400 IU/mL UTI were instilled into the amniotic cavity of the gastroschisis plus meconium embryos, respectively. Serosal thickness of the intestines in each group was measured histopathologically. The contractions of the intestines were evaluated by in vitro organ bath technique and the responses were expressed as maximal contraction induced by acetylcholine.. The serosal thickness was significantly increased in the gastroschisis plus meconium, 100 IU/mL, 200 IU/mL UTI groups compared to control and gastroschisis only groups. The serosal thickness of the 400 IU/mL UTI group was similar to control and gastroschisis only groups. Contractility of the intestines was diminished in the gastroschisis plus meconium, 100 IU/mL and 200 IU/mL UTI groups. There was no significant difference regarding contractility among control, gastroschisis only and 400 IU/mL UTI groups.. Intra-amniotic administration of UTI preserves intestinal contractility in chick embryos with gastroschisis. However, preservation of intestinal dysmotility by using UTI in the human gastroschisis cases needs further experimental and clinical trials.

Topics: Amnion; Animals; Chick Embryo; Gastrointestinal Motility; Gastroschisis; Glycoproteins; Injections; Intestines; Meconium; Trypsin Inhibitors

Contact with amniotic fluid causes intestinal damage (ID) in fetuses with gastroschisis. Intraamniotic meconium has been shown to be responsible for ID, and ID has been shown to correlate with intraamniotic meconium concentrations. ID can be prevented by lowering the intraamniotic meconium concentration. A new method to lower intraamniotic meconium concentration might consist in the induction of fetal diuresis with intraamniotic diuretic injection. This hypothesis was tested in a rat model.. There were 4 experimental groups.. Rat fetuses without any manipulation. Fetuses were harvested by cesarean section for examination at E21.5 (Term). SHAM GROUP: On E18.5, the hind limb of the rat fetuses were exteriorized by hysterotomy and replaced in the uterus. GASTROSCHISIS GROUP: Gastroschisis was surgically created in rat fetuses on E18.5, under a dissection microscope (16×). GASTROSCHISIS+FUROSEMIDE GROUP: After surgical creation of gastroschisis on E18.5, intraamniotic furosemide (5 mg/kg) was administered to the fetuses on E20. All fetuses were harvested on E21.5.. There was no significant difference between intestinal serosal thicknesses of the control and sham groups. The serosal thickness was significantly higher in the gastroschisis group compared to the control group. In the gastroschisis+furosemide group, the intestinal serosal thickness was found significantly decreased compared with the gastroschisis group.. Intraamniotic furosemide injection caused a substantial decrease in ID encountered in gastroschisis. The induction of fetal diuresis with intraamniotic furosemide injection seems promising as a prenatal treatment modality.

Topics: Amnion; Animals; Disease Models, Animal; Diuresis; Diuretics; Fetal Therapies; Furosemide; Gastroschisis; Injections; Intestinal Diseases; Meconium; Rats; Rats, Sprague-Dawley

Despite the good survival rate of fetuses with gastroschisis, the length and cost of hospitalization for surgically repaired gastroschisis are high. In gastroschisis, prolonged exposure of the intestine to amniotic fluid (AF) containing intestinal waste products results in intestinal damage, including intestinal wall thickening and fibrous peel formation. The deleterious effects of AF on gastroschisis can be prevented by lowering the concentration of intestinal waste products. We describe the treatment of a case of fetal gastroschisis by repeated AF exchange and infusion. Following repeated, successful transabdominal AF exchange and infusion, the concentrations of various intestinal waste products were decreased. AF exchange and infusion may prevent intestinal damage and improve postnatal outcome in gastroschisis by diluting the AF, probably by lowering the concentrations of intestinal waste products.

Topics: Adult; Amniocentesis; Amniotic Fluid; Female; Fetal Diseases; Gastroschisis; Humans; Infant, Newborn; Inflammation; Meconium; Pregnancy; Prenatal Care; Ultrasonography, Prenatal

Contact with amniotic fluid causes intestinal damage in gastroschisis, and intraamniotic meconium has been shown to be responsible. Meconium has been shown to contain a significant amount of IL-8, which may be the responsible cytokine for harmful effects of meconium. Neonatal urine contains high amount of urinary trypsin inhibitor (UTI) compared with adult human urine. Urinary trypsin inhibitor has been shown to exert inhibitory effects on IL-8. Therefore, far from being destructive, presence of fetal urine in the amniotic fluid might be beneficial because human urine contains UTI. An experimental study has been performed to investigate whether presence of intraamniotic human urine (consequently UTI) besides meconium is beneficial on intestines of chick embryo with gastroschisis.. Five-day-old fertilized chick eggs were used. Gastroschisis was created through amniotic cavity without opening the allantoic cavity. Sterile urine and meconium were obtained from newborn humans. Study was conducted in 2 stages. In the first stage, gastroschisis was created, and meconium suspensions at minimal harmful meconium concentration were prepared using natural and denatured human neonatal urine and instilled into the amniotic cavity. In the second stage of study, various concentrations of UTI plus meconium suspension at minimal harmful meconium concentration was instilled into the amniotic cavity.. Serosal thickening, inflammation, and focal fibrin deposits were observed in intestines of the groups with meconium and meconium in denatured urine. Histopathologic features of intestines of the group with meconium in natural urine did not differ from the intestines of the control group. Histopathologic examination of intestines of groups with meconium and meconium plus 50 U/mL UTI showed serosal thickening, inflammation, focal fibrin, and collagen deposits. Histopathologic features of intestines of the groups with 1:400 intraamniotic meconium plus 100 and 200 U/mL UTI did not differ from the intestines of control group.. Urinary trypsin inhibitor 100 U/mL prevented the intestinal damage via inhibiting IL-8, which is contained by 1:400 concentration of meconium. Therefore, besides the existence of threshold level of meconium, the existence of UTI, which is capable of inhibiting IL-8 contained by threshold level of meconium, may be a factor in the occurrence of intestinal damage in gastroschisis.

Topics: Amniotic Fluid; Animals; Chick Embryo; Gastroschisis; Glycoproteins; Humans; Infant, Newborn; Interleukin-8; Intestinal Diseases; Meconium; Urine

Topics: Amniotic Fluid; Animals; Disease Models, Animal; Gastroschisis; Inflammation; Intestinal Diseases; Meconium; Rats

Topics: Amniocentesis; Amniotic Fluid; beta-Endorphin; Diuresis; Diuretics; Female; Fetal Diseases; Furosemide; Gastroschisis; Humans; Intestinal Diseases; Meconium; Oligohydramnios; Pregnancy; Prognosis; Sodium Chloride; Therapeutic Irrigation

Topics: Amniotic Fluid; beta-Endorphin; Biomarkers; Diuretics; Fetal Diseases; Furosemide; Gastroschisis; Humans; Intestines; Meconium; Nerve Tissue

Several studies in animal models demonstrate that peel formation in gastroschisis is due to the accumulation and activation of intestinal waste products (IWP) in the amniotic fluid. We reviewed our recent experience with gastroschisis and asked the following questions: First, does staining of the bowel and amniotic fluid with IWP correlate with intestinal peel formation? Second, what prenatal ultrasound findings indicate that peel formation is occurring in utero? Over two years, 16 neonates were treated for gastroschisis; twelve had been diagnosed by prenatal ultrasound and followed closely. Patients were grouped based on the presence of IWP in the amniotic fluid at the time of delivery (staining or no staining), and outcomes were reviewed. All neonates in the staining group (n=7) had a fibrinous peel present at the time of birth whereas a peel was absent in all neonates in the no-staining group (n=9). Matting of the bowel was seen by prenatal ultrasound in four patients in the staining group (0/8 in the no-staining group) and correlated with peel formation (Fisher's exact test p =0.007). Primary closure was done in 14 of the infants, and two required silo closure. In neonates with gastroschisis, staining of the amniotic fluid and bowel serosa with IWP correlated with intestinal peel formation. The ultrasound findings of matting correlated with both peel formation and staining with IWP. These results suggest that spillage of IWP into the amniotic fluid is one of the factors in peel formation in gastroschisis. Identification of matting of the bowel by prenatal ultrasound indicates formation of a peel.

Topics: Amniotic Fluid; Female; Gastroschisis; Humans; Infant, Newborn; Meconium; Pregnancy; Ultrasonography, Prenatal; United States

Topics: Amniotic Fluid; Animals; Deglutition; Enterocolitis; Esophagus; Female; Fetal Diseases; Gastroesophageal Reflux; Gastroschisis; Intestines; Ligation; Meconium; Models, Animal; Pregnancy; Sheep

Topics: Amniotic Fluid; Animals; Biological Therapy; Diuresis; Diuretics; Endoscopy; Female; Fetus; Furosemide; Gastroschisis; Intestines; Meconium; Meningomyelocele; Oligohydramnios; Osmolar Concentration; Pregnancy; Sheep; Sodium Chloride; Trauma, Nervous System

Contact with amniotic fluid (AF) causes intestinal damage in gastroschisis. Intraamniotic meconium has been shown to be responsible for intestinal damage, and occurrence of this damage has been shown to depend on the concentration of intraamniotic meconium. When intraamniotic meconium concentration is lowered below threshold level by exchanging AF with saline in gastroschisis, intestinal damage can be prevented. Theoretically, induction of fetal diuresis with intraamniotic furosemide may increase AF volume and fetal swallowing rate, thus, increase absorption of AF by intestines; therefore, the clearance of meconium from the AF may increase. An experimental study was planned to investigate the effects of intraamniotic diuretic injection on the clearance of intraamniotic substances.. Pregnant rabbits on the 23rd to 25th gestational day were divided into 2 groups as furosemide and control. Technetium tc99m labeled "tin colloid" was injected into the amniotic cavity, and AF sample was taken 10 minutes later. Furosemide was injected into the amniotic cavity afterwards. Two and 6 hours later, AF samples were obtained. Intestines were harvested at the end of the study. Control group received intraamniotic saline instead of furosemide. Radioactivities of the AF samples and intestines were determined by gamma counter. Clearance of the radioisotope from AF and intestinal accumulation were calculated.. The clearance of the radioisotope from AF was increased significantly in the furosemide group (n = 10) compared with the control group (n = 8; P <.01). Gastrointestinal accumulation of the radioisotope in the furosemide group was 4-fold higher than that the control group (P <.01).. Induction of fetal diuresis with intraamniotic furosemide accelerates the clearance of intraamniotic substances. This is probably caused by increased urinary output rate, which increases AF volume and consequently results in increased fetal swallowing of AF. In the diseases like gastroschisis and myelomeningocele, in which the contact with AF causes tissue damage, the elimination of meconium from AF in a somewhat natural manner like this method, should be studied further because it may be an alternative minimal invasive in utero treatment modality.

Topics: Amniotic Fluid; Animals; Diuresis; Diuretics; Female; Fetal Diseases; Furosemide; Gastroschisis; Meconium; Pregnancy; Rabbits

Topics: Amniotic Fluid; Animals; Coproporphyrins; Gastroschisis; Intestinal Diseases; Meconium; Meningomyelocele; Rats; Spinal Cord

In gastroschisis, contact with amniotic fluid (AF) causes intestinal damage. Intraamniotic meconium has been shown to be responsible for the intestinal damage, and intestinal damage has been shown to correlate with intraamniotic meconium concentrations. Intraamniotic meconium below a threshold level does not cause intestinal damage. Intraamniotic meconium concentrations can be lowered by AF exchange. Can induction of foetal diuresis by an intraamniotic injection of furosemide be used as an alternative method for the same purpose?. Pregnant rabbits on the 23rd - 25th gestational days (normal gestation time: 31 - 33 days) were divided into two groups, the control group and the furosemide group. Initial AF samples were taken, then either 5 mg/kg furosemide or a placebo was injected into the amniotic cavity. Final AF samples were obtained 6 hours later. AF urea nitrogen, creatinine, amylase, alkaline phosphatase and bilirubin levels were determined.. There was no significant difference between the initial and final levels of AF urea nitrogen, creatinine, bilirubin, amylase, and alkaline phosphatase in the control group, while the final AF urea nitrogen and creatinine levels of the furosemide group were not significantly different from the initial levels (p > 0.05). Final AF bilirubin, amylase and alkaline phosphatase levels of the furosemide group were significantly decreased compared with initial levels (p < 0.01).. Induction of foetal diuresis with intraamniotic furosemide is effective for the removal of intestinal waste products from amniotic fluid.

Topics: Amnion; Animals; Diuretics; Female; Fetal Diseases; Furosemide; Gastroschisis; Injections; Intestinal Diseases; Meconium; Pregnancy; Rabbits; Statistics, Nonparametric

Increasing evidence of physiologic in utero defecation supports the hypothesis that bowel damage in gastroschisis may be meconium dependent. In this study, the author investigated the role of meconium on parameters of bowel damage in a fetal rat model of gastroschisis.. Pregnant rats underwent laparotomy at 18 1/2 days gestational age (GA). There were 4 experimental groups of 11 fetuses each; the G(M) group consisted of fetuses with isolated gastroschisis and was considered to have moderate meconium contamination of the amniotic fluid (MCAF); the G(L) group consisted of fetuses with gastroschisis and anal ligation, performed to prevent MCAF; the G(H) group consisted of fetuses with gastroschisis and colon perforation, performed to increase MCAF; and the Sham group consisted of sham operated controls. All fetuses were harvested by cesarean section at 21 1/2 days GA, and the fetal intestine was assessed for peel, intestinal length, intestinal weight per unit length, and histologic appearance.. The authors achieved the following fetal survival rates: G(M) group, 91% (10 of 11); G(L) group, 78% (7 of 9, the ligation was not successful in 2 fetuses); G(H) group, 82% (9 of 11). Sham group, 100% (11 of 11). Intestinal length was decreased in fetuses with gastroschisis, and this reduction was related directly to the grade of MCAF (Sham, 18.4 +/- 0.6; G(L), 11.5 +/- 0.5; G(M), 10.2 +/- 0.6; G(H), 9.1 +/- 0.6 cm; P <.01). In contrast, intestinal weight per unit length increased in fetuses with gastroschisis, and this increase was related directly to the grade of MCAF (Sham, 7.8 +/- 0.5; G(L), 9.4 +/- 0.5; G(M), 11.3 +/- 0.5; G(H), 16.9 +/- 0.7 mg/cm; P <.01). In comparison with the G(M) group, the degree of peel coverage and bowel adherence were increased markedly in the G(H) group, whereas the fetuses of the G(L) group had neither peel nor bowel adherence.. All bowel damage parameters were affected by MCAF supporting the hypothesis that bowel damage in gastroschisis is at least partially dependent on meconium exposure. Further research is required to clarify other factors that contribute to bowel damage and to identify risk factors that may allow prenatal identification of severely affected fetuses.

Topics: Amniotic Fluid; Anal Canal; Animals; Female; Fetal Diseases; Gastroschisis; Intestinal Diseases; Intestines; Ligation; Meconium; Organ Size; Rats; Rats, Wistar

Topics: Animals; Disease Models, Animal; Gastroschisis; Humans; Meconium; Species Specificity

Contact with amniotic fluid (AF) causes intestinal damage in gastroschisis, which has been shown to be caused by intraamniotic meconium. However, whether this intraamniotic meconium-induced intestinal damage is concentration dependent has not been investigated previously. The purpose of this study is to investigate the effects of intraamniotic human meconium at various concentrations on the intestines of chick embryo with gastroschisis.. Five-day-old fertilized chick eggs were used. Gastroschisis was created through the amniotic cavity without opening the allantoic cavity. Sterile meconium was obtained from newborn humans. Meconium suspensions at various concentrations were prepared using saline and instilled into the amniotic cavity.. Intraamniotic 1:200 and 1:400 meconium was found to cause intestinal damage. Meconium concentrations lower than 1:400 did not cause intestinal damage. Histopathologic examination of the intestines of the 1:200 and 1:400 meconium groups showed serosal thickening, inflammation, focal fibrin, and collagen deposits. Histopathologic features of the intestines of the 1:600 and 1:800 meconium groups did not differ from the intestines of the control group.. Intraamniotic meconium, which is responsible for intestinal damage in gastroschisis, must reach a threshold level to induce intestinal damage. J Pediatr Surg 36:1811-1815.

Topics: Amniotic Fluid; Animals; Chick Embryo; Gastroschisis; Humans; Infant, Newborn; Intestinal Diseases; Intestinal Mucosa; Intestines; Meconium

Urinary waste products in the amniotic fluid has been implicated as a cause of intestinal damage (ID) in gastroschisis based on the fact that fetus urinates physiologically into the amniotic cavity. However, experimental and clinical data suggest that intrauterine defecation is a physiological event, thus gastrointestinal waste products also may be responsible for ID in gastroschisis. An experimental study was performed to investigate the effects of intraamniotic human neonatal urine and diluted meconium on the intestines of chick embryo with gastroschisis.. Five-day-old fertilized chick eggs (Gallus domesticus) were used. Gastroschisis was created through amniotic cavity without opening the allantoic cavity. Sterile urine and meconium were obtained from newborn humans, and 1% meconium suspension was prepared. The eggs were divided in to 3 groups. In the first group, gastroschisis was created, and amniotic fluid was reinstilled without changing its composition (control group). Equal amounts of amniotic fluid and urine mixture was instilled into the amniotic cavity in second group (urine group) and 1% meconium suspension was instilled in similar fashion in the third group after creation of gastroschisis (meconium group).. Histopathologic features of the intestines of the urine group did not differ from the intestines of the control group. The meconium group's bowel showed serosal thickening, inflammation, focal fibrin, and collagen deposits. Histopathologic changes of intestines induced by intraamniotic diluted meconium are consistent with the ones described for human gastroschisis specimens.. Gastrointestinal waste products seem responsible for the ID in gastroschisis rather than urinary waste products.

Topics: Amniotic Fluid; Animals; Chick Embryo; Gastroschisis; Humans; Intestines; Meconium; Rats; Urine

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.

Topics: Animals; Gastroschisis; Humans; Infant, Newborn; Injections, Intraperitoneal; Intestines; Male; Meconium; Rats; Urine