SEARCH

SEARCH BY CITATION

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. METHODS
  5. RESULTS
  6. DISCUSSION
  7. References

Objectives To investigate the relationship between intestinal atresia and fetal growth, intrapartum cardiotocograph abnormalities and staining of the amniotic fluid in gastroschisis pregnancies.

Design Observational study of 115 gastroschisis pregnancies conceived between 1980 and 1996.

Setting South West Region of England.

Main outcome measures Birthweight, intrapartum cardiotocograph abnormality, staining of amniotic fluid and Apgar score.

Results There was no statistically significant difference between the Apgar scores or the frequency of amniotic fluid staining of gastroschisis cases with or without atresia. Patent bowel gastroschisis was associated significantly with more cardiotocograph abnormalities (61%vs 26%, P= 0.026) and reduced growth (P= 0.02), when compared with cases with intestinal atresia.

Conclusions Bile vomiting may be an important cause of amniotic fluid staining. Bowel atresia protects against the increased incidence of cardiotocograph and growth abnormality found in cases of gastroschisis which may reflect their aetiology.


INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. METHODS
  5. RESULTS
  6. DISCUSSION
  7. References

Stillbirth rates of up to 12.5%1 and high perinatal mortality2,3 have been reported in pregnancies complicated by gastroschisis. This raises questions about the optimal gestational age for delivery and soon after 35 weeks has been recommended by one group4 if lung maturity is indicated by amniocentesis. Alternatively, if regular biophysical profile and Doppler studies are reassuring, waiting until 37–38 weeks of gestation before inducing labour has also been advocated1.

Gastroschisis is an increasingly common problem with the national incidence in the United Kingdom having doubled from 0.65 in 1987 to 1.35 per 10,000 births in 19935. Its incidence was even higher in the South West region of England at 4.4 per 10,000 in 19956. Fetal growth restriction, defined as a birthweight less than 3rd centile for gestational age, is common in gastroschisis fetuses with an incidence between 16%4 and 46%1 but the mechanism of the growth restriction in gastroschisis is not understood. The increased incidence of fetal growth restriction, cardiotocograph abnormalities and staining of amniotic fluid is often taken to suggest that fetuses with gastroschisis suffer from uteroplacental insufficiency. Crawford et al.1 reported a 47% incidence of pathological cardiotocograph during labour in fetuses with gastroschisis which is often a baseline tachycardia with decelerations. The incidence of ‘meconium’ stained amniotic fluid in gastroschisis labours is up to 79%7 and it has a significant association with an abnormal cardiotocograph1. However, there may be difficulty in differentiating between meconium and bile stained amniotic fluid, because at corrective surgery all babies in one study had bile stained gastric aspirates1. Cardiotocograph abnormality and stained amniotic fluid gives an increased incidence of ‘intrapartum fetal distress’ in gastroschisis fetuses1 with a reported caesarean section rate for this indication between 10% and 32%4,8–10. However the aetiology of these observations is unclear and in our experience we encountered little objective evidence of intrapartum hypoxia despite the abnormal cardiotocographs and meconium.

We wished to test the hypothesis that the above observations related to exposed bowel and that bowel atresia might be protective. Our aim was to compare the events in labour, the condition at birth and birthweight of neonates with patent gastroschisis to those with intestinal atresia.

METHODS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. METHODS
  5. RESULTS
  6. DISCUSSION
  7. References

We studied 115 pregnancies with live born babies with gastroschisis delivered after 30 weeks of gestational age between 1980 and 1996 and complicated by gastroschisis. Details of fetal gestational age by early pregnancy ultrasound measurement, mode of delivery, reason for delivery, Apgar scores at 1 and 5 minutes, gender, birth-weight, presence of stained amniotic fluid and cardiotocograph abnormalities were retrieved from the medical notes. Cardiotocograph abnormalities recorded were tachycardia (> 160 beats per minute (bpm), late decelerations (nadir of deceleration occurs more than 30 s after the peak of the uterine contraction), variable decelerations (early and late decelerations), reduced baseline variability (< 5 bpm) or bradycardia (< 100 bpm). The presence or absence of intestinal atresia was confirmed by the pathology or paediatric surgery records. Our management protocol in otherwise uncomplicated gastroschisis pregnancy was to induce labour at 38 weeks of gestational age.

To allow comparison between neonates of different gestational age and sex, birthweights were expressed as a multiple of the standard deviation of birthweight for a given gestational age and sex using tables published by Yudkin11 calculated as follows:

  • image

where MSD = multiple of the standard deviation of birthweight, Wn = birthweight, Wm = population mean birthweight for that gestational age, and SD = population birthweight standard deviation for that gestational age.

Statistical analysis

Statistical analysis was performed using Arcus Pro-Stat Version 3.2.3. Statistical comparisons between groups with normally distributed continuous variables was performed using the unpaired, two-tailed t test. Comparisons between unpaired groups with respect to continuous variables that were not normally distributed were performed using the Mann-Whitney U test. The χ2 test (with Yates correction) was used to analyse differences in categorical variables between the groups. Statistical significance was taken at the 5% level.

RESULTS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. METHODS
  5. RESULTS
  6. DISCUSSION
  7. References

Intestinal atresia was present in 19 cases (16%) and the bowel was patent in the other 96 cases. The comparison of gastroschisis neonates with intestinal atresia and those with patent bowel is shown in Table 1. There was no significant difference in 1-minute and 5-minute Apgar scores in the intestinal atresia and patent groups (P= 0.06 and P= 0.095, respectively, Mann-Whitney U test).

Table 1.  The results of gastroschisis neonates with intestinal atresia compared with those with patent bowel. Values are given as median [range] or n (%), unless otherwise indicated
 Patent bowel (n= 96)Intestinal atresia (n= 19)P
Proportion (%)8416 
Gestation at delivery (weeks)37 [30–40]34 [32–391≤ 0.001
Mean birthweight standard   
 deviation−1.02−0.4420.02
Apgar score   
 1 min7 [2.10]9 [2.10]0.06
 5 min9 [4.10]9 [5.10]0.095
Spontaneous vaginal delivery62 (65)14 (74)0.25
Meconium79 (82)16 (84)0.21
Cardiotocograph abnormality59 (61)5 (26)0.026

The average birthweight (expressed as the multiple of standard deviation to correct for gestational age and gender) in the intestinal atresia and patent bowel groups was −0.442 and −1.02 respectively. This difference was significant (P= 0.02, Mann-Whitney U test) showing that the patent group were significantly more growth restricted than the atresia group.

Stained amniotic fluid occurred in 95 of 115 (83%) deliveries and there was no significant difference in the incidence of stained amniotic fluid in the intestinal atresia and patent bowel groups (Yates corrected χ2 P = 0.21). Fifty-six percent of deliveries had a significant cardiotocograph abnormality. The most common cardiotocograph abnormalities were tachycardia (n= 28 (43%)) and variable or late decelerations (n= 26 (40%)). Cardiotocograph abnormalities were present in five of 19 in the intestinal atresia group and 59 of 96 in the patent bowel group, respectively, and these rates were significantly different (Yates corrected χ2P= 0.026).

The median gestational age at delivery of the whole study group was 36 weeks. Gestational age at delivery was significantly lower in gastroschisis fetuses with atresia (median gestational age = 34 weeks) compared with those with patent bowel (median gestational age = 37 weeks) (P= 0.0005). This difference was not iatrogenic because only one of the 19 intestinal atresia cases was induced and this was at 38 weeks of gestational age. Only two intestinal atresia cases were delivered by caesarean section (at gestational week 32 and 38).

The modes of delivery were spontaneous vaginal (76 (66%)), operative vaginal (11 (10%)) or caesarean section (28 (24%)). The indications for caesarean section were fetal distress in labour (21 (75%)), breech (3 (11%)), failure to progress in labour (2 (7%)) and gastroschisis alone (2 (7%)). There was no significant difference in the incidence of spontaneous vaginal and operative delivery between the intestinal atresia and patent groups (Yates corrected χ2P= 0.25). The neonatal mortality rate (4 (3.5%)) was lower than previous reports.

DISCUSSION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. METHODS
  5. RESULTS
  6. DISCUSSION
  7. References

The proportion of gastroschisis neonates with atresia was 16% and was similar to 10% reported in a recent study of 50 cases8. An association between fetal growth restriction and gastroschisis has been reported before and this was confirmed by this study. However, we were unaware that bowel atresia significantly protected against fetal growth restriction. We found that the mean multiple of standard deviation of birthweight corrected for gestational age of gastroschisis neonates with patent bowel was significantly less than those with intestinal atresia. The mechanism of fetal growth retardation in gastroschisis is not fully understood but this difference may help to identify the cause. Nutrients pass from maternal blood circulation across the chorionic villi into the fetal circulation and this mechanism should be unaffected by the presence of gastroschisis. Transmural loss of proteins across exposed bowel wall may cause a nutritional drain on the fetus and impair fetal growth. Indeed, hypoalbuminaemia, hypoglobulinaemia and low transferrin concentration are common in neonates with gastroschisis12. The transmural loss of protein may be greater when the herniated bowel is patent (rather than distal to an atresia) because patent bowel is functional, has an intact vascular supply and a greater surface area from which to lose protein. Also our finding that atresia appears to be protective against reduced growth is evidence that the hypothesis that an intact bowel may be required to absorb nutrients from the amniotic fluid at the end of pregnancy is not likely to be the cause of reduced growth in gastroschisis13–15.

In this study, there was a 84% (16 of 19) incidence of amniotic fluid staining in gastroschisis fetuses with atresia. It is very surprising if fetuses with atresia passed ‘meconium’, since gastroschisis atresias are usually located in the midgut10,16,17. Since bile acids enter the gut at the ampulla of Vater proximal to an atresia, any meconium passed should not have the characteristic green/black colour. Consequently, the cause of amniotic fluid staining reported in 84% of fetuses with intestinal atresia is almost certainly bile vomiting. Therefore, intrapartum amniotic fluid staining in gastroschisis may not indicate fetal hypoxia.

The 56% incidence of abnormal cardiotocograph traces in the labours of fetuses with gastroschisis is similar to the 47% incidence of pathological cardiotocograph reported by Crawford et al.1. However, as a new finding we found significantly more cardiotocograph abnormalities in gastroschisis fetuses with patent bowel compared with those with intestinal atresia. Since these cases did not have an increased incidence of asphyxia at birth as indicated by the Apgar scores, an alternative explanation for the increased incidence of cardiotocograph abnormalities in gastroschisis fetuses should be sought. In fetuses with gastroschisis the presence of staining of the amniotic fluid and/or cardiotocograph abnormalities (particularly tachycardias) are not a reliable sign of fetal hypoxia and alternative methods of fetal monitoring such as fetal scalp blood sampling or fetal pulse oximetry should be considered instead.

The median gestational age at delivery of gastroschisis neonates with atresia was significantly earlier than those with patent bowel. This was not an iatrogenic effect due to either induction of labour or caesarean section and the cause is not known. One possibility was if atresia led to an increased incidence of polyhydramnious but this did not appear to be the case. The caesarean section rate was at the lower end of the 10% to 66% range reported for gastroschisis deliveries7,9.

In gastroschisis, bowel atresia was associated with both fewer cardiotocograph abnormalities and less fetal growth restriction. This supports the hypothesis that these complications may be caused by uterine compression of the herniated bowel and protein and fluid loss into the amniotic space.

References

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. METHODS
  5. RESULTS
  6. DISCUSSION
  7. References
  • 1
    Crawford RAF, Ryan G, Wright VM, Rodeck CH. The importance of serial biophysical assessment of fetal wellbeing in gastroschisis. Br J Obstet Gynaecol 1992; 99: 899902.
  • 2
    Gabriel R, Leroux B, Quereux C, Daoud S, Wahl P. Gastroschisis: what part can the obstetrician play Eur J Obstet Gynecol Reprod Biol 1992; 45: 101105.
  • 3
    van de Geijn EJ, van Vujt JMG, Sollie JE, van Geijn HP. Ultrasonographic diagnosis and perinatal management of fetal abdominal wall defects. Fetal Diagn Ther 1991; 6: 210.
  • 4
    Poulain P, Milon J, Fremont B et al. Remarks about the prognosis in case of antenatal diagnosis of gastroschisis. Eur J Obstet Gynecol Reprod Biol 1994; 54: 185190.
  • 5
    Tan KH, Kilby MD, Whittle MJ et al. Congenital anterior abdominal wall defects in England and Wales 1987–1993: retrospective analysis of OPCS data. BMJ 1996; 313: 903906.
  • 6
    Penman DG, Fisher RM, Noblett HR, Soothill PW. Increase in the incidence of gastroschisis in the south west of England in 1995. Br J Obstet Gynaecol 1998; 105: 328331.
  • 7
    Adair CD, Rosnes J, Frye AH, Burrus DR, Nelson LH, Veille JC. The role of antepartum surveillance in the management of gastroschisis. Int J Gynaecol Obstet 1996; 52: 141144.
  • 8
    Haddock G, Davis CF, Raine PAM. Gastroschisis in the decade of prenatal diagnosis: 1983–1993. Eur J Pediatr Surg 1996; 6: 1822.
  • 9
    Moretti M, Khoury A, Rodriguez J, Lobe T, Shaver D, Sibai B. The effect of mode of delivery on the perinatal outcome in fetuses with abdominal wall defects. Am J Obstet Gynecol 1990; 163: 833838.
  • 10
    Stringer MD, Brereton RJ, Wright VM. Controversies in the management of gastroschisis: a study of 40 patients. Arch Dis Child 1991; 66: 3436.
  • 11
    Yudkin PL, Aboualfa M, Eyre JA, Redman CW, Wilkinson AR. New birthweight and head circumference centiles for gestational ages 24 to 42 weeks. Early Hum Dev 1987, 15: 4552.
  • 12
    Fries MH, Filly RA, Callen PW, Goldstein RB, Goldberg JD, Golbus MS. Growth retardation in prenatally diagnosed cases of gastroschisis. J Ultrasound Med 1993; 12: 583588.
  • 13
    O'Neill JA, Grosfeld JL. Intestinal malfunction after antenatal exposure of viscera. Am J Surg 1974; 127: 129132.
  • 14
    Blakelock R, Upadhyay V, Kimble R, Pease P, Kolbe A, Harding J. Is a normally functioning gastrointestinal tract necessary for normal growth in late gestation Pediatr Surg Int 1998; 13: 1720.
  • 15
    Morrison JJ, Klein N, Chitty LS et al. Intra-amniotic inflammation in human gastroschisis: possible aetiology of postnatal bowel dysfunction. Br J Obstet Gynaecol 1998; 105: 12001204.
  • 16
    Hoyme HE, Jones MC, Jones KL. Gastroschisis: abdominal wall disruption secondary to early gestational disruption of the omphalomesenteric artery. Semin Perinatol 1983; 7: 294298.
  • 17
    Caniano DA, Brokaw B, Ginn-Pease ME. An individualised approach to the management of gastroschisis. J Pediatr Surg 1990; 25: 297300.