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Small intestinal atresia: Effect on fetal nutrition
Small
Intestinal
Atresia:
Effect on Fetal Nutrition
By R. Surana and P. Puri Dublin, l The peak velocity for fetal weight gain occurs in the last few weeks of pregnancy. As the fetus matures, it swallows and absorbs an increasing amount of amniotic fluid, which contributes to the growth of the fetus. The authors studied cases of small intestinal atresia (IA) treated over g years to determine whether amniotic fluid has any nutritive role in the development of human fetus, and if it does, at what stage of gestation is the contribution of amniotic fluid significant to fetal nutrition. Fifty-nine newborns had IA (24 jejunal, 35 ileal). Ten of the patients had associated anomalies (3 cystic fibrosis, 2 congenital heart disease, 1 neural tube defect, 1 microcephaly, 2 malrotation, 1 vesicoureteric reflux). Among the 24 babies with jejunal atresia, one was a twin, and birth weight was not recorded for another. These two patients were excluded from the study. of the remaining 22 patients with jejunal atresia, 10 were born before 36 weeks’ gestation; only five of 35 patients with ileal atresia were born before 36 weeks’ gestation. Fourteen patients were below the 10th percentile for birth weight after correction for gestational age, one was born before 36 weeks, and 13 were born after 36 weeks. Five (41.7%) of the 12 patients with jejunal atresia who were born after 36 weeks’ gestation were underweight, as were eight (26.7%) of the 30 patients with ileal atresia. Thus, it appears that amniotic fluid contributes to the fetal growth in the last few weeks of gestation, and the higher the obstruction in the small intestine, the more pronounced the effect on the nutrition of the fetus. Copyright o 1994 by WA Saunders Company
Ireland
whether the amniotic fluid has any nutritive significance.4 Recently, Lopez de Torre et al3 examined the effects of experimental prenatal intestinal obstruction on the growth of chick embryos. They showed that, compared with controls, chicks with intestinal atresia were severely undernourished. However, in the late stages of gestation, chicks rely on the amniotic fluid to a greater extent than do humans. We undertook a study in patients with intestinal atresia to address two questions: does the amniotic fluid have any nutritive role in the development of the human fetus, and, if it does, at what stage of gestation is the contribution of amniotic fluid significant to fetal nutrition. MATERIALS
A retrospective review of the records of all patients presenting with small bowel atresia (jejunal and ileal) over a 9-year period (from 1980 to 1988) admitted to Our Lady’s Hospital for Sick Children, Crumlin, and the Children’s Hospital, Dublin, was undertaken. Data were collected regarding sex, gestational age, birth weight, level and type of atresia, and presence of other congenital anomalies. Birth weight was plotted on the percentile charts, according to gestational age and sex. Intrauterine growth retardation (IUGR) was defined as birth weight below the 10th percentile when adjusted for gestational age and sex.5,h
INDEX WORDS: Atresia, jejunal, ileal, intrauterine.
T
HE HUMAN fetus is primarily dependent on the placenta for its nutrition. However, as the fetus matures, it swallows increasing amounts of amniotic fluid-up to 750 mL per day in the last month of gestation.’ At term, amniotic fluid contains 3 g of protein per liter. Thus, 1.5 to 2.25 g of protein passes through the fetal gut every day.’ The proteins involved are not only fetal (lanugo, desquamated cells) but also low molecular weight maternal proteins transferred through the placenta and passed into the amniotic fluid by filtration through fetal kidneys.3 Although the fetal gut is potentially able to carry out its digestive function, there is still doubt as to
From the Children’s Research Centre, Our Lady’s Hospital for Sick Children, Dublin, Ireland. Presented at the 25th Annual Meeting of the Canadian Association of Paediatric Surgeons, Victoria, British Columbia, September 13-15, 1993. Address reprint requests to Prem Puri, FACS, Director of Research. Children’s Research Centre, Our Lady’s Hospital for Sick Children, Crumlin, Dublin 12, Ireland. Copyright o 1994 by W B. Saunders Company 0022-3468/94/2909-0023$03.00/O 1250
AND METHODS
RESULTS
Fifty-nine patients were treated during this period. Twenty-four had jejunal atresia, and 3.5 had ileal atresia. Among the 24 patients with jejunal atresia, one was a twin, and birth weight was not recorded for another. These two patients were excluded from the study. Gestational age and birth weight were available for all other patients. Forty-two patients were born after 36 weeks’ gestation, and 15 were born before 36 weeks. Ten (45%) babies with jejunal atresia were born before 36 weeks’ gestation, as were five (14%) patients with ileal atresia. Fourteen babies’ (25%) birth weights were below the 10th percentile; six were born with jejunal atresia and eight with ileal atresia. Thirteen (31%) of the 42 babies born after 36 weeks and one (7%) of the 15 born before 36 weeks were growth-retarded. Table 1 shows the analysis of growth retardation according to gestational age and level of atresia. Among patients born after 36 weeks, growth retardation occurred in 42% of those with jejunal atresia and 27% of those with ileal atresia. Among the babies born before 36 weeks, 10% of patients with jejunal atresia were growth-retarded, and none with ileal atresia were growth retarded. Associated congenital anomalies were found in 10 Journatoffediatric
Surgery, Vol29, No 9 (September), 1994: pp 1250-1252
1251
FETAL GROWTH IN SMALL INTESTINAL ATRESIA
Table 2. Associated Anomalies
Table 1. Relationship Between Gestational Age, Level of Atresia, and IUGR ~36 Weeks’ Gestation Group
Jejunal lleal Total
IUGR/Total
l/10 o/5 1115
Group
> 36 Weeks’ Gestation
Jejunal atresia
Anomaly
NO.
Congenital heart disease
2 1
%
IUGR/Total
%
Microcephaly
10 0 7
5112 8/30 13142
42 27 31
Neural tube defect
1
Malrotation
2
Cystic fibrosis Total lleal atresia
Vesicoureteric reflux Total
patients; nine had jejunal atresia and one had ileal atresia (Table 2). Only one (11%) of the nine patients who had jejunal atresia and other associated congenital anomalies had IUGR. The patient with ileal atresia who had an associated congenital anomaly did not have growth retardation. DISCUSSION
The peak velocity for fetal weight gain occurs at 33 weeks’ gestation and continues until after birth.5,7-9 The human fetus obtains most of its nutrition from the mother, via the placenta. However, as the fetus matures, it swallows and absorbs increasing amounts of amniotic fluid.lJ” Various experimental studies have shown the nutritional role of amniotic fluid deglutition. Gitlin et al l1 demonstrated that 63% of the radionuclide-tagged exogenous proteins injected into the amniotic fluid in the uterus of pregnant women in the last month of gestation are absorbed, and that a fraction of these are metabolized by the fetus. They showed that 10% to 15% of the daily nitrogen requirements are supplied by this route. Other investigators have shown that carbohydrates are also absorbed by the fetus when administered intragastrically.‘? In animal experiments, ligation of the esophagus and creation of intestinal atresia have been shown to cause undernutrition of the fetus.3J3 Our data support these experimental studies and show that the role of amniotic fluid as a nutritional avenue for the fetus is more pronounced in the last month of pregnancy and results in IUGR if this pathway is interrupted. Other investigators have indicated that there is only slight interference with fetal growth in the presence of conditions such as esophageal atresia with tracheoesophageal fistula, malrotation, and anorectal malformations, in which there is partial obstruction.2 From our study, it appears that
3 9122
1 1I35
the effect of the total interruption of this nutritional avenue is more pronounced if the obstruction is in the jejunum rather than distal to it. Similar findings were reported by Pierro et al. ia However, some patients in their study who had esophageal atresia with fistula may not represent complete interruption of the amniotic IIuid swallowing and absorption. Kimura and Warsha@ speculated that IUGR may be caused by associated anomalies. However, only 11% of the patients who had associated anomalies in the present series were growth-retarded. The findings of the present series and of that reported by Pierro et ali0 do not support this hypothesis. Another significant finding in our study was the high incidence of premature delivery among patients with high atresia. It has been suggested that high intestinal atresia results in impairment of swallowing and/or absorption of amniotic fluid, and in the absence of other pathways for water exchange, leads to hydramnios. ia Mechanical distension of the uterus may precipitate premature delivery.“’ The fetus and neonate with IUGR have a substantially high perinatal mortality rate. The growthretarded infant is subject to increased morbidity in the immediate neonatal period and beyond. Sequelae include peripartum asphyxia and acidosis, hypoglycemia, hypocalcemia, hypothermia, and polycythemia.5 Because interruption of the amniotic fluid pathway results in growth retardation in the last month of pregnancy, the role of early induction of delivery must be evaluated. The results of the present study indicate that absorption of amniotic fluid by the fetal gut contributes to fetal growth in the last month of pregnancy, and that the higher the obstruction, the more pronounced the effect on the nutrition of the fetus.
REFERENCES 1. Pritchard JA: Fetal swallowing and amniotic fluid volume. Obstet Gynecol28:606-610, 1966 2. Jolleys A: An examination of the birth weights of babies with some abnormalities of the alimentary tract. J Pediatr Surg 16:160163,198l 3. Lopez de Torre B, Tovar JA, Uriat S, et al: The nutrition of
the fetus with intestinal atresia: Studies in the chick embryo model. J Pediatr Surg 27:1325-1328, 1992 4. Kimura RE, Warshaw JB: Intrauterine development of gastrointestinal function, in Lebenthal E (ed): Textbook of Gastroenterology and Nutrition in Infancy, New York, NY, Raven, 1981, pp 39-46
1252
5. Lockwood CJ, Weiner S: Assessment of fetal growth. Clin Perinatol 13:3-35, 1986 6. Arias F: The diagnosis and management of intrauterine growth retardation. Obstet Gynecol49:293-298, 1977 7. Streeter G: Weight, sitting height, head size, foot length and menstrual age of the human embryo. Contrib Embryo1 1:143,1920 8. Tanner JM: Fetus Into Man. Boston, MA, Harvard University, 1978, pp 40-42 9. Vorherr H: Factors influencing fetal growth. Am J Obstet Gynecol142:577-58X,1982 10. Pierro A, Cozzi F, Colarossi G, et al: Does fetal gut
SUAANA AND PURI
obstruction cause hydramnios and growth retardation? J Pediatr Surg 22:4.54-457,1987 11. Gitlin 0, Kumate J, Morales C, et al: The turnover of amniotic fluid protein in the human conceptus. Am J Obstet Gynecol113:632-645,1975 12. Charlton Char V, Rudolph AM: Digestion and absorption of carbohydrates by the fetal lamb in the utero. Pediatr Res 13:10181023,1979 13. Wesson N, Muraji T, Kent G, et al: The effect of intrauterine esophageal ligation on growth of fetal rabbits. J Pediatr Surg 19:398-399, 1984
Intestinal
Atresia:
Effect on Fetal Nutrition
By R. Surana and P. Puri Dublin, l The peak velocity for fetal weight gain occurs in the last few weeks of pregnancy. As the fetus matures, it swallows and absorbs an increasing amount of amniotic fluid, which contributes to the growth of the fetus. The authors studied cases of small intestinal atresia (IA) treated over g years to determine whether amniotic fluid has any nutritive role in the development of human fetus, and if it does, at what stage of gestation is the contribution of amniotic fluid significant to fetal nutrition. Fifty-nine newborns had IA (24 jejunal, 35 ileal). Ten of the patients had associated anomalies (3 cystic fibrosis, 2 congenital heart disease, 1 neural tube defect, 1 microcephaly, 2 malrotation, 1 vesicoureteric reflux). Among the 24 babies with jejunal atresia, one was a twin, and birth weight was not recorded for another. These two patients were excluded from the study. of the remaining 22 patients with jejunal atresia, 10 were born before 36 weeks’ gestation; only five of 35 patients with ileal atresia were born before 36 weeks’ gestation. Fourteen patients were below the 10th percentile for birth weight after correction for gestational age, one was born before 36 weeks, and 13 were born after 36 weeks. Five (41.7%) of the 12 patients with jejunal atresia who were born after 36 weeks’ gestation were underweight, as were eight (26.7%) of the 30 patients with ileal atresia. Thus, it appears that amniotic fluid contributes to the fetal growth in the last few weeks of gestation, and the higher the obstruction in the small intestine, the more pronounced the effect on the nutrition of the fetus. Copyright o 1994 by WA Saunders Company
Ireland
whether the amniotic fluid has any nutritive significance.4 Recently, Lopez de Torre et al3 examined the effects of experimental prenatal intestinal obstruction on the growth of chick embryos. They showed that, compared with controls, chicks with intestinal atresia were severely undernourished. However, in the late stages of gestation, chicks rely on the amniotic fluid to a greater extent than do humans. We undertook a study in patients with intestinal atresia to address two questions: does the amniotic fluid have any nutritive role in the development of the human fetus, and, if it does, at what stage of gestation is the contribution of amniotic fluid significant to fetal nutrition. MATERIALS
A retrospective review of the records of all patients presenting with small bowel atresia (jejunal and ileal) over a 9-year period (from 1980 to 1988) admitted to Our Lady’s Hospital for Sick Children, Crumlin, and the Children’s Hospital, Dublin, was undertaken. Data were collected regarding sex, gestational age, birth weight, level and type of atresia, and presence of other congenital anomalies. Birth weight was plotted on the percentile charts, according to gestational age and sex. Intrauterine growth retardation (IUGR) was defined as birth weight below the 10th percentile when adjusted for gestational age and sex.5,h
INDEX WORDS: Atresia, jejunal, ileal, intrauterine.
T
HE HUMAN fetus is primarily dependent on the placenta for its nutrition. However, as the fetus matures, it swallows increasing amounts of amniotic fluid-up to 750 mL per day in the last month of gestation.’ At term, amniotic fluid contains 3 g of protein per liter. Thus, 1.5 to 2.25 g of protein passes through the fetal gut every day.’ The proteins involved are not only fetal (lanugo, desquamated cells) but also low molecular weight maternal proteins transferred through the placenta and passed into the amniotic fluid by filtration through fetal kidneys.3 Although the fetal gut is potentially able to carry out its digestive function, there is still doubt as to
From the Children’s Research Centre, Our Lady’s Hospital for Sick Children, Dublin, Ireland. Presented at the 25th Annual Meeting of the Canadian Association of Paediatric Surgeons, Victoria, British Columbia, September 13-15, 1993. Address reprint requests to Prem Puri, FACS, Director of Research. Children’s Research Centre, Our Lady’s Hospital for Sick Children, Crumlin, Dublin 12, Ireland. Copyright o 1994 by W B. Saunders Company 0022-3468/94/2909-0023$03.00/O 1250
AND METHODS
RESULTS
Fifty-nine patients were treated during this period. Twenty-four had jejunal atresia, and 3.5 had ileal atresia. Among the 24 patients with jejunal atresia, one was a twin, and birth weight was not recorded for another. These two patients were excluded from the study. Gestational age and birth weight were available for all other patients. Forty-two patients were born after 36 weeks’ gestation, and 15 were born before 36 weeks. Ten (45%) babies with jejunal atresia were born before 36 weeks’ gestation, as were five (14%) patients with ileal atresia. Fourteen babies’ (25%) birth weights were below the 10th percentile; six were born with jejunal atresia and eight with ileal atresia. Thirteen (31%) of the 42 babies born after 36 weeks and one (7%) of the 15 born before 36 weeks were growth-retarded. Table 1 shows the analysis of growth retardation according to gestational age and level of atresia. Among patients born after 36 weeks, growth retardation occurred in 42% of those with jejunal atresia and 27% of those with ileal atresia. Among the babies born before 36 weeks, 10% of patients with jejunal atresia were growth-retarded, and none with ileal atresia were growth retarded. Associated congenital anomalies were found in 10 Journatoffediatric
Surgery, Vol29, No 9 (September), 1994: pp 1250-1252
1251
FETAL GROWTH IN SMALL INTESTINAL ATRESIA
Table 2. Associated Anomalies
Table 1. Relationship Between Gestational Age, Level of Atresia, and IUGR ~36 Weeks’ Gestation Group
Jejunal lleal Total
IUGR/Total
l/10 o/5 1115
Group
> 36 Weeks’ Gestation
Jejunal atresia
Anomaly
NO.
Congenital heart disease
2 1
%
IUGR/Total
%
Microcephaly
10 0 7
5112 8/30 13142
42 27 31
Neural tube defect
1
Malrotation
2
Cystic fibrosis Total lleal atresia
Vesicoureteric reflux Total
patients; nine had jejunal atresia and one had ileal atresia (Table 2). Only one (11%) of the nine patients who had jejunal atresia and other associated congenital anomalies had IUGR. The patient with ileal atresia who had an associated congenital anomaly did not have growth retardation. DISCUSSION
The peak velocity for fetal weight gain occurs at 33 weeks’ gestation and continues until after birth.5,7-9 The human fetus obtains most of its nutrition from the mother, via the placenta. However, as the fetus matures, it swallows and absorbs increasing amounts of amniotic fluid.lJ” Various experimental studies have shown the nutritional role of amniotic fluid deglutition. Gitlin et al l1 demonstrated that 63% of the radionuclide-tagged exogenous proteins injected into the amniotic fluid in the uterus of pregnant women in the last month of gestation are absorbed, and that a fraction of these are metabolized by the fetus. They showed that 10% to 15% of the daily nitrogen requirements are supplied by this route. Other investigators have shown that carbohydrates are also absorbed by the fetus when administered intragastrically.‘? In animal experiments, ligation of the esophagus and creation of intestinal atresia have been shown to cause undernutrition of the fetus.3J3 Our data support these experimental studies and show that the role of amniotic fluid as a nutritional avenue for the fetus is more pronounced in the last month of pregnancy and results in IUGR if this pathway is interrupted. Other investigators have indicated that there is only slight interference with fetal growth in the presence of conditions such as esophageal atresia with tracheoesophageal fistula, malrotation, and anorectal malformations, in which there is partial obstruction.2 From our study, it appears that
3 9122
1 1I35
the effect of the total interruption of this nutritional avenue is more pronounced if the obstruction is in the jejunum rather than distal to it. Similar findings were reported by Pierro et al. ia However, some patients in their study who had esophageal atresia with fistula may not represent complete interruption of the amniotic IIuid swallowing and absorption. Kimura and Warsha@ speculated that IUGR may be caused by associated anomalies. However, only 11% of the patients who had associated anomalies in the present series were growth-retarded. The findings of the present series and of that reported by Pierro et ali0 do not support this hypothesis. Another significant finding in our study was the high incidence of premature delivery among patients with high atresia. It has been suggested that high intestinal atresia results in impairment of swallowing and/or absorption of amniotic fluid, and in the absence of other pathways for water exchange, leads to hydramnios. ia Mechanical distension of the uterus may precipitate premature delivery.“’ The fetus and neonate with IUGR have a substantially high perinatal mortality rate. The growthretarded infant is subject to increased morbidity in the immediate neonatal period and beyond. Sequelae include peripartum asphyxia and acidosis, hypoglycemia, hypocalcemia, hypothermia, and polycythemia.5 Because interruption of the amniotic fluid pathway results in growth retardation in the last month of pregnancy, the role of early induction of delivery must be evaluated. The results of the present study indicate that absorption of amniotic fluid by the fetal gut contributes to fetal growth in the last month of pregnancy, and that the higher the obstruction, the more pronounced the effect on the nutrition of the fetus.
REFERENCES 1. Pritchard JA: Fetal swallowing and amniotic fluid volume. Obstet Gynecol28:606-610, 1966 2. Jolleys A: An examination of the birth weights of babies with some abnormalities of the alimentary tract. J Pediatr Surg 16:160163,198l 3. Lopez de Torre B, Tovar JA, Uriat S, et al: The nutrition of
the fetus with intestinal atresia: Studies in the chick embryo model. J Pediatr Surg 27:1325-1328, 1992 4. Kimura RE, Warshaw JB: Intrauterine development of gastrointestinal function, in Lebenthal E (ed): Textbook of Gastroenterology and Nutrition in Infancy, New York, NY, Raven, 1981, pp 39-46
1252
5. Lockwood CJ, Weiner S: Assessment of fetal growth. Clin Perinatol 13:3-35, 1986 6. Arias F: The diagnosis and management of intrauterine growth retardation. Obstet Gynecol49:293-298, 1977 7. Streeter G: Weight, sitting height, head size, foot length and menstrual age of the human embryo. Contrib Embryo1 1:143,1920 8. Tanner JM: Fetus Into Man. Boston, MA, Harvard University, 1978, pp 40-42 9. Vorherr H: Factors influencing fetal growth. Am J Obstet Gynecol142:577-58X,1982 10. Pierro A, Cozzi F, Colarossi G, et al: Does fetal gut
SUAANA AND PURI
obstruction cause hydramnios and growth retardation? J Pediatr Surg 22:4.54-457,1987 11. Gitlin 0, Kumate J, Morales C, et al: The turnover of amniotic fluid protein in the human conceptus. Am J Obstet Gynecol113:632-645,1975 12. Charlton Char V, Rudolph AM: Digestion and absorption of carbohydrates by the fetal lamb in the utero. Pediatr Res 13:10181023,1979 13. Wesson N, Muraji T, Kent G, et al: The effect of intrauterine esophageal ligation on growth of fetal rabbits. J Pediatr Surg 19:398-399, 1984