Gastroschisis is a congenital abdominal wall defect that is characterized by a full-thickness defect to the right of the umbilical cord. The defect is present as early as the 6th week of gestation. There are several theories in regard to what causes gastroschisis.

Duhamel (1963) suggested a discrete teratogenic insult to the somatopleural mesenchyme resulting in an isolated defect in differentiation. Another theory is that the physiologic hernia of the cord ruptures in utero, before closure of the umbilical ring (Shaw, 1975 and Glick et al. 1985). Others have suggested that in-utero regression of the right umbilical vein leaves a weakness on right side of the abdominal cord insertion, or that there is a disruption of the right omphalomesenteric artery again leading to a weakness predisposing to what we clinically recognize as gastroschisis (Hoyme et al., 1983 and Torfs et al., 1990).

At birth, in patients with gastroschisis, the bowel may have an abnormal appearance which is referred to as an intestinal “peel”. The peel is a layer of fibrin and collagen on the serosal surface of the bowel, which likely is caused by the combination of inflammatory reaction to constituents in the amniotic fluid and constriction of the bowel as it herniates through the abdominal wall defect. In addition, the bowel in fetuses with gastroschisis is often foreshortened (Amoury et al., 1977; Klein et al., 1983; Tibboel et al., 1986 a, b; Amoury et al., 1988; Langer et al., 1990, Moore, 1992).

Most cases of gastroschisis are detected prenatally. Ultrasound will often detect an abdominal wall defect at the time of the “dating” ultrasound, which is usually done around 20 weeks of gestation. Occasionally the abdominal wall defect is seen before 20 weeks gestation, if an ultrasound is obtained late in the first trimester. In the second trimester, maternal serum alpha-fetoprotein (MSAFP) screening will be elevated in most mothers pregnant with a fetus with gastroschisis, but the test is not specific for gastroschisis. MSAFP is also elevated in twin pregnancies as well as in fetuses with neural tube defects, omphalocele, and in autosomal chromosomal anomalies.

Would you like to schedule an appointment with our Fetal Care Center?

For Medical Professionals

The incidence of gastroschisis is 4.7 per 10,000 live births (Mowrer 2022). The number of babies born with gastroschisis has increased over the last 2 decades, but the incidence has abruptly decreased during the pandemic. The reason for the increase is not known. Epidemiologic data have shown that young maternal age is associated with an increased risk of gastroschisis.

Goldbaum et al (1990) studied infants with gastroschisis in the state of Washington and found a 4-fold increased risk in mothers less than 20 years of age. Cigarette smoking has been associated with gastroschisis (Haddow et al., 1993). Medications and recreational drugs that can cause vascular constriction have been linked to an increased risk of gastroschisis (Van Allen, 1981; Colorado et al., 1997; Plessinger, 1998)

It is difficult to diagnose gastroschisis in the first trimester because of the normal herniation of the intestine into the umbilical cord (Cyr et al., 1986). The intestine reduces back into the abdominal cavity by 11 weeks gestation; therefore, it is difficult to differentiate between a physiologic and a pathologic sonographic finding. The earliest reported diagnosis of gastroschisis is 13 weeks 3 days gestation (Guzman, 1990).

Ultrasound findings typically demonstrate a full-thickness abdominal wall defect, almost always, to the right of the umbilical cord. There is a bowel floating freely in the amniotic fluid without a limiting membrane, which is seen in the omphalocele. In omphalocele, the bowel is contained within the omphalocele sac, which is comprised of the parietal peritoneum and the amnion with a layer of hyaluronic acid in between. Omphalocele can be confused with gastroschisis if the omphalocele sac ruptures, which is a relatively rare event.

The prenatal detection rate for gastroschisis is over 80% (Barisic et al., 2001). Gastroschisis and omphalocele were shown to be accurately distinguished in 79.3% of cases on initial diagnosis and in 84.5% of cases after referral for further evaluation (Walkinshaw et al., 1992).

A ruptured hernia of the umbilical cord can present late as gastroschisis. In these cases, the gastroschisis may develop later in pregnancy and may not be present on ultrasound early in pregnancy (Knott and Colley, 1987).

The differential diagnosis of gastroschisis should include omphalocele, ruptured omphalocele, hernia of the cord, and limb-body wall complex. Omphalocele and gastroschisis are differentiated by the presence of a sac in omphalocele with cord insertion on the sac. In gastroschisis, the umbilical cord inserts into the abdominal wall with the abdominal wall defect immediately to the right of its insertion. In gastroschisis, there is no sac and the intestine floats freely in the amniotic cavity. In addition, the abdominal wall defect is small, usually less than 4 cm in diameter, even at term.

In contrast, the abdominal wall defect in omphalocele is quite large often with herniated liver and stomach, which is typically not the case with gastroschisis. A ruptured omphalocele may be mistaken for gastroschisis, however, if the abdominal wall defect is sufficiently large that it allows the liver to herniate through the abdominal wall defect, the diagnosis is more likely to be omphalocele and not gastroschisis. A ruptured hernia of the cord will present later in pregnancy and may be impossible to differentiate from gastroschisis unless a prior ultrasound shows a hernia of the cord without an abdominal wall defect.

Limb body wall complex is characterized by very severe limb defects and anterior wall defects, these can be of the head, chest, or abdomen, and are usually not in the midline. These fetuses also have spinal abnormalities, which together are rarely mistaken for gastroschisis.

Chromosomal anomalies are rare in gastroschisis (Mayer et al., 1980; Mann and Ferguson-Smith, 1984; Sermer et al., 1987; Romero et al., 1988; Lewinsky et al., 1990; Sipes et al., 1990). Only in cases where sonographic abnormalities in addition to gastrointestinal abnormalities are seen, is chromosomal evaluation recommended.

In a study of 24 international birth defects registries including over 3300 cases of gastroschisis, 10% were found to have associated major unrelated defects, with 2% part of a recognized syndromes and cardiac abnormalities detected in 2-3% (Mastroiacovo 2007). A report from the Texas Birth Defects Registry found up to a third of cases of gastroschisis had associated anomalies (Benjamin 2014). However, in a prospectively collected database of 4700 infants with gastroschisis discharged from 348 neonatal intensive care units in North America found associated anomalies in only 8% of cases and cardiac defects in 1% (Corey 2014).

Postnatally, gastroschisis is classified into one of two categories: simple and complex. In patients with complex gastroschisis, there may be a concomitant atresia, perforation, volvulus, stenosis, and necrosis. Between 10 and 25% of cases of gastroschisis will be complex. The focus of prenatal diagnosis has been on trying to distinguish simple from complex gastroschisis in order to better understand the prenatal natural history of gastroschisis that might influence the rate of intrauterine fetal demise, fetal distress, and prematurity.

Additionally, understanding which fetuses are at risk of having complex gastroschisis will allow us to better guide prenatal management. Simple gastroschisis has a survival of over 98% and low morbidity rates (Bradnoch et al 2011, Gamba et al 2014), but complex gastroschisis is associated with survival rates of 70 to 80% with prolonged hospital stay and higher long-term morbidity rates with feeding difficulties and need for parenteral nutrition (Bradnoch et al 2011, Cowan et al 2012).

In utero bowel dilatation is one of the most commonly noted abnormalities on fetal ultrasound. Its significance for the outcome has not been established. A large study from Canada including 100 patients diagnosed prenatally with gastroschisis did not find that prenatal bowel dilatation over 18 mm was associated with a worse outcome (Skarsgaard et al., 2007). Piper and Jaksic (2006) reviewed the experience at Boston Children’s Hospital and found no difference in length of stay, time on TPN, mortality, or time in the NICU for babies who had bowel dilatation over 6 mm prenatally.

Bowel dilatation and bowel thickening may indicate bowel damage, but the existing data does not provide evidence for changing the delivery time or mode if these features are present on ultrasound. A more recent meta-analysis of 2023 fetuses with gastroschisis found a positive association between intra-abdominal bowel dilation, polyhydramnios, and bowel atresia. In addition, prenatal gastric dilation was found to be associated with an increased risk of neonatal death (D’Antonio et al 2018).

Intrauterine growth retardation (IUGR) is common and may affect as many as 77% of babies (Carpenter et al., 1984; Molenaar and Tibboel, 1993). A study by Royner and Richards (1977) found a large difference between predicted IUGR (43%) and actual IUGR at birth (23%). The weight of the fetus is often underestimated because the abdominal circumference is taken into account. In babies with gastroschisis, the abdominal circumference is small because most of the bowel is outside the abdomen.

A few studies (Crawford et al.,1992; Burge and Ade-Ajayi, 1997) have reported an up to 10% rate of stillbirth in the third trimester in babies with gastroschisis. This is now thought to be an overestimate of the rate of intrauterine fetal demise in gastroschisis. The cause of death is thought to be mid-gut volvulus or cord compression. More recently, the CAPSNET data from Canada reported a fetal loss rate of only 1.4% among 700 cases of gastroschisis (

Premature birth is common in pregnancies with gastroschisis. At least one-third of babies are born prematurely, and possibly the most important reason for premature labor is polyhydramnios (Mayer et al., 1980; Kirk and Wah, 1983; Carpenter et al., 1984; Caplan and McGregor, 1989; Molenaar and Tibboel, 1993). Also, oligohydramnios is seen in gastroschisis (Bair et al., 1986; Crawford et al., 1992). Mercer et al. (1988) reported amniotic fluid staining in 73% of their series of 22 babies with gastroschisis. The significance of this is unclear, but it may indicate fetal distress.

There are several considerations in the management of pregnancies with gastroschisis including imaging guidelines, methods of monitoring, and timing of delivery. A recent national survey of maternal-fetal specialists suggests that the common management strategy includes close surveillance in conjunction with weekly nonstress tests, biophysical profile, and amniotic fluid levels starting at 32 weeks gestation (Amin R, et al 2019).

Additional ultrasound findings that are assessed include the development of in-utero growth restriction, polyhydramnios, oligohydramnios, gastric distention, and intra-abdominal bowel dilation that can be indicative of higher postnatal complications. For example, intra-abdominal bowel dilation, gastric distention, and polyhydramnios have been shown to be associated with a higher incidence of neonatal death (D’Antonio, et al 2015).

Gastroschisis is not an indication for cesarean section (C-section) as outcomes are similar for babies delivered via vaginal birth (Boutros et al., 2009). In the absence of routine maternal and fetal indications for C-sections, vaginal delivery has been demonstrated to be safe and is recommended for patients with gastroschisis. In patients with gastroschisis, the risk of fetal demise is greater, suggesting that proceeding with an elective early delivery may mitigate this risk (Sparks TN, et al. 2017). However, several studies have explored this and studies have demonstrated that delivery at less than 35 weeks gestation is associated with worse outcomes (Shamshirsaz AA, et al 2020; Overcash RT, et al; Landisch RM, et al 2017).

The optimal timing of delivery is something that is debated and is presently under investigation in a multicenter, prospective, randomized control trial (Gastroschisis Outcome of Delivery Study, Identifier: NCT02774746). Patients are randomized to delivery at either 35 weeks or 38 weeks gestation, and in this study outcomes being evaluated include rates of stillbirth, neonatal death, and overall morbidity. If fetal growth, amniotic fluid volume, and antenatal testing are normal, the risk of intrauterine fetal demise is minimal, and delivery prior to 37 weeks is generally not recommended. It is important to note, however, that fetuses that meet these criteria are in the minority.

In general, at the Fetal Care Center at Connecticut Children’s, we schedule patients for induction of labor at 37 weeks if they haven’t already delivered.

There are currently no fetal treatment options that will improve outcomes in gastroschisis. Amnioexchange has been proposed as a possible fetal treatment for gastroschisis. The rationale is that there are two mechanisms that cause bowel damage: constriction of the abdominal wall defect with resultant hypo-perfusion of the bowel and various irritants in the amniotic fluid (Langer et al., 1989, 1990). In France, Luton et al. (2003) performed a trial of amnio exchange, but there was no significant improvement in outcomes with this intervention.

After the delivery of the patient with gastroschisis, the major concerns are fluid loss and hypothermia due to the exposed viscera. Therefore, immediately after delivery, the newborn with gastroschisis is placed in a plastic “bowel” bag. This is done to reduce evaporative fluid and heat losses and to help keep the baby warm. The baby should be placed on the right side and the bowel should be supported to prevent kinking of the mesenteric vessels at the abdominal wall defect.

An orogastric or nasogastric tube is placed into the stomach for gastric decompression. Intravenous (IV) access is important and necessary immediately after birth for the administration of crystalloid intravenous fluids and antibiotics. Newborn babies with gastroschisis have large ongoing fluid losses and will often need in excess of 10-30 ml/kg in IV fluid boluses.

Soon after birth, the pediatric surgeon will assess the bowel for any abnormalities and decide on the next steps in the surgical treatment.

There are two primary methods to closing the abdominal wall defect in gastroschisis. The surgeon’s preference, degree of viscero-abdominal disproportion, the appearance of the bowel, and how the newborn is doing clinically are some of the factors that will guide the surgical treatment. Additionally, depending on patient characteristics, the abdominal defect may be closed immediately or delayed and either the sutured or sutureless closure may be employed. It is important to note that studies have not demonstrated any differences in outcomes in patients who have undergone sutureless closure versus silo placement and closure within 5 days (Hawkins, RB et al 2020). Therefore, several factors are taken into consideration to guide the optimal closure strategy for each patient with gastroschisis.

1. Sutureless Closure

Primary closure can be achieved in a significant percentage of patients with gastroschisis. It is important that the baby is doing well and is not significantly premature and that the bowel is not very dilated and there is minimal viscero-abdominal disproportion to be able to close the defect primarily.

This can be accomplished at the bedside, without intubation, general anesthesia and with minimal sedation (Bianchi et al 1998) using the umbilical cord as a flap in a suture-less closure after reduction of herniated bowel (Sandler et al 2004). This technique also requires a clinically well neonate and that the bowel is not very dilated, the difference is that the bowel is reduced and the defect covered with the umbilical stump and a Duoderm dressing.

The sutureless closure avoids an operation around the time of birth, but it may increase the risk for an umbilical hernia which will require surgical closure later in life. Studies have also found decreased use of general anesthesia, antibiotics, time on the ventilator, and surgical site infections in patients who underwent sutureless closure (Fraser JD, et al 2020).

2. Silo Placement

If reduction of the bowel with primary flap closure is not possible without causing respiratory compromise due to pressure on the diaphragm, then placement of a preformed silo can be performed at the bedside. This will allow for the bowel to be elevated, which facilitates the resolution of bowel wall edema and allows the reduction of the loops into the abdominal cavity over time.

This reduction can be encouraged by manual reduction of the loops of bowel tying umbilical tape around the silo to prevent re-herniation. This reduction can be repeated daily or twice daily as needed until all the bowel is reduced. The abdominal wall defect can then be either closed operatively (i.e., with sutures) or an umbilical cord flap can be used (i.e., delayed suturess closure).

The most common approach and the safest approach for babies who are in distress, significantly premature, those who have dilated bowel, or in patients with complex gastroschisis is to place the bowel in a preformed silo bag and then sequentially reduce it. When all of the bowel has been reduced into the abdominal cavity, the fascia is closed with sutures or a sutureless closure can be used.

In patients with complex gastroschisis who are known to have an associated bowel atresia, the primary goal in gastroschisis is the closure of the abdominal wall defect. Any attempt at resection of the bowel atresia at the time of delivery should be avoided as the bowel wall is edematous and inflamed and resection and primary anastomosis will result in anastomotic leak and sepsis. Once the bowel has been reduced into the abdomen the inflammatory peel begins to regress, and definitive surgery is considered where the atresia can be safely addressed and a primary anastomosis safely performed.

Lastly, either a peripherally inserted central venous catheter (PICC) is placed in the NICU prior to surgery or a tunneled central venous catheter (Broviac) is placed by the surgeon. The central line is critical for the newborn with gastroschisis, as it allows for the administration of IV nutrition and medications.

Postnatally, the most common problem affecting babies with gastroschisis is intestinal dysmotility and inability to absorb nutrients. In the first few weeks of life, all babies with gastroschisis will require total parenteral nutrition (TPN) as they slowly adjust to enteral feeds. During this time a nasogastric (or orogastric) tube will drain the secretions from the stomach until the baby has bowel function.

The mean time to first enteral feed was 16 days in a Canadian study (Boutros et al., 2009) and the median time to full enteral feeds in babies with simple gastroschisis was 24 days (Bradnock et al., 2011). In patients with complex gastroschisis, the time to full enteral feeds was 81 days in a cohort study from England and Ireland (Bradnock et al., 2011). More contemporary studies where there has been an attempt to standardize feeding protocols have demonstrated that early closure of the gastroschisis defect is associated with earlier feed initiation and decreased time to when patients reach enteral autonomy (first feed on average was initiated in 17 days and enteral autonomy was reached in 25 days) (Harris J, et al 2015).

Additionally, feeding advancement strategies are also actively being investigated in order to safely shorten the time to when patients reach enteral autonomy (Utria AF, et al 2022).

Rates of patients with complex gastroschisis are variable. Bradnock et al. (2011) identified 11% with atresia, necrosis or bowel perforation in their cohort study and Emil et al. (2011) identified 23% with complex gastroschisis in a smaller cohort. Boutros et al., found that 22% of the patients in the Canadian study required multiple operations, likely related to complex gastroschisis. This group of patients with gastroschisis has a significantly longer NICU stay, ranging from 84 days (Bradnock et al., 2011) to 104 days (Emil et al., 2011), and will more likely develop short bowel syndrome and be at risk for TPN-induced liver failure. These studies highlight that there is a subset of patients with gastroschisis who are at risk of higher complication rates, need for reoperation, and have a longer length of stay.

Intestinal failure may result from gastroschisis. It can either be secondary to short bowel syndrome as a result of loss of bowel length, or it can be a result of severe dysmotility and chronic intestinal pseudo-obstruction. Both conditions will require long-term TPN dependency, which can result in liver failure, and sepsis and may require bowel and liver transplantation. Fortunately, it is rare that patients born with gastroschisis end up needing bowel and liver transplantation.

Pneumatosis intestinalis is seen in up to 10% of infants with gastroschisis. Pneumatosis is a sign of necrotizing enterocolitis (NEC) in newborn babies, but in gastroschisis medical NEC is more common than surgical NEC which requires laparotomy to address perforation or medically refractory systemic illness. Medical NEC is managed with bowel rest and IV antibiotics for 7-10 days until pneumatosis resolves.

Cryptorchidism is common in baby boys with gastroschisis, about a third of baby boys with gastroschisis will have cryptorchidism at birth and a third of these babies will need to undergo orchidopexy (Hill and Durham, 2011). Hernias, both inguinal and incisional are common in infants with gastroschisis which may not present for several months after discharge from the NICU.

Infants born with gastroschisis are often small typically < 5% of body weight at delivery and their small size tends to persist through the end of the first year of life. Linear growth failure is common in patients with gastroschisis and requires ongoing monitoring after discharge from the hospital (Strobel KM, et al 2021). Most children will begin catching up in somatic growth after their first year of life.

The duration of hospitalization is directly related to the degree of gastrointestinal compromise or presence of gastrointestinal atresia. Approximately 10% of patients with gastroschisis will have hypoperistalsis syndrome. These infants remain dependent on parenteral nutrition for an indefinite period, sometimes permanently.

The average hospital stay following the primary closure of gastroschisis is usually on the order of 7 to 14 days. Often feeding difficulties after repair of gastroschisis will delay discharge because of the need for gavage feedings. Although primary closure may be achieved and infants are weaned from mechanical ventilatory support, they often remain quite tachypneic, which impairs their ability to suckle. Once further abdominal wall relaxation and accommodation have had time to occur, there is less tension and pressure on the diaphragm and the respiratory rate decreases. Once a respiratory rate of less than 60 breaths per minute is achieved, infants can suckle effectively and be weaned from supplemental gavage feeding.

Hospitalization for infants with gastroschisis requiring staged closure is much longer, related to the need for gradual reduction, greater visceroperitoneal disproportion, and a second procedure to achieve fascial closure. The hospitalization in these infants may be prolonged by several weeks.

Inguinal hernias will develop in most infants with gastroschisis because of increased intraabdominal pressure. Occasionally, incisional hernias seen as bulging from attenuated fascia at the closure site will require remedial surgery months or years later. There are no long-term sequelae from gastroschisis if there is no associated hypoperistalsis syndrome.

Gastroschisis has been generally considered a sporadic event, with a multifactorial cause, but there have been reports of familial recurrence (Hershey et al. 1989; Lowry and Baird 1982; Salinar et al. 1979). Torfs et al. (1991) described a 4.3% sibling recurrence rate in a population-based study. A 4.3% recurrence risk implies a mixture of genetic predisposition with environmental factors. In one study, Torfs and Curry (1993) found only 6 published reports of familial occurrence of gastroschisis.

Therefore, a single-gene defect is unlikely for this condition. Families should receive genetic counseling regarding recurrence risk and they should be offered MSAFP testing and prenatal sonography in future pregnancies.

Abdel-Latif ME, Bolisetty S, Abeywardana S, Lui K; Australian and New Zealand Neonatal Network. Mode of delivery and neonatal survival of infants with gastroschisis in Australia and New Zealand. J Pediatr Surg. 2008 Sep;43(9):1685-90. doi: 10.1016/j.jpedsurg.2008.03.053. PMID: 18779007.

Amin R, Domack A, Bartoletti J, Peterson E, Rink B, Bruggink J, Christensen M, Johnson A, Polzin W, Wagner AJ. National Practice Patterns for Prenatal Monitoring in Gastroschisis: Gastroschisis Outcomes of Delivery (GOOD) Provider Survey. Fetal Diagn Ther. 2019;45(2):125-130. doi: 10.1159/000487541. Epub 2018 May 23. PMID: 29791899.

Amoury RA, Beatty EC, Wood WI, et al. Histology of the intestine in human gastroschisis relationship to intestinal malfunction: dissolution of the “peel” and its ultrastructural characteristics. J Pediatr Surg 1988;23:950–956.

Amoury RA, Holder TM. Gastroschisis complicated by intestinal atresia. Surgery 1977;82:373–381.

Bair JH, Russ PD, Pretorius DH. Fetal omphalocele and gastroschisis: a review of 24 cases. Am J Radiol 1986;147: 1047–1051.

Baird PA, MacDonald EC. An epidemiologic study of congenital malformations of the anterior abdominal wall in more than half a million consecutive live births. Am J Hum Genet 1981;33:470–478.

Barisic I, Clementi M, Häusler M, et al. Evaluation of prenatal ultrasound diagnosis of fetal abdominal wall defects by 19 European registries. Ultrasound Obstet Gynecol 2001; 18:309.

Benjamin B, Wilson GN. Anomalies associated with gastroschisis and omphalocele: analysis of 2825 cases from the Texas Birth Defects Registry. J Pediatr Surg 2014; 49:514.

Bianchi A, Dickson AP: Elective delayed reduction and no anesthesia: “minimal intervention management” for gastroschisis. J Pediatr Surg 1998; 33: 1338-1340

Bond SJ, Harrison MR, Filly RA, et al. Severity of intestinal damage in gastroschisis: correlation with prenatal sonographic findings. J Pediatr Surg 1988;23:520–525.

Baud D, Lausman A, Alfaraj MA, et al. Expectant management compared with elective delivery at 37 weeks for gastroschisis. Obstet Gynecol 2013; 121:990

Boutros 2009

Bowerman R, Aulla N, Ginsberg H. High resolution sonographic identification of fetal midgut herniation into the umbilical cord: differentiation from fetal anterior abdominal wall defects. J Ultrasound in Med 1988;109(suppl):7.

Bradnock TJ, Marven S, Owen A et al: BAPS-CASS. Gastroschisis: one year outcomes from national cohort study. BMJ 2011; 343; d6749

Brock DJ, Barron L, Duncan P, et al. Significance of elevated mid-trimester maternal plasma AFP values. Lancet 1979;1:1281.

Bryant MS, Tepas JJ, Mollitt DL, et al. The effect of initial operative repair on the recovery of intestinal function in gastroschisis. Am Surg 1985;55:210

Burge DM, Ade-Ajayi N. Adverse outcome after prenatal diagnosis of gastroschisis: the role of fetal monitoring. J Pediatr Surg 1997; 32:441.

Calzolari E, Volpato S, Bianchi F, et al. Omphalocele and gastroschisis: a collaborative study of five Italian congenital malformation registries. Teratology 1993;47:47–55.

Caniano DA, Brokaw B, Ginn-Pease ME. An individualized approach to the management of gastroschisis. J Pediatr Surg 1990;25:287–300.

Caplan MS, MacGregor SN. Perinatal management of congenital diaphragmatic hernia and anterior abdominal wall defects. Clin Perinatol 1989;16:917.

Carlan SJ, Knuppel RA, Perez J, et al. Antenatal fetal diagnosis and maternal transport gastroschisis. Clin Pediatr 1990;29:378.

Carpenter MW, Curci MR, Dibbins AW, et al. Perinatal management of ventral wall defects. Obstet Gynecol 1984;64: 646.

Colombani PM, Cunningham MD. Perinatal aspects of omphalocele and gastroschisis. Am J Dis Child 1977;131:1386.

Colado ML, O’Shea E, Granados R, et al: A study of the neurotoxic effect of MDMA (‘ecstasy’) on 5-HT neurones in the brains of mothers and neonates following administration of the drug during pregnancy. Br J Pharmacol 1997;121:827–833

Corey KM, Hornik CP, Laughon MM, et al. Frequency of anomalies and hospital outcomes in infants with gastroschisis and omphalocele. Early Hum Dev 2014; 90:421.

Coughlin JP, Drucker DE, Jewell MR et al. Delivery room repair of gastroschisis. Surgery 1993;114:822–827.

Cowan KN, Puligandla PS, Laberge JM et al: Canadian Pediatric Surgical Network. The gastroschisis prognostic score: reliable outcome prediction in gastroschisis. 2012; 47(6) 1111-1117

Crandall BF, Robinson L, Grau P. Risks associated with an elevated maternal serum alpha-fetoprotein level. Am J Obstet Gynecol 1991;165:581–586.

Crawford RAF, Ryan G, Wright VM, et al. The importance of serial biophysical assessment of fetal well being in gastroschisis. Br J Obstet Gynaecol 1992;99:899–902.

Cyr DR, Mack LA, Schoenecker SA, et al. Bowel migration in the normal fetus: US detection. Radiology 1986;161: 119–121.

D’Antonio F, Virgone C, Rizzo G, Khalil A, Baud D, Cohen-Overbeek TE, Kuleva M, Salomon LJ, Flacco ME, Manzoli L, Giuliani S. Prenatal Risk Factors and Outcomes in Gastroschisis: A Meta-Analysis. Pediatrics. 2015 Jul;136(1):e159-69. doi: 10.1542/peds.2015-0017. PMID: 26122809.

DeLorenzo M, Yazbeck S, Ducharme JC. Gastroschisis: a 15-year experience. J Pediatr Surg 1987;22:710–712.

deVries PA. The pathogenesis of gastroschisis and omphalocele. J Pediatr Surg 1980;15:245.

Duhamel B. Embryology of exomphalos and allied malformations. Arch Dis Child 1963;38:142.

Egenaes J, Bjerkedal T. Forekomst av gastroschisis og omfalocele i Norge 1967–1979. Tidsskr Nor Laegeforen 1982;102:172–176.

Ein SH, Rubin SZ. Gastroschisis: primary closure or silo pouch. J Pediatr Surg 1980;15:549.

Ein SH, Superina R, Bagwell C, et al. Ischemic bowel after primary closure for gastroschisis. J Pediatr Surg 1988;23: 728–730.

Emil S, Canvasser N, Chen T et al: Contemporary 2-year outcomes of complex gastroschisis. J Pediatr Surg 2012 47(8): 1521-1528

Ewigman BG, Crane JP, RADIUS Study Group. Effect of prenatal ultrasound screening on perinatal outcome. N Engl J Med 1993;329:821–827.

Fonkalsrud EW. Selective repair of neonatal gastroschisis based on degree of visceroabdominal disproportion. Surgery 1980;139:138.

Fraser JD, Deans KJ, Fallat ME, Helmrath MA, Kabre R, Leys CM, Burns RC, Corkum K, Dillon PA, Downard CD, Gadepalli SK, Grabowski JE, Hernandez E, Hirschl RB, Johnson KN, Kohler JE, Landman MP, Landisch RM, Lawrence AE, Mak GZ, Minneci PC, Rymeski B, Sato TT, Scannell M, Slater BJ, Wilkinson KH, Wright TN, St Peter SD; Midwest Pediatric Surgery Consortium. Sutureless vs sutured abdominal wall closure for gastroschisis: Operative characteristics and early outcomes from the Midwest Pediatric Surgery Consortium. J Pediatr Surg. 2020 Nov;55(11):2284-2288. doi: 10.1016/j.jpedsurg.2020.02.017. Epub 2020 Feb 20. PMID: 32151403.

Gamba P, Midrio P:Abdominal wall defects: prenatal diagnosis, newborn management and long-term outcomes. Semin Pediatr Surg 2014;23(5) 283-290

Glick PL, Harrison MR, Adzick NS, et al. The missing link in the pathogenesis of gastroschisis. Pediatr Surg 1985;20: 406–409.

Goldbaum G, Daling J, Milham S. Risk factors for gastroschisis. Teratology 1990;42:397–403.

Goldfine C, Haddow JE, Knight GJ, et al. Amniotic fluid alpha-fetoprotein and acetylcholinesterase measurements in pregnancies associated with gastroschisis. Prenat Diag 1989;8:697–700.

Gornall P. Management of intestinal atresia complicating gastroschisis. J Pediatr Surg 1989;24:522–525.

Green JJ, Hobbins JC. Abdominal ultrasound examination of the first-trimester fetus. Am J Obstet Gynecol 1988;159: 165–175.

Gutenberger JE, Miller DL, Dibbins AW, et al. Hypogammaglobulinemia and hypoalbuminemia in neonates with ruptured omphaloceles and gastroschisis. J Pediatr Surg 1973;8:353–359.

Guzman ER. Early prenatal diagnosis of gastroschisis with transvaginal ultrasonography. Am J Obstet Gynecol 1990;162:1253–1254.

Haddow JE, Palomaki GE, Holman MS. Young maternal age and smoking during pregnancy as risk factors for gastroschisis. Teratology 1993;47:225–228.

Harris J, Poirier J, Selip D, Pillai S, N Shah A, Jackson CC, Chiu B. Early Closure of Gastroschisis After Silo Placement Correlates with Earlier Enteral Feeding. J Neonatal Surg. 2015 Jul 1;4(3):28. PMID: 26290810; PMCID: PMC4518187.

Hawkins RB, Raymond SL, St Peter SD, Downard CD, Qureshi FG, Renaud E, Danielson PD, Islam S. Immediate versus silo closure for gastroschisis: Results of a large multicenter study. J Pediatr Surg. 2020 Jul;55(7):1280-1285. doi: 10.1016/j.jpedsurg.2019.08.002. Epub 2019 Aug 22. PMID: 31472924; PMCID: PMC7731615.

Hemmenki K, Saloniemi I, Kyronen P, et al. Gastroschisis and omphalocele in Finland in the 1970’s: prevalence at birth and its correlates. J Epidemiol Commun Health 1982;36:289–293.

Hershey DW, Haesslein HC, Marr CC, et al. Familial abdominal wall defects. Am J Med Genet 1989;34:174.

Hill LM, Breckle R, Gehrking WC. Prenatal detection of congenital malformations by ultrasonography. Am J Obstet Gynecol 1985;151:44–50.

How HY, Harris BJ, Pietrantoni M, et al. Is vaginal delivery preferable to elective cesarean delivery in fetuses with a known ventral wall defect? Am J Obstet Gynecol 2000; 182:1527.

Hoyme HE, Jones MC, Jones KL. Gastroschisis: abdominal wall disruption secondary to early gestational interruption of the omphalomesenteric artery. Semin Perinatol 1983;7: 294–298.

Killam WP, Miller RC, Seeds JW. Extremely high maternal serum alpha-fetoprotein levels at second-trimester screening. Obstet Gynecol 1991;78:257.

King DR, Savrin R, Boles ET. Gastroschisis update. J Pediatr Surg 1980;15:553.

Kirk EP, Wah RH. Obstetric management of the fetus with omphalocele or gastroschisis: a review and report of 112 cases. Am J Obstet Gynecol 1983;146:512.

Klein M, Kluck P, Tibboel D, et al. The effect of fetal urine on the development of the bowel in gastroschisis. J Pediatr Surg 1983;18:47.

Knott PD, Colley NV. Can fetal gastroschisis always be diagnosed prenatally? Prenat Diagn 1987;7:607–610.

Landisch RM, Yin Z, Christensen M, Szabo A, Wagner AJ. Outcomes of gastroschisis early delivery: A systematic review and meta-analysis. J Pediatr Surg. 2017 Dec;52(12):1962-1971. doi: 10.1016/j.jpedsurg.2017.08.068. Epub 2017 Sep 7. PMID: 28947324.

Langer JC, Longaker MT, Crombleholme TM, et al. Etiology of intestinal damage in gastroschisis. I. Effects of amniotic fluid exposure and bowel constriction in a fetal lamb model. J Pediatr Surg 1989;24:992–997.

Langer JC, Bell JG, Castillo RO, et al. Etiology of intestinal damage in gastroschisis. II. Timing and reversibility of histological changes, mucosal function, and contractility. J Pediatr Surg 1990;25:1122–1126.

Langer JC, Khanna J, Caco C, et al. Prenatal diagnosis of gastroschisis: development of objective sonographic criteria for predicting outcome. Obstet Gynecol 1993;81:53–56.

Larson JM, Pretorius DH, Budorick NE, et al. Value of maternal serum alpha-fetoprotein levels of 5.0 MoM or greater and prenatal sonography in predicting fetal outcome. Radiology 1993;189:77–81.

Lenke RR, Hatch EI. Fetal gastroschisis: a preliminary report advocating the use of cesarean section. Obstet Gynecol 1986;67:395.

Lenke RR, Persutte WH, Nemes J. Ultrasonographic assessment of intestinal damage in fetuses with gastroschisis: is it of clinical value? Am J Obstet Gynecol 1990;163: 995–998.

Lewinsky RM, Jonson JM, Lao TT, et al. Fetal gastroschisis associated with monosomy 22 mosaicism and absent cerebral diastolic flow. Prenat Diagn 1990;10:605–608.

Lewis DF, Towers CV, Garite TH, et al. Fetal gastroschisis and omphalocele: is cesarean section the best mode of delivery? Am J Obstet Gynecol 1990;163:773–775.

Lindham S. Omphalocele and gastroschisis in Sweden 1965–1976. Acta Paediatr Scand 1981;70:55–60.

Lowry RB, Baird PA. Familial gastroschisis and omphalocele. Am J Hum Genet 1982;34:517–518.

Luck SR, Sherman JO, Raffensperger JG, et al. Gastroschisis in 106 consecutive newborn infants. Surgery 1985;98:677.

Luton D, Guibourdenche J, Vuillard E et al: Prenatal management of gastroschisis: the place of the amnioexchange procedure. Clin Perinatol 2003 30(3): 551-572

McKeown T, McMahon B, Record RG. An investigation of 69 cases of exomphalos. Am J Hum Genet 1953;5: 168–175.

Mann L, Ferguson-Smith MA. Prenatal assessment of anterior abdominal wall defects and their prognosis. Prenatal Diag 1984;14:427.

Martinez-Frias ML, Prieto SL, Zaplana J. Epidemiological study of gastroschisis and omphalocele in Spain. Teratology 1984;29:337–382.

Mastroiacovo P, Lisi A, Castilla EE. The incidence of gastroschisis: research urgently needs resources. BMJ 2006; 332:423.

Mayer T, Black R, Matlak ME, et al. Gastroschisis and omphalocele. Ann Surg 1980;192:783.

Mercer S, Mercer B, D’Alton MA, et al. Gastroschisis: ultrasonographic diagnosis, perinatal embryology, surgical and obstetric treatment and outcomes. Can J Surg 1988; 31:25. Molenaar JC, Tibboel D. Gastroschisis and omphalocele. World J Surg 1993;17:337–341.

Molenaar J, Tibboel D: Gastroschisis and omphalocele. World J Surg 1993 17(3): 337-341

Moore KL, Persaud TVN. The developing human: clinically oriented embryology. 5th ed. Philadelphia: Saunders, 1993.

Moore T, Stokes GF. Gastroschisis. Surgery 1953;33:112–120.

Moore TC. Gastroschisis with antenatal evisceration of intestines and urinary bladder. Ann Surg 1962;157:263.

Moore TC. The role of labor in gastroschisis bowel thickening and prevention by elective pre-term and pre-labor cesarean section. Pediatr Surg Int 1992;7:256–259.

Moretti M, Khoury A, Rodriquez J, et al. The effect of mode of delivery on the perinatal outcome in fetuses with abdominal wall defects. Am J Obstet Gynecol 1990;163: 833–838.

Muraji T, Tsugawa C, Nishijima E, et al. Gastroschisis: a 17-year experience. J Pediatr Surg 1989;24:343–345.

Nicholls G, Upadhyaya V, Gornall P, et al. Is specialist center delivery of gastroschisis beneficial? Arch Dis Child 1993;69:71–73.

Nicolaides KH, Snijders RJM, Cheng HH, et al. Fetal gastrointestinal and abdominal wall defects: associated malformations and chromosomal abnormalities. Fetal Diagn Ther 1992;7:102–115.

Novotny A, Klein RJ, Boeckman CR: Gastroschisis: an 18-year review. J Pediatr Surg 1993;28:650–652.

Nyberg DA, Mahony BS, Pretorius DH. Diagnostic ultrasound of fetal anomalies. Yearbook Medical Publisher, Chicago, 1993; 385–432.

Oh KS, Dorst JP, Dominguez R, et al. Abnormal intestinal motility in gastroschisis. Radiology 1978;127:457–460.

Oldham KT, Coran AG, Drongowski RA, et al. The development of necrotizing enterocolitis following repair of gastroschisis: a surprisingly high incidence. J Pediatr Surg 1988;23:945–949.

O’Neill JA, Grosfeld JL. Intestinal malfunction after antenatal exposure of viscera. Am J Surg 1974;127:129–132.

Overcash RT, DeUgarte DA, Stephenson ML, Gutkin RM, Norton ME, Parmar S, Porto M, Poulain FR, Schrimmer DB; University of California Fetal Consortium*. Factors associated with gastroschisis outcomes. Obstet Gynecol. 2014 Sep;124(3):551-557. doi: 10.1097/AOG.0000000000000425. PMID: 25162255; PMCID: PMC4147679.

Paidas M, Crombleholme TM, Robertson FM. Prenatal diagnosis and management of the fetus with an abdominal wall injury. Semin Perinatol 1994:18(3):182–195.

Palomaki GE, Hill LE, Knight GJ, et al. Second-trimester maternal serum alpha-fetoprotein levels in pregnancies associated with gastroschisis and omphalocele. Obstet Gynecol 1988;71:906.

Paulozzi LJ. Seasonality of omphalocele in Washington state. Teratology 1986;33:133–134.

Piper HG, Jaksin T: The impact of prenatal bowel dilation on clinical outcomes in neonates with gastroschisis. J Pediatr Surg 2006 41(5): 897-900

Plessinger MA (1998) Prenatal exposure to amphetamines. Risks and adverse outcomes in pregnancy. Obstet Gynecol Clin North Am 25: 119–38.

Pokorny WJ, Harberg, FJ, McGill CW. Gastroschisis complicated by intestinal atresia. J Pediatr Surg 1981;16:261.

Puligandla PS, Janvier A, Flageole H, et al. Routine cesarean delivery does not improve the outcome of infants with gastroschisis. J Pediatr Surg 2004; 39:742.

Redford RHA, McNay MB, Whittle MJ. Gastroschisis and exomphaloceles: precise diagnosis by mid-pregnancy ultrasound. Br J Obstet Gynaecol 1985;92:54.

Roeper PJ, Harris J, Lee G, et al. Secular rates and correlates for gastroschisis in California (1968–1977). Teratology 1987;35:203–210.

Romero R, Pilu G, Jeanty P, et al. The abdominal wall: prenatal diagnosis of congenital anomalies. Norwalk, CT: Appleton & Lange, 1988.

Rosendahl H, Kivinen S. Antenatal detection of congenital malformations by routine ultrasonography. Obstet Gynecol 1989;73:947.

Royner BD, Richards D. Growth retardation in fetuses with gastroschisis. J Ultrasound Med 1977;16:13–16.

Salihu HM, Emusu D, Aliyu ZY, et al. Mode of delivery and neonatal survival of infants with isolated gastroschisis. Obstet Gynecol 2004; 104:678.

Salinar CF, Bartoshefsky L, Othersen HB, et al. Familial occurrence of gastroschisis. Am J Dis Child 1979;133: 514–517.

Sandler A, Lawrence J, Meehan J et al: A “plastic” surtureless abdominal wall closure in gastroschisis 2004 39(5): 738-741J Pediatr Surg

Sawin R, Glick P, Schaller R, et al. Gastroschisis wringer clamp: a safe, simplified method for delayed primary closure. J Pediatr Surg 1992;27:1346–1348.

Schmidt D, Rose E, Greenberg F. An association between fetal abdominal wall defects and elevated levels of human chorionic gonadotropin in mid-trimester. Prenat Diag 1993;13:9–12.

Schuster S. A new method for the staged repair of large omphaloceles. Surg Gynecol Obstet 1967;125:261–266.

Sermer M, Benzie RJ, Pitson L, et al. Prenatal diagnosis and management of congenital defects of the anterior abdominal wall. Am J Obstet Gynecol 1987;156:308–312.

Shah R, Woolley MM. Gastroschisis and intestinal atresia. J Pediatr Surg 1991;26:788–790.

Shamshirsaz AA, Lee TC, Hair AB, Erfani H, Espinoza J, Shamshirsaz AA, Fox KA, Gandhi M, Nassr AA, Abrams SA, Mccullough LB, Chervenak FA, Olutoye OO, Belfort MA. Elective delivery at 34 weeks vs routine obstetric care in fetal gastroschisis: randomized controlled trial. Ultrasound Obstet Gynecol. 2020 Jan;55(1):15-19. doi: 10.1002/uog.21871. Epub 2019 Dec 3. PMID: 31503365.

Shaw A. The myth of gastroschisis. J Pediatr Surg 1975;10: 235–244.
Sipes SL, Weiner CP, Sipes DR, et al. Gastroschisis and omphalocele: does either antenatal diagnosis or route of delivery make a difference in perinatal outcome? Obstet Gynecol 1990a;76:195–199.

Sipes SL, Weiner CP, Wiliamson RA, et al. Fetal gastroschisis complicated by bowel dilation: an indication for imminent delivery? Fetal Diagn Ther 1990b;5:100.

Skarsgaard 2007

Snyder CL, St Peter SD: Trends in mode of delivery of gastroschisis infants. Am J Perinatol 2005 22(7)391-396

Sparks TN, Shaffer BL, Page J, Caughey AB. Gastroschisis: mortality risks with each additional week of expectant management. Am J Obstet Gynecol. 2017 Jan;216(1):66.e1-66.e7. doi: 10.1016/j.ajog.2016.08.036. Epub 2016 Sep 3. PMID: 27596619.

Stiller RJ, Haynes, de Regt R, et al. Elevated maternal serum alpha-fetoprotein concentration and fetal chromosomal abnormalities. Obstet Gynecol 1990;75:994.

Stoodley N, Sherma A, Noblett H, et al. Influence of place of delivery on outcome of babies with gastroschisis. Arch Dis Child 1993;69:71–73.

Stringel G. Large gastroschisis: primary repair with Gore-Tex patch. J Pediatr Surg 1993;28:653–655.

Stringel G, Filler RM. Prognostic factors in omphalocele and gastroschisis. J Pediatr Surg 1978;14: 515–519.

Strobel KM, Romero T, Kramer K, Fernandez E, Rottkamp C, Uy C, Keller R, Moyer L, Poulain F, Kim JH, DeUgarte DA, Calkins KL; University of California Fetal Consortium. Growth Failure Prevalence in Neonates with Gastroschisis : A Statewide Cohort Study. J Pediatr. 2021 Jun;233:112-118.e3. doi: 10.1016/j.jpeds.2021.02.013. Epub 2021 Feb 26. PMID: 33647253; PMCID: PMC8154735.

Tibboel D, Raine P, McNee M, et al. Developmental aspects of gastroschisis. J Pediatr Surg 1986a;21:865–869.

Tibboel D, Vermey-Keers C, Kluck P, et al. The natural history of gastroschisis during fetal life: development of the fibrous coating on the bowel loops. Teratology 1986b;33: 267–272.

Timor-Tritsch IE, Warren WB, Peisner DB, et al. First trimester midgut herniation: a high-frequency transvaginal sonographic study. Am J Obstet Gynecol 1989;161: 831–833.

Torfs C, Curry C, Roeper P. Gastroschisis. J Pediatr 1990; 116:1.

Torfs CP, Curry CJR. Familial cases of gastroschisis in a population-based registry. Am J Med Genet 1993;45: 465–467.

Utria AF, Wong M, Faino A, Jacobson E, Javid PJ. The role of feeding advancement strategy on length of stay and hospital costs in newborns with gastroschisis. J Pediatr Surg. 2022 Mar;57(3):356-359. doi: 10.1016/j.jpedsurg.2021.04.011. Epub 2021 Apr 19. PMID: 34020775.

Van Allen MI. Fetal vascular disruptions: mechanisms and some resulting birth defects. Pediatr Annu 1981;10:31–50.

Walkinshaw SA, Renwick M, Hebisch G, et al. How good is ultrasound in the detection and evaluation of anterior abdominal wall defects? Br J Radiol 1992;65:298–301.

Werler MM, Mitchell AA, Shapiro S. First trimester maternal medication use in relation to gastroschisis. Teratology 1992b;45:361–367.

Yaster M, Scherer TLR, Stone MM, et al. Prediction of successful primary closure of congenital abdominal-wall defects using intraoperative measurements. J Pediatr Surg 1989;24:1217–1220.

Zivkovle SM. Repair of gastroschisis using umbilical cord as patch. J Pediatr Surg 1991;26:1179–1180.