Introduction
Background
Gastroschisis represents a herniation of abdominal contents through a paramedian full-thickness abdominal fusion defect. The abdominal herniation is usually to the right of the umbilical cord. No genetic association exists. A gastroschisis usually contains small bowel and has no surrounding membrane. The herniated bowel is not rotated and is devoid of secondary fixation to the posterior abdominal wall.
Gastroschisis usually is detected in the second trimester using antenatal sonography.1,2,3,4,5,6,7,8,9 The maternal serum alpha-fetoprotein (AFP) level is elevated in 77-100% of mothers. The mortality rate is approximately 17%. Surgical repair should be offered within the first day after delivery to avoid infection. The outcome is no different in infants delivered in tertiary obstetric centers than in infants delivered in smaller peripheral hospitals, although delivery within easy access of a neonatal surgical unit is advised. Cesarean delivery is performed in many mothers of fetuses with gastroschisis, although this does not convey any advantage over vaginal delivery.
For excellent patient education resources, visit eMedicine's Pregnancy and Reproduction Center. Also, see eMedicine's patient education articles Hernia and Cesarean Childbirth.
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Abdominal Hernias
Omphalocele
Omphalocele and Gastroschisis
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Ward reduction without general anaesthesia versus reduction and repair under general anaesthesia for gastroschisis in newborn infants
Pathophysiology
Controversy exists regarding the cause of gastroschisis. Some authorities suggest that the defect is caused by abnormal involution of the right umbilical vein, resulting in rupture of the anterior abdominal wall at a point of weakness. Others suggest that gastroschisis results from rupture of an exomphalos. Rupture of a small omphalocele and transformation into a gastroschisis has been described in utero. This observation has led to speculation that gastroschisis could represent an omphalocele that ruptures before the somatic components of the anterior abdominal wall become folded. However, the much-increased incidence of associated anomalies in patients with omphalocele does not support this theory.
Another theory for the etiology of gastroschisis is premature interruption of the right omphalomesenteric artery, which results in ischemic injury to the anterior abdominal wall through which herniation of abdominal contents occurs. This artery persists under normal circumstances.
The use of recreational drug use has been quoted as a significant risk factor for gastroschisis.10 Maternal hair analysis proved an acceptable and valuable method of independently verifying recreational drug use.
Because the herniated bowel is bathed by amniotic fluid, both maternal serum and amniotic fluid AFP levels are elevated, more so than in exomphalos. In early pregnancy, the bowel loops can be seen floating in the amniotic fluid. The thickness and the diameter of the bowel are normal. Later in pregnancy, bowel obstruction, peritonitis, bowel perforation, and fetal growth restriction may occur. Intrauterine growth restriction (IUGR) occurs in 38-77% of fetuses and is usually secondary to nutrient loss through exposed bowel. Approximately 48% of infants with gastroschisis are small for their gestational age.11
A bowel diameter greater than 17 mm usually represents significant bowel dilatation, and diameters greater than 11 mm are usually associated with a greater number of postnatal bowel complications. Sonographic findings of bowel abnormalities are associated with difficult abdominal wall repair and an increased incidence of complications.
Tibboel and associates reviewed a number of studies in which prenatal and postnatal autopsy material showed no evidence of abnormal histologic results in ganglion cells or in the myenteric nervous system to explain the motility disorder that accompanies some cases of gastroschisis.12 Tibboel et al also showed that a fibrous peel surrounds the herniated bowel beginning at approximately 30 weeks' gestation. Ischemic changes in the bowel loops are usually not seen in fetuses with gastroschisis who were aborted before 30 weeks' gestation. However, ischemic changes are seen in postnatal infants who have hypoperistalsis, which suggests that bowel vascular compromise may occur at the abdominal wall defect late in pregnancy.
The cause of bowel injury in gastroschisis has been controversial for several years. Experimental animal models have shown that when bowel is exposed to allantoic contents, it thickens, becomes edematous, and develops a fibrous peel, whereas bowel exposed to amniotic fluid alone develops normally. Results from animal models have led to the suggestion that the urine in amniotic fluid causes the bowel damage.13 The fibrous peel consists of type 1 collagen and fibrin, and it usually dissolves after surgical repair. Some authors suggest that the peel itself may cause the bowel motility disorder.
Another animal study showed that bowel damage in gastroschisis at least partially depends on meconium exposure in utero.14 The authors of this study suggested that the increasing evidence of physiologic in utero defecation supports the hypothesis that bowel damage in gastroschisis may be meconium dependent.
Gastroschisis is classified as an open fetal defect by virtue of the finding that it is not covered by skin. Open fetal defects allow diffusion of AFP from the fetal circulation into amniotic fluid. Because the fetal AFP level is 200-300 times as high as the concentration in amniotic fluid, the diffusion is not only reflected as higher amniotic fluid AFP levels, but it is also reflected in higher maternal serum AFP levels, albeit to a lesser degree.
AFP levels in gastroschisis are usually higher than those found with omphalocele. The lower maternal serum AFP level in open fetal defects reflects the fact that the amnion represents a significant barrier to the diffusion of AFP from the amniotic fluid into the maternal circulation. Maternal serum AFP levels are usually higher than 2.5 multiples of the median (MoM) in 77-100% of mothers of fetuses with gastroschisis.
Major malformations and chromosomal anomalies are common in association with omphalocele. However, these anomalies are rare in gastroschisis, with the exception of intestinal atresia, which appears to be a direct consequence of in utero herniation. Bowel anomalies occur in 5% of patients with gastroschisis and include intestinal atresia or stenosis resulting from vascular compromise. Rarely, ectopia cordis has been recorded.6 Chromosomal anomalies in gastroschisis are extremely rare, and most centers do not recommend karyotyping in infants with gastroschisis.
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Frequency
United States
The incidence of gastroschisis is 1.75-2.5 cases per 10,000 live births. Most cases are sporadic, although a few familial cases have been reported. Occurrence in twins has been reported.
International
The incidence is the same as in the United States.
Mortality/Morbidity
Although reported survival rates are good in gastroschisis, the postoperative hospital stay is often lengthy, and complications occur frequently, especially complications related to the gastrointestinal tract.15 Evidence of bowel damage, such as atresia, necrosis, or severe dilatation or thickening of the bowel, or the inability to close the abdominal defect primarily indicates a poor prognosis. Prenatally, bowel obstruction, peritonitis, bowel perforation, prematurity, and fetal growth restriction may be complications of gastroschisis. Postnatally, malrotation, small bowel atresia or stenosis, bowel infarction, prolonged intestinal motility dysfunction, necrotizing enterocolitis, chronic short-gut syndrome, and hyperalimentation hepatitis may occur.
Deformations of the fetal urinary tract can develop secondary to gastroschisis. These do not represent separate malformations, and karyotyping is not indicated. When hydronephrosis is present, ongoing urologic evaluation of the neonate is indicated.
Survival rates after surgery are 87-100%. Mortality rates are 17%, and most deaths occur as a result of premature delivery, sepsis, and bowel infarction. The clinical outcome cannot be correlated with the size of the abdominal defect as estimated using sonography or with the known time of exposure to amniotic fluid. Gastroschisis diagnosed antenatally can resolve in utero — causing necrosis of portions of the small and large bowel, leading to short-bowel syndrome and increased mortality and morbidity rates. Spontaneous resolution of gastroschisis and closure of the anterior abdominal wall defect have been described.16,17,18,19
Associated anomalies are more uncommon than in omphalocele. The reported overall incidence of associated anomalies is 7-30%. The anomalies are not related directly to the defect and include anencephaly, cleft lip and palate, ectopia cordis, atrial septal defect, diaphragmatic hernia, scoliosis, syndactyly, and amniotic band. These anomalies add to the morbidity.
Neonatal outcome of live-born infants following a prenatal diagnosis of gastroschisis is not different from a diagnosis at birth. The presence of intestinal atresia is the most important prognostic factor for morbidity.20 However, it is not always possible to determine whether the gastroschisis defect is simple or complex by antenatal scans, although this information is obviously valuable to families with infants with gastroschisis because the length of hospital stay and ultimate prognosis is dependent on this knowledge.
Vachharajani and associates described the outcomes of 70 infants with gastroschisis who were admitted to their neonatal intensive care unit between 2001 and 2005.21 In this study, 72% of the patients had isolated gastroschisis, whereas 28% had more complex anomalies (intestinal atresia, perforation, bowel necrosis, or volvulus). The authors concluded that not only was the type of gastroschisis (simple vs complex) an important factor in the infants' outcomes, but also the duration of parenteral nutrition, length of hospital stay, and survival were affected.
Improvements in short-term results of gastroschisis treatment can be attributed to more recent developments in prenatal diagnosis and the advancements of centralized perinatal care. There has also been considerable improvement in long-term results of babies treated for gastroschisis. The initial gastrointestinal problems and developmental delays are made up during the first 2 years of life, and therefore, a more optimistic prenatal counseling can now be given.
Mortality was quoted as nil following surgery in 40 patients with gastroschisis.22 In this group of 40 patients, delivery was by cesarean section in 93%, but the outcomes following vaginal delivery were no worse. Twenty-eight percent of the gastroschisis cases demonstrated congenital abnormalities that were limited to the gastrointestinal tract.22
Sex
A slight male predilection exists.
Age
The diagnosis can often be made by using antenatal sonography before 20 weeks' gestation. With transvaginal sonograms, the diagnosis has been made as early as 12 weeks' gestation.
Anatomy
The anterior abdominal wall and umbilical cord insertion are readily recognized on antenatal scanning because the wall provides a direct interface between itself and the amniotic fluid. The anterior abdominal wall is best demonstrated by axial scans. Assessment of the lower anterior abdominal wall is occasionally made difficult by flexed fetal limbs. The inner aspect of the anterior abdominal wall is difficult to see because its echodensities are identical to the remainder of the abdominal viscera unless fetal ascites is present.
Gastroschisis results from herniation/evisceration of small bowel into the amniotic cavity through a small defect (2-5 cm) in the right paraumbilical region. Reportedly, the defect can be located in the left paraumbilical region, but this site is extremely rare. No covering membrane exists. The large bowel (common), pancreas, stomach, liver (rare), spleen, bladder, uterus, ovaries, and fallopian tubes may also be herniated. The attachment of the umbilical cord is normal.
Presentation
Gastroschisis is found incidentally or because of an elevated maternal AFP level. Rarely, polyhydramnios may prompt an antenatal sonographic examination. Fetal growth restriction is a frequent association. Oligohydramnios is rare. Chromosomal anomalies are not associated with gastroschisis, and familial occurrence is exceptionally rare. Approximately 50% of fetuses with gastroschisis are small for their gestational dates. Fetal abdominal circumference, which is regarded as a standard reference for assessment of fetal size, does not apply to this group of fetuses; therefore, obstetric management may be difficult.
The presence of the bowel in amniotic fluid may affect cardiotocographic monitoring. As a result of the difficulty in monitoring fetal maturity and fetal well-being, cesarean delivery is performed with many fetuses, although this does not convey an advantage in terms of fetal mortality or morbidity. Postnatal management requires a sterile covering of cling film over the herniated viscera to prevent infection, heat and evaporative loss, and the need for immediate transfer to a neonatal surgical unit.23 Hospital stays for these infants are lengthy, and although most of these infants are usually on normal feedings by 4 weeks from the date of delivery, many affected infants require months of intravenous feeding because of the many bowel complications associated with gastroschisis.
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Preferred Examination
Antenatal sonography is the key imaging examination available, with detection rates of 70-72%. Prenatal sonography is the primary imaging modality in pregnancy because it is noninvasive, is rapid, and allows real-time fetal examination. Plain radiographs and bowel contrast studies may be indicated in the postnatal postoperative period to assess bowel complications.
Limitations of Techniques
Sonography remains operator dependent, and artifacts are a problem. Despite the straightforward nature of the defect, a diagnosis of gastroschisis can be missed.
Misdiagnosis of exomphalos as gastroschisis has occurred in 5% of patients. This misdiagnosis has serious implications because exomphalos is often associated with chromosomal and other severe anomalies and karyotyping is not performed in patients with gastroschisis.
In one case series, gastroschisis was misdiagnosed as exomphalos at a rate of 14.7%. This misdiagnosis results in unnecessary amniocentesis, which exposes the fetus to the risks involved in amniocentesis and which also exposes the mother to psychological trauma.
Assessment of fetal size by using abdominal circumference measurements is difficult in the presence of gastroschisis. Postnatal plain radiographs and bowel-contrast studies lack specificity and expose the infant to a radiation burden. However, Siemer et al have developed a sonographic weight formula for fetuses with abdominal wall defects.11 The authors evaluated their formula in a group of 97 fetuses with either gastroschisis or omphalocele and concluded that it provided a significantly greater accuracy in estimating fetal weight than a more commonly used formula. More data will be necessary to determine the utility of Siemer et al's formula.
Differential Diagnoses
Other Problems to Be Considered
Physiologic bowel herniation
Physiologic herniation occurs at 10-13 weeks. The best method for differentiating this from an omphalocele is to obtain a repeat sonogram after 15 weeks' menstrual age. A large defect with the liver exteriorized indicates an omphalocele at any gestational age.
Omphalocele
Omphalocele is herniation of a variable amount of abdominal viscera through a defect (2-10 cm) at the base of the umbilical cord. A membrane covers the herniation, differentiating it from gastroschisis, and the umbilical vessel inserts into the apex. Association with liver herniation, ascites, cardiac defects, and chromosomal anomalies is frequent. Association with holoprosencephaly and limb anomalies is occasional. The incidence of chromosomal abnormalities is high at approximately 33%. The prognosis is related to the karyotype, associated abnormalities, and contents of the omphalocele.24
Umbilical hernia
Umbilical hernia results from a defect in the linea alba; the protruding bowel is covered by subcutaneous tissues and skin. Umbilical hernia is common in the first months in 20% of black neonates and in 3% of white neonates, as well as common in premature infants, namely, in more than 5% of premature infants weighing less than 1500 g. Sonographic findings include a prominent bulge of the anterior abdominal wall that may contain omentum and/or bowel, which may protrude into the umbilical cord. Amniotic fluid AFP levels may be elevated when the bowel is herniated into the umbilical cord.
Amniotic band syndrome
Amniotic band syndrome (ABS) is a common cause of an abdominal wall defect. Involvement of the abdominal wall may produce appearances similar to gastroschisis. However, an atypical location of the abdominal wall defect suggests the diagnosis of ABS. Membranes contiguous with such a defect may be identified.
Bladder extrophy
Sonographically, bladder extrophy may present as an external, well-defined, solid or complex mass immediately superior to the fetal genitalia. Prolonged and repeated scans fail to reveal the fetal bladder. The renal collecting system and ureters need not be dilatated, and unilateral or horseshoe kidneys may be found. Uterine and adnexal anomalies are relatively frequent. The pubis is abnormally wide, and the umbilical cord insertion may be abnormal.
Cloacal extrophy
Cloacal extrophy consists of a low omphalocele; bladder or cloacal extrophy; and, frequently, other caudal anomalies. These other conditions may include meningomyelocele anal atresia and lower limb anomalies. Most affected fetuses have a single umbilical artery. Sonographic findings include a low anterior abdominal mass below the umbilical cord that is associated with an absent urinary bladder.
Limb-body-wall complex
Limb-body-wall complex (LBWC) is a lethal condition with a severe anterior abdominal wall defect. The defect is placed laterally and involves the size of the umbilical cord insertion. The abdominal contents lie outside within a sac of amnion and mesoderm. Association with congenital heart defects (CHDs), cranial anomalies (encephalocele), limb abnormalities, and scoliosis is frequent. Chromosomal defects are usually not present.
Cavernous hemangioma
Cavernous hemangiomas are most frequently found over the lower body and are often associated with Klippel-Trenaunay-Weber syndrome, which is diagnosed in the presence of multiple surface masses, producing limb hypertrophy. Hydrops may occur.
Thoracoabdominal pentalogy of Cantrell
Ectopia cordis associated with a ventral wall defect should prompt the diagnosis of pentalogy of Cantrell. The syndrome is often associated with other anomalies.
Blood clot
A blood clot around the umbilicus secondary to traumatic amniocentesis or abruptio placenta may mimic gastroschisis.
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Further Reading
Keywords
omphalocele, exomphalos, paromphalocele, embryonal ruptured omphalocele, laproschisis, abdominoschisis, full-thickness abdominal fusion defect, abdominal herniation
