Aetiology
The aetiology of gastroschisis and omphalocele is unclear, and many theories have been proposed to explain these abdominal wall defects. Due to the poor understanding of the aetiology of these conditions, it is difficult to propose modifiable factors for prevention. Some studies suggest that maternal use of recreational drugs may be a risk factor for gastroschisis.[11] Others suggest that the incidence of gastroschisis is less in young mothers taking daily multivitamins during pregnancy.[12] Conversely, the incidence of gastroschisis in babies of teenage mothers who smoke is increasing.[3][4][9][10]
Evidence supporting an association between smoking during pregnancy and the development of abdominal wall defects in the fetus is well described for both gastroschisis and omphalocele. It is suggested that cigarette smoke causes vasoconstriction that contributes to placental insufficiency and failed development of the vascular system.[11][13][14][15] Maternal infections and illness during pregnancy are seen in mothers who deliver infants with omphalocele and gastroschisis. It is proposed that maternal illness can contribute to placental insufficiency that may, in turn, contribute to the development of abdominal wall defects.[4] Genitourinary infection during pregnancy has also been shown to be associated with abdominal wall defects.[16]
Pathophysiology
Several theories have been proposed to explain the development of gastroschisis. One theory suggests that the full-thickness defect results from abnormal involution of the right umbilical vein causing rupture of the anterior abdominal wall at the weakened point.[17] Another theory suggests that premature interruption of the right omphalomesenteric artery results in ischaemia of the anterior abdominal wall, allowing herniation of abdominal contents.[1][18] In utero rupture of an omphalocele leading to the development of gastroschisis has also been suggested.[19] However, the lack of associated anomalies in gastroschisis does not support this theory. The thickened peel covering the intestine in gastroschisis may be due to exposure of the extruded abdominal contents to fetal urine or meconium in utero or mesenteric venous obstruction resulting in oedema.
Many theories have also been suggested to explain the development of omphalocele. These include failure of intestinal migration into the abdomen by 10 to 12 weeks of embryological development, failure of central migration of the lateral body folds of mesoderm, and persistence of a body stalk beyond 12 weeks' gestation.[20]
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