Congenital ventral body wall defects encompass a number of distinct entities including ectopia cordis, bladder exstrophy and abdominal wall defects i.e. omphalocele and gastroschisis.1 Ectopia Cordis (incidence of 5.5-7.9/million live births) and bladder exstrophy (incidence of 1/40,000 live births) are considerably rarer than gastroschisis and omphalocele.1 The incidence of gastroschisis appears to be increasing. A study using cases identified in 15 states by the National Birth Defects Prevention Network noted an increasing temporal trend in the incidence of gastroschisis ranging from 2.32 to 4.42/10,000 live births over a 11-year study period.2 The incidence of omphalocele is considerably lower, a multistate retrospective cohort study performed from 1995 to 2005 using multiple population-based birth defects registries estimated the prevalence to be 1.92 per 10,000 live births in the United States.3 The incidence of omphalocele, however, as seen on ultrasonography at 14-18 weeks is as high as 1 in 1,100 and therefore the overall perinatal mortality has been estimated to be as high as 52.7%.4, 5 This discrepancy stems from the relatively high rate of fetal demise along with planned termination of pregnancies.6 The main focus of this manuscript will be to review the anatomy and embryology of abdominal wall defects i.e. gastroschisis and omphalocele.

The two abdominal wall defects omphalocele and gastroschisis are often considered together, however, there are marked differences in their presentation, etiology and management principles.7 One of the major points of distinction stems from the considerably differential rates of associated anomalies seen in ∼ 50% of the patients (27-88%) with omphalocele, but very rarely in patients with gastroschisis except for the patients with intestinal atresias.4, 8, 9, 10, 11 Among patients with omphalocele these associated anomalies have a considerable impact on prognosis.