Gastroschisis and omphalocele are defects of the abdominal wall that occur in utero, can be detected prenatally using fetal ultrasonography, and result in herniation of abdominal contents.
In contrast to omphalocele, there is no sac covering the intestines in gastroschisis.
The significant fluid balance changes and heat loss from exposed intestines in gastroschisis require emergency surgical intervention to establish abdominal wall closure or temporary coverage.
The lack of a protective sac in gastroschisis exposes the intestines to amniotic fluid in utero, leading to a thick inflammatory film or peel overlying the intestine and causing delay of return of normal bowel function after closure.
The most commonly associated anomaly of gastroschisis is intestinal atresia, which occurs in 10% to 15% of cases, and is related to ischemia of the exposed gut caused by constriction of its mesenteric blood supply at the level of the abdominal wall defect.
The most common cause of mortality in omphalocele relates to associated organ system and chromosomal anomalies such as pentalogy of Cantrell and Beckwith-Wiedemann syndrome, which are characterized by cardiac anomalies and chromosomal defects.
Successful postnatal management of all abdominal wall defects is focused on timely abdominal wall closure, maintenance of euthermia, fluid resuscitation, and prevention of additional fluid loss from the abdominal contents, as well as prevention of ischemia and infarction of the intestine.
Gastroschisis and omphalocele are congenital defects of the abdominal wall resulting in intestinal herniation from the abdominal cavity. They can be detected prenatally using fetal ultrasonography. Limited studies have attempted to categorize gastroschisis defects into subsets of simple or complex defects, with simple gastroschisis existing as an isolated defect, and complex gastroschisis occurring with other gastrointestinal anomalies such as intestinal atresia, perforation, necrosis, or volvulus.
University of Florida College of Medicine
CLL declares that she has no competing interests.
Dr Cynthia L. Leaphart would like to gratefully acknowledge Dr Joseph T. Tepas, a previous contributor to this monograph. JTT declares that he has no competing interests.
Emeritus Nuffield Professor of Paediatric Surgery
Institute of Child Health
LS declares that he has no competing interests.
Assistant Professor of Surgery
Division of Pediatric Surgery
Johns Hopkins University School of Medicine
FA declares that he has no competing interests.
Consultant in Paediatric and Neonatal Surgery
Royal Alexandra Children's Hospital
RH declares that she has no competing interests.
Department of Pediatrics
University of Washington Medical Center
SC declares that he has no competing interests.
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