PubMed · 11462663
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S Sakazume. 2001. [Gastroschisis].. https://pubmed.ncbi.nlm.nih.gov/11462663/
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Gastroschisis, a ventral body wall defect, is a continuing challenge and concern to researchers, clinicians, and epidemiologists seeking to identify its cause(s) and pathogenesis. Concern has been renewed in recent years because, unlike most other birth defects, rates of gastroschisis are reportedly increasing in many developed and developing countries. No tenable explanation or specific causes have been identified for this trend. Rates of gastroschisis are particularly high among pregnancies of very young women. Such an intriguing association, not observed to this degree with other birth defects, may afford clues to the defect's cause. Understanding the causes of gastroschisis may provide insight to the defect's origin. In pursuing such causal studies, it would be helpful to understand the embryogenesis of gastroschisis. To date, four main embryologic hypotheses have been proposed: (1) Failure of mesoderm to form in the body wall; (2) Rupture of the amnion around the umbilical ring with subsequent herniation of bowel; (3) Abnormal involution of the right umbilical vein leading to weakening of the body wall and gut herniation; and (4) Disruption of the right vitelline (yolk sac) artery with subsequent body wall damage and gut herniation. Although based on embryological phenomena, these hypotheses do not provide an adequate explanation for how gastroschisis would occur. Therefore, we propose an alternative hypothesis, based on well described embryonic events. Specifically, we propose that abnormal folding of the body wall results in a ventral body wall defect through which the gut herniates, leading to the clinical presentation of gastroschisis. This hypothesis potentially explains the origin of gastroschisis as well as that of other developmental defects of the ventral wall.
The use of a silo for temporary coverage of exposed viscera for newborns with gastroschisis has allowed gradual reduction of the externalized intestine into the abdominal cavity. However, there has not been an easy way to monitor blood perfusion to the intestine within the silo other than with visual examination. In addition, visual examination of bowel through the silo is sometimes difficult for medical staff due to serositis and peel over the bowel. We have adopted an approach to monitor oxygen saturation of silo-contained intestine by placing a pulse oximeter sensor on the surface of the transparent silo to detect intestinal ischemia. Pulse oximeter sensors were applied on both a patient's distal extremity and the silo on five consecutive patients who were born with gastroschisis. The sensor was left on the silo during the entire period of gradual reduction. Perfusion index, pulse and oxygen saturation were observed and checked against the sensor placed on a peripheral extremity. The silo-placed pulse oximeter and peripheral pulse oximeter sensors showed a similar pulse and oxygen saturation throughout the reduction period in all five patients. In general, perfusion index was higher from the silo pulse oximeter compared to the peripheral pulse oximeter reading. A pulse oximeter can be used to monitor intestinal oxygen saturation contained within a silo and help modulate the rate of manual reduction of intestine.
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