PubMed · 4238326
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K Yamase. 1969. [Abdominal wall].. https://pubmed.ncbi.nlm.nih.gov/4238326/
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It is known that neonates with congenital abnormalities of the intestine tend to be growth-retarded. We wished to explore the hypothesis that normal fetal gut function is needed for normal growth in late gestation. If this is true, then different populations of babies with different congenital gut abnormalities would be expected to have similar impairments of growth and be small at birth. This growth retardation would be more marked in term than in preterm babies and would be independent of other congenital anomalies. To test these hypotheses, we examined 43 babies born with gastroschisis (GS) in Auckland, New Zealand; 69 babies born with GS in Birmingham, England; and 60 babies born with intestinal atresia (IA) in Auckland. For Auckland babies with GS, the mean weight standard deviation score (WSDS) (i.e., birth weight relative to the mean birth weight for gestation) for term babies was lower than that for preterm babies (-0.932+/-0.180 vs -0.064+/-0.237, P=0.014). This was also true for Birmingham babies with GS (-0.991+/-0.193 vs -0.36 +/-0.153, P=0.028). For babies with IA, the mean WSDS for term babies was lower than that for preterm babies (-0.627+/-0.266 vs 0. 057+/-0.211, P=0.034). There was no significant difference between the mean WSDS of babies with and without major congenital abnormalities (-0.402+/-0.201 vs -0.271, P=0.70). Our results demonstrate that term babies born with GS are significantly growth-retarded compared with premature babies born with GS. Term babies born with a proximal IA are also growth-retarded. This strongly suggests that in late gestation, the normal growth is dependent on a normally functioning gastrointestinal tract that allows exposure of the proximal intestinal mucosa to ingested amniotic fluid.
This paper reports a premature infant with a congenital diaphragmatic hernia (CDH) who underwent an abdominal wall plasty to enlarge the abdominal cavity, one of twin infants born at 32 weeks weighing 1,255 g. After stabilization, the herniated viscera were reduced from the pleural cavity and the abdominal wall muscle and skin layers were replaced by a Gore-tex patch without closure of the diaphragmatic defect. Respiratory and circulatory conditions were stable during the perioperative period. Postoperatively, a roentogenogram showed expansion of the lung. However, his condition deteriorated 24 h after surgery, triggered by intratracheal suction, and he died on the 4th day of life despite the use of high-frequency oscillation, catecholamines, and vasodilators. Postmortem examination showed severely hypoplastic lungs. Abdominal wall plasty may be a less invasive initial procedure, however, further studies, such as comparison with the standard method or conservative management, are needed using a large clinical group or animal models to justify the usefulness of this procedure.
We have used a retrograde labeling technique to identify motorneurons for each of the 30 body wall muscles of an abdominal hemisegment in the late stage 16 Drosophila embryo. Each motorneuron has a characteristic cell body position, dendritic arborization, and axonal projection. In addition, we have determined the neuroblasts of origin for most of the motorneurons we describe. Some organizational principles for the neuromuscular system have become apparent: (1) There is no obvious topographic relationship between the cell body positions of motorneurons and the position or orientation of the muscles they innervate; (2) motorneurons that innervate muscles of similar position and orientation are often clustered and have overlapping dendritic trees; (3) morphologically similar motorneurons are generally derived from a common neuroblast and innervate operationally related muscles; and (4) neuroblasts can give rise to more than one morphological type of motorneuron.