BACKGROUND/ PURPOSE: The mechanisms of intrauterine vascular disruptions that result in the development of jejunoileal atresia (JIA) are not fully understood. Monochorionic twinning with fetal death of a cotwin is known to be correlated with the development of JIA in the survivor through placental communication. The aim of this study was to evaluate whether other placental vascular compromises might contribute to the development of JIA. METHODS: Forty-five newborns (23 boys and 22 girls) who were treated for JIA at Tsukuba University Hospital from 1978 to 2003 were reviewed. Placental findings were informative in 23 cases. RESULTS: No or slight abnormality of the placenta was found in 19 cases. Significant placental abnormalities were found in 4 patients who also had a low birth weight. One patient with apple peel atresia (APA) had excessive torsion of the umbilical cord (UC), which was inserted at the margin of the placenta, and there was an adjacent area of infarction. One patent with multiple atresia (MA) was a surviving monochorionic twin with intrauterine fetal death of the other. Another case of MA showed marginal insertion of the UC. Severe placental abnormalities including wide infarction, cyst formation, and marginal insertion of the UC were found in 1 case of MA. These 3 cases of MA were complicated with other anomalies including brain anomaly. CONCLUSIONS: Placental vascular compromises were involved infrequently in JIA but might possibly be responsible for the development of JIA as well as associated anomalies and a low birth weight as chronic insults since an early stage of gestation in some cases.
BACKGROUND/ PURPOSE: The mechanisms of intrauterine vascular disruptions that result in the development of jejunoileal atresia (JIA) are not fully understood. Monochorionic twinning with fetal death of a cotwin is known to be correlated with the development of JIA in the survivor through placental communication. The aim of this study was to evaluate whether other placental vascular compromises might contribute to the development of JIA. METHODS: Forty-five newborns (23 boys and 22 girls) who were treated for JIA at Tsukuba University Hospital from 1978 to 2003 were reviewed. Placental findings were informative in 23 cases. RESULTS: No or slight abnormality of the placenta was found in 19 cases. Significant placental abnormalities were found in 4 patients who also had a low birth weight. One patient with apple peel atresia (APA) had excessive torsion of the umbilical cord (UC), which was inserted at the margin of the placenta, and there was an adjacent area of infarction. One patent with multiple atresia (MA) was a surviving monochorionic twin with intrauterine fetal death of the other. Another case of MA showed marginal insertion of the UC. Severe placental abnormalities including wide infarction, cyst formation, and marginal insertion of the UC were found in 1 case of MA. These 3 cases of MA were complicated with other anomalies including brain anomaly. CONCLUSIONS: Placental vascular compromises were involved infrequently in JIA but might possibly be responsible for the development of JIA as well as associated anomalies and a low birth weight as chronic insults since an early stage of gestation in some cases.