Abstract
Background: The causes of intrauterine fetal demise are varied and not entirely well-understood. Multiple observational studies have shown that both perinatal and infant mortality rates are increased in children of diabetic mothers when compared to those of nondiabetic mothers. Case: We present a case involving a 22-year-old G4P0120 with poorly controlled type 1 diabetes mellitus and a complex medical history including two first trimester fetal losses, and second trimester intrauterine fetal demise who presented during the second trimester for care and was found to have a fetus with ultrasound findings consistent with caudal regression syndrome. When she presented in labor at term intrauterine fetal demise was identified. Discussion: Infants and fetuses of diabetic mothers are at a higher risk for congenital anomalies, one of which is the potentially devastating caudal regression syndrome. However, it appears that this risk may be lowered with strict glycemic control both before and during pregnancy.
Highlights
DiscussionInfants and fetuses of diabetic mothers are at a higher risk for congenital anomalies, one of which is the potentially devastating caudal regression syndrome
Fetal death, though relatively more prevalent in low- and middle-income countries, remains an issue in the United States with a fetal mortality rate of 5.96 of 1000 live births and fetal deaths.[1,2] Several risk factors for fetal death and stillbirth have been identified that allow practitioners to identify which patients may be at greater risk for these outcomes
Infants and fetuses of diabetic mothers are at a higher risk for congenital anomalies, one of which is the potentially devastating caudal regression syndrome
Summary
Fetal death can be a highly emotional event, which may make searching for and determining an etiology difficult. The pathogenesis of CRS is poorly understood It likely arises from an issue with the gastrulation process leading to a defect in the mesoderm and induction of caudal elements in the embryo before the 4th week of gestation.[12, 14] Several gene/protein pathways, including the Shh, Cdx[2], Acd, and Lrp[6] pathways appear to be involved.[14] It has been suggested that in mothers with diabetes, hyperglycemia leads to decreased myoinositol intake in the embryo, which in turn may cause abnormal fusion and folding events in the embryo.[12] It is likely that the pathogenesis of CRS is multifactorial, with both genetic and environmental components. Multiple studies have shown that while mothers with higher glycated hemoglobin levels early in pregnancy have higher rates of fetal anomalies, tight glycemic control both before and throughout the pregnancy may decrease these rates.[18,19,20,21] pregnant women with diabetes should be counseled extensively about the benefits of maintaining good control of their diabetes
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