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A defect in the abdomen of the developing fetus can allow the internal organs (intestines, bladder, liver, stomach or spleen) to protrude out of the abdomen. When the organs come out of the abdomen at the point where the umbilical cord is attached to the fetus, the defect is called an omphalocele. In this case, the internal organs are located in a sac or membrane connecting the umbilical cord to the fetus. When the internal organs are floating freely in the fluid surrounding the fetus (amniotic fluid), it is called gastroschisis. Both of these conditions can be diagnosed during a routine ultrasound examination of the fetus performed between weeks 18 and 22 of pregnancy. It is estimated that omphalocele occurs once in every 5,800 births, and gastroschisis occurs once in every 12,000 live births. Omphalocele can be accompanied by chromosome abnormalities (trisomy 13, 15, 16, or 18), heart defects, kidney defects and abnormal development of the nervous system. The prognosis is poor if the omphalocele is large and contains the liver, and if chromosome abnormalities or other organ defects are present. This article describes the case of a 29-year-old pregnant woman who had a routine ultrasound examination performed during week 20 of pregnancy. The ultrasound showed that the fetus had an omphalocele. The parents elected to terminate the pregnancy. It should be noted that not all pregnancies complicated by omphalocele need to be terminated. If an omphalocele is diagnosed, then amniocentesis should be performed to determine if there are any genetic defects. In some cases, surgery can be performed to place the organs back into the abdominal cavity. (Consumer Summary produced by Reliance Medical Information, Inc.)

Prolonged pregnancies complicated by oligohydramnios may be characterized by changes in the blood flow of the fetal kidneys. An oligohydramnio is a deficiency of amniotic fluid. Among 50 women who were 40 or more weeks pregnant, 33 had a normal amniotic fluid index and 17 had a low amniotic fluid index. The amniotic fluid index is a measurement of amniotic fluid volume. Fetuses with a low amniotic fluid index were more likely to have changes in the blood flow of the renal artery of the fetus. Blood flow in the umbilical artery was the similar for the two groups. A significant decrease in amniotic fluid is associated with both term and post-term pregnancies.

Studies indicate that abnormally high blood sugar, or glucose, levels in pregnant diabetic women may affect the developing fetus. Hyperglycemia, high blood glucose, has been associated with fetal loss, abnormal development, and growth retardation. To see how glucose affects the cells of the fetus, rapidly growing cells were removed from placentas after delivery and grown in the laboratory in varying levels of glucose. Fewer cells grew in the specimens exposed to higher levels of glucose. The proliferation of cells is essential for normal development throughout pregnancy. When cell growth is adversely affected, particularly during critical stages of fetal development, severe abnormalities can result. Previous studies examining the effects of high glucose on fetal development in diabetic pregnancies have used animal models. This model, which uses human cells derived from products of conception, may provide a more accurate assessment. However, these cells were obtained from completed pregnancies which may not be representative of cellular activity during early embryonic development. (Consumer Summary produced by Reliance Medical Information, Inc.)

Pulmonary hypoplasia, the underdevelopment of fetal lung tissue, can cause fetal death. Within the uterus the fetus is surrounded by amniotic fluid. Although there are many factors predisposing the fetus to pulmonary hypoplasia, one theory suggests that an inadequate amount of amniotic fluid, oligohydramnios, is responsible. Pulmonary hypoplasia occurs because the uterine wall compresses the fetal chest which in turn compresses the lung tissue, inhibiting growth. This theory does not explain why tissue compression does not affect the development of other organs. Another theory explains that the pressure of the amniotic fluid, amniotic pressure, is decreased when the fluid volume is reduced; decreased amniotic pressure causes too much fluid to be lost from the fetal lungs. Pressure inside the small structures of the lungs must be greater than the amniotic pressure to promote growth and function. If that balance is upset, as in oligohydramnios, too much fluid escapes from the fetal lungs. To prevent this from happening the amniotic fluid volume must be increased by adding more fluid artificially. Amniotic fluid replacement was attempted in one pregnancy with oligohydramnios. Although the fetus died from other complications, the fetal lungs had no evidence of fetal lung hypoplasia.