The association of maternal glucose values and fetal macrosomia was limited to the fasting glucose values between 32-35 weeks while maternal obesity appeared to be a strong risk factor for macrosomia throughout pregnancies with GDM. In obese women the high fetal macrosomia rate did not appear be normalized by therapy based on maternal euglycemia.

OBJECTIVE -To determine maternal parameters with the strongest influence on fetal growth in different periods of pregnancies complicated by an abnormal glucose tolerance test (GTT).RESEARCH DESIGN AND METHODS -Retrospective study of 368 women with gestational diabetes mellitus (GDM; Ն2 abnormal GTT values, n ϭ 280) and impaired glucose tolerance (IGT; one abnormal value, n ϭ 88) with 869 ultrasound examinations at entry to and during diabetic care. Both groups were managed comparably. Abdominal circumference (AC) Ն90th percentile defined fetal macrosomia. Maternal historical and clinical parameters, and diagnostic and glycemic values of glucose profiles divided into five categories of 4 weeks of gestational age (GA; Ͻ24 weeks, 24 weeks/0 days to 27 weeks/6 days, 28/0 -31/6, 32/0 -35/6, and 36/0 -40/0 [referred to as Ͻ24 GA, 24 GA, 28 GA, 32 GA, and 36 GA categories, respectively]) were tested by univariate and multiple logistic regression analysis for their ability to predict an AC Ն90th percentile at each GA group and large-for-gestational-age (LGA) newborn. Data obtained at entry were also analyzed separately irrespective of the GA.RESULTS -Maternal weight, glycemia after therapy, rates of fetal macrosomia, and LGA were not significantly different between GDM and IGT; thus, both groups were analyzed together.LGA in a previous pregnancy, (odds ratio [OR] 3.6; 95% CI 1.8 -7.3) and prepregnancy obesity (BMI Ն30 kg/m 2 ; 2.1; 1.2-3.7) independently predicted AC Ն90th percentile at entry. When data for each GA category were analyzed, no predictors were found for Ͻ24 GA. Independent predictors for each subsequent GA category were as follows: at 24 GA, LGA history (OR 9.8); at 28 GA, LGA history (OR 4.2), and obesity (OR 3.3); at 32 GA, fasting glucose of 32 GA (OR 1.6 per 5-mg/dl increase); at 36 GA, fasting glucose of 32 GA (OR 1.6); and for LGA at birth, LGA history (OR 2.7), and obesity (OR 2.4).CONCLUSIONS -In the late second and early third trimester, maternal BMI and LGA in a previous pregnancy appear to have the strongest influence on fetal growth, while later in the third trimester coincident with the period of maximum growth described in diabetic pregnancies, maternal glycemia predominates.

ABSTRACT

Critical fetal organs are preferentially supplied with oxygenated blood from the umbilical vein (UV) by way of the ductus venosus (DV). Under normal conditions a significant part of UV-blood flows steadily forward through the left portal vein (LPV). Blood flow through the LPV could reverse, however, in cases of absent or reversed endodiastolic flow in the umbilical arteries. We tested when fetal blood flow reversal occurs by studying 28 cases with pathological flow in the umbilical artery. In the LPV we observed normal nonpulsatile forward flow in 9 cases, pulsatile forward flow in 10 cases, and reversed flow in 9 cases. Reverse flow in the LPV correlated significantly with an elevated resistance index of the umbilical arteries. This reversal could have major physiological implications: Deoxygenated blood may be added via the LPV to the blood shifted through the DV and ultimately reach critical fetal organs. In extremis there could be a waterhose effect, whereby more blood flows through the DV than the UV that supplies it. The LPV is thus the watershed of the venous circulation of the fetus.

In this study we compared the distribution of blood flow to the liver in growth-retarded fetuses whose estimated weight was < 5th centile with normal-weight fetuses. As expected, the relative venous blood flow to the liver was reduced, with blood flowing preferentially through the ductus venosus. However, the total blood supply seemed to be maintained by a concomitant, significant increase in arterial blood flow through the hepatic artery. Absolute flow velocities such as the peak, minimum diastolic and temporal average velocities were changed, as was the flow waveform. Effectively, the deficiency in venous supply was made up for by an increase in arterial blood flow. This compensatory effect may be crucial for maintaining liver function in times of low portal venous blood supply. It thus makes sense to regard the liver as the fourth preferential organ for arterial blood supply in the compromised fetus, besides heart, brain, and adrenals.