Acute reversible placental dysfunction and abnormal fetal heart rate at delivery.

UNLABELLED: Acute placental dysfunction induced by malaria is characterized by umbilical artery resistance increase and cerebral artery resistance decrease during the crisis. The objective was to evaluate the sensitivity and specificity of fetal Doppler indices and crisis duration for predicting abnormal fetal heart rate (aFHR) at delivery several weeks after the crisis. METHOD: Every day during the crisis, the umbilical and cerebral resistance indices were measured by Doppler. These indices allowed evaluation of the amplitude of the fetal flow redistribution (C/U = cerebral resistance/umbilical resistance ratio), the duration of the flow redistribution period (i.e. crisis duration) and the Hypoxic index (HI) (mean %C/U change x crisis duration). POPULATION: 46 pregnancies. Mean duration of the flow redistribution period 8+/-3.2 days, mean C/U change -9%+/-6; Hypoxic index -86+/-75; prematures 48%; aFHR 30%). Hypoxic index >150 predicted occurrence of aFHR with high sensitivity and specificity (83%/88%). The presence of abnormal flow distribution (C/U<1.1) and the duration of the period with flow disturbance (>8 days) predicted aFHR at delivery with a sensitivity of 45 and 48% and a specificity of 82 and 84%. CONCLUSION: The Hypoxic index was more predictive of aFHR at delivery than the amplitude or the duration of the fetal flow redistribution triggered by placental insufficiency.

Doppler assessment of the fetal cerebral hemodynamic response to moderate or severe maternal anemia.

OBJECTIVE: The purpose of this study was to evaluate the fetal vascular adaptation to moderate and severe maternal anemia. STUDY DESIGN: Biometry; amniotic fluid index; uterine, cerebral, and umbilical Doppler; and maternal hemoglobin level were measured at admission and 8 days after treatment. RESULTS: Group 1 consisted of 16 pregnancies (maternal hemoglobin level, 6.9 +/- 0.6 g/100 mL); group 2 consisted of 23 pregnancies (maternal hemoglobin level, 5 +/- 0.6 g/100 mL). At admission the cerebral and cerebral/umbilical Doppler indexes, amniotic index, and biometry were lower in group 2. The uterine index was normal in both groups. An abnormal fetal heart rate was found in group 2 only (48%). At day 8, maternal hemoglobin level and amniotic index increased more in group 2 than in group 1. The cerebral index and the cerebral-to-umbilical resistance ratio increased only in group 2. The abnormal fetal heart rate disappeared in group 2. CONCLUSION: Only severe maternal anemia (maternal hemoglobin level, <6 mg/L) triggered fetal cerebral vasodilation and reduced amniotic volume.

Fetal flow redistribution to the brain in response to malaria infection: does protection of the fetus against malaria develop over time?

OBJECTIVE: Malaria during pregnancy induces deterioration of placental function, resulting in transient fetal hypoxia. Our objective was to evaluate the sensitivity and specificity of fetal Doppler indices for prediction of abnormal fetal heart rate at delivery and to compare the amplitude of the fetal vascular response to malaria in 2 groups of fetuses (1994 and 1996) separated by an interval of 2 years. METHODS: Every day during the crisis, the umbilical and cerebral resistance indices, the cerebral-umbilical resistance ratio, and the hypoxic index (mean percent cerebral-umbilical resistance ratio change x crisis duration) were calculated. RESULTS: In group 2 (1996), the duration of the flow redistribution period was about 7 days (mean cerebral-umbilical resistance ratio change +/- SD, 7%+/-4%; hypoxic index, 49+/-26; premature, 35%; and abnormal fetal heart rate, 17.5%). A hypoxic index greater than 150 predicted abnormal fetal heart rate with high sensitivity and specificity (group 1, 80% and 85%; and group 2, 100% and 91 %). Moreover, in group 2 (1996), the amplitude of the fetal vascular response and the rate of long-duration crisis were significantly lower than in group 1 (1994; P < .01). Nevertheless, the hypoxic index was much more predictive of fetal heart rate at delivery than the amplitude or duration (i.e., crisis duration) of the flow redistribution. CONCLUSIONS: The hypoxic index value during the crisis allowed prediction of abnormal fetal heart rate at delivery. In group 2, the absence of a long-term flow redistribution period and the smaller hemodynamic changes (lower hypoxic index) associated with a lower occurrence of abnormal fetal heart rate could be related to improvement of pregnancy management, acquired protection during the interval between the 2 studies, or both.