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ORIGINAL RESEARCH |
From the Department of Obstetrics and Gynecology, Chaim Sheba Medical Center; and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer, Ramat Gan, Israel.
Address reprint requests to: Yaron Zalel, MD, The Chaim Sheba Medical Center, Tel-Hashomer, Department of Obstetrics and Gynecology, Ramat Gan 52621; E-mail: zalel_y{at}netvision.net.il.
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ABSTRACT |
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METHODS: The study is a prospective cohort evaluation of 430 singleton male and female fetuses between 20 and 40 weeks’ normal gestation. Abdominal ultrasonography and Doppler measurements were performed to measure the fetal atrial ventricular size and resistance index (RI) of the middle cerebral artery.
RESULTS: The mean (± standard deviation) ventricular width was 6.2 ± 1.2 mm. The modification in the RI of the middle cerebral artery throughout gestation showed a biphasic mode, increasing gradually to a peak at 30 weeks’ gestation and decreasing progressively thereafter. No significant correlation was found between the middle cerebral artery flow and the lateral cerebral ventricular width (r = .11). In addition to the 430 cases studied, three cases of mild ventriculomegaly and three cases of hydrocephalus were evaluated. The RI of the middle cerebral artery was within the normal range in all six of these cases.
CONCLUSION: Fetal middle cerebral artery blood flow is not affected by the width of the lateral ventricles, even in enlarged ventricles.
Sonographic evaluation of the fetal cerebral ventricles is one of the most diagnostically powerful and prognostically important features of the antepartum ultrasound examination.1 Abnormal ventricular size has been shown to be a useful marker for congenital infection, other central nervous system anomalies, and fetal aneuploidy.2
Doppler examination of fetal middle cerebral artery flow plays an important role in the monitoring of fetal well-being.3 Altered middle cerebral artery flow is associated with various fetal conditions, including asphyxia, twin-to-twin transfusion syndrome, anemia, and intracranial anomalies or hemorrhage.4
Reports on fetal intracerebral flow velocities in ventriculomegaly or hydrocephalus have been contradictory.5–7 Hypothetically, fetal ventricular enlargement, especially in the extreme cases of hydrocephalus, can cause elevation in the flow resistance index (RI) due to increased intracranial pressure. Alternatively, RI may increase through direct compression of the small branches of the middle cerebral artery, which supplies the lateral ventricle.
There is also a controversy regarding the change in middle cerebral artery impedance during gestation.8–14 Some investigators found decreasing resistance with advancing gestation,10,12,13 whereas others observed a peak around the beginning of the third trimester,8,9,14 and still others found no change with advancing gestation.11 The objective of the present prospective cohort study was therefore to evaluate a possible correlation between ventricular size and the flow resistance in the middle cerebral artery. In addition, we used the large database obtained to create reference values for middle cerebral artery blood flow throughout gestation.
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MATERIALS AND METHODS |
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During the follow-up period, eight cases had to be excluded: three cases of intrauterine growth retardation, three cases of pregnancy-induced hypertension/preeclampsia, and two cases of diabetes. In addition, three cases of ventriculomegaly and three cases with hydrocephalus were referred to our unit during the study period. Blood flow indices in the middle cerebral artery were measured in these six fetuses as well.
Measurements were performed during ultrasound examination performed to rule out malformations, as well as during routine third-trimester sonographic follow-up. Measurements of ventricular width, middle cerebral artery RI, and systolic-diastolic ratio (S/D) were obtained in all 430 fetuses. We could not obtain measurements in less than 1% of examinations owing to maternal obesity or fetal position. Each patient (fetus) was evaluated only once during the study. All cases were evaluated by a single examiner (YZ).
Ultrasonography was performed with an abdominal 3.5–5-MHz curvilinear transducer (Ultramark HDI 3000, ATL, Bothwell, WA). Freeze-frame ultrasound capabilities and electronic on-screen calipers were used for the measurements. Each measurement was repeated three times in each fetus, and the mean value was determined.
Ventricular width at the atria was measured at the level of the thalami just above the standard image used to measure biparietal diameter. The cursor was uniformly placed perpendicular to the falx, just touching the choroids plexus. To measure middle cerebral artery flow velocity, the transducer was moved toward the base of the skull to identify the circle of Willis. At this plane the middle cerebral artery is easily distinguishable from the internal carotid and the anterior cerebral arteries. After localization of the middle cerebral artery, Doppler flow velocity was measured at the middle third of the middle cerebral artery, away from the internal carotid and anterior cerebral arteries. Multiple waveform recordings were obtained using pulsed-waved Doppler. Averaged S/D and RI were calculated. Resistance index was calculated according to the following formula: (S–D)/S.
Results are given as mean ± standard deviation (SD). According to power analysis, 200 cases were the estimated minimum number of subjects required to identify a correlation coefficient of 0.2 as significant (at 
of 5% and 90% power). Owing to possible nonlinear (biphasic) association, we have considered twice as many as the minimum.
Linear regression of atrial width and second-order polynomial regression equation of RI on gestational age were calculated. Means, 95% confidence interval (CI) of the ventricular width, and the RI for consecutive gestational ages were calculated. Differences between normal fetuses and those with ventriculomegaly were assessed using the nonparametric Mann-Whitney test. All data processing was performed by SPSS for Windows 9.0 (SPSS, Chicago, IL) and a P value of 5% or less was considered statistically significant.
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RESULTS |
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The mean ± SD of the ventricular width was 6.2 ± 1.2 mm. The ventricular width showed an upward trend throughout gestation. The intraobserver variability, as determined by coefficient of variation, was 2.2%.
Table 1
presents the mean, SD, and 95% CI of the RI for consecutive gestational ages from 20 to 40 weeks.
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presents a scatter plot of the mean middle cerebral artery RI in relation to gestational age (weeks). The trend of RI in the fetal middle cerebral artery throughout gestation was biphasic, increasing to a peak at 30 weeks’ gestation and decreasing progressively thereafter. Resistance index as a function of gestational age was expressed by the following second-order polynomial regression equation: RI = 0.2497 + 0.0358 x GA - 0.0006 x GA2, where GA = gestational age. This equation was found to be highly statistically significant (P < .001).
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shows the middle cerebral artery indices in relation to ventricular size. No statistically significant correlation was found between the middle cerebral artery flow and the cerebral lateral ventricular width (r = .11).
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DISCUSSION |
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Accordingly, antenatal studies have been performed investigating a possible correlation between fetal ventriculomegaly or hydrocephalus and cerebral blood flow. These studies have yielded contradictory findings.5–7 Some investigators found high resistance for the cerebral blood flow in some cases of hydrocephalus,6,7 whereas others obtained normal results.5 One possible mechanism explaining the disturbed cerebral blood flow in cases of ventriculomegaly could be previously undiagnosed intracranial hemorrhage. It is well recognized that cerebral ventriculomegaly can be a secondary phenomenon following a hemorrhagic accident. Previous studies18,19 have shown high resistance in cerebral blood flow in such cases. Therefore, cerebral blood flow abnormalities can persist even after a resolved hemorrhagic event, leaving ventriculomegaly as the sole sonographic finding. A second possible mechanism is that the lateral ventricles lie in the middle cerebral artery distribution area, and thus locally increased pressure on small blood vessels by the expanding ventricle could increase the RI without substantially increasing the intracranial pressure.
In the present study, we did not find any correlation between the size of the ventricle and disturbance in the cerebral blood flow. Moreover, no significant change in the middle cerebral artery indices was found even in the six cases of ventriculomegaly or hydrocephalus. The discrepancy between the findings of fetal and newborn hydrocephalus may be explained by the lower rigidity and higher compliance of the fetal skull. Whether fetal hydrocephalus does not elevate the intracranial pressure is a matter for further investigation. Future studies should also avoid the limitation of our study, namely its being cross-sectional in nature rather than a longitudinal follow-up.
Controversy exists regarding the change in middle cerebral artery impedance during gestation. Mari et al8,9 and Hsieh et al14 demonstrated a lower middle cerebral artery pulsatility index (PI) in the early second trimester and late third trimester, with the highest PI value at around 28 or 30 weeks’ gestation. Other investigators have demonstrated that the PI values of the proximal and distal middle cerebral artery or the S/D decreased progressively with advancing gestational age.10,12,13 In contrast, Veille et al11 showed that the PI and RI values did not change significantly with advancing gestation. In this series, we observed a significant increase in middle cerebral artery RI values between 20 and 30 weeks’ gestation. We also concur with the observations of Mari et al,8,9 Locci et al,10 and Hsieh et al14 in demonstrating a decrease in PI/RI values of middle cerebral artery after 30 weeks’ gestation. The decrease in RI may reflect the increased cellular multiplication, oxygenation, metabolism, and deoxyribonucleic acid synthesis in the fetal brain during the third trimester.9
We conclude that, according to our series, there is no change in the middle cerebral artery blood flow in correlation with the ventricular width. It appears that the increase in the ventricular size does not alter cerebral blood flow, in contrast to observations made in the newborn. Further investigation of cerebral blood flow in the hydrocephalic fetus is warranted.
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Footnotes |
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Received March 4, 2002. Received in revised form May 18, 2002. Accepted May 30, 2002.
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REFERENCES |
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2. Kramer RL, Yaron Y, Johnson MP, Evans MI, Treadwell MC, Wolfe HM. Differences in measurements of the atria of the lateral ventricle: Does gender matter? Fetal Diagn Ther 1997;12:304–5.[Medline]
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18. Achiron R, Pinchas OH, Reichman B, Heyman Z, Schimmel M, Eidelman A, et al. Fetal intracranial haemorrhage: Clinical significance of in utero ultrasonographic diagnosis. Br J Obstet Gynaecol 1993;100:995–9.[Medline]
19. Hadi HA, Finley J, Mallette JQ, Strickland D. Prenatal diagnosis of cerebellar hemorrhage: Medicolegal implications. Am J Obstet Gynecol 1994;170:1392–5.[Medline]
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