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ORIGINAL RESEARCH |
From the Department of Obstetrics and Gynecology, University of Brescia, Brescia, Italy.
Address reprint requests to: Tiziana Frusca, Department of Obstetrics and Gynecology, University of Brescia, Piazzale Spedali Civili 1, 25100 Brescia, Italy; E-mail: tifrusca{at}tin.it.
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ABSTRACT |
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METHODS: A retrospective study was conducted on 344 hypertensive pregnant women who underwent uterine artery Doppler investigation. Patients were classified as either preeclamptic or with gestational hypertension at follow-up 2 months after delivery. Pregnancy outcomes of patients with preeclampsia and gestational hypertension were correlated to uterine artery velocimetry. A further analysis was done dividing patients into mild and severe groups.
RESULTS: An abnormal uterine Doppler was related to a significantly earlier week of delivery (32.5 versus 35.3 in preeclampsia, 33.6 versus 38.1 in gestational hypertension), a lower mean birth weight (1494 g versus 2320 g in preeclampsia, 1690 g versus 2848 g in gestational hypertension), and a higher number of growth-restricted fetuses (70% versus 23% in preeclampsia, 75% versus 20% in gestational hypertension). In both mild and severe hypertensive groups, abnormal uterine velocimetry was associated with a worse pregnancy outcome (delivery at week 33.1, versus 37.9 in the mild group; 32.7 versus 37.3 in the severe group; birth weight 1574 g versus 2741 g in the mild group; 1539 g versus 2742 g in the severe group). A multivariable analysis of the presence of proteinuria, severity of hypertension, and uterine Doppler revealed that only an abnormal uterine Doppler was significantly related to adverse perinatal outcome (P < .001)
CONCLUSION: Abnormal uterine Doppler was the variable that was more frequently associated with adverse pregnancy outcome.
Hypertension in pregnancy is associated with a high rate of adverse perinatal outcomes, particularly if significant proteinuria and severe hypertension are present.1,2 A better outcome of pregnancy has generally been reported with gestational hypertension without proteinuria.3 More recently, maternal and fetal complications have been reported in patients without proteinuria but with severe gestational hypertension, suggesting that in these patients intensive prenatal surveillance is as necessary as in patients with preeclampsia.4–6
Abnormal uterine artery velocimetry has been related to the lack or the incomplete development of physiologic changes in the spiral arteries of the placental bed by various authors.7,8 Abnormal uterine artery velocimetry has also been shown to identify pregnancies at risk for growth-restricted fetuses and preeclampsia.9–14
The purpose of this study was to evaluate whether abnormal uterine artery velocimetry in gestational hypertension is more predictive of pregnancy outcome than the presence of proteinuria and the severity of hypertension.
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MATERIALS AND METHODS |
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Hypertension was defined either as mild or as severe based on diastolic blood pressure (mild diastolic blood pressure less than 110, severe at least 110 mm Hg). Exclusion criteria were gestational age at admission of greater than 37 weeks, chronic hypertension, renal disease, twin gestation, and associated medical or obstetric complications. Uterine artery velocimetry investigation was performed at admission by means of a color Doppler PowerVision 6000 (Toshiba Corp., Tokyo, Japan) using a 3.5–5-MHz transabdominal transducer.
Patients were examined in a semirecumbent position. The recording was performed at the apparent crossover point of the uterine and external iliac arteries, after identification of the main uterine artery on a longitudinal scan lateral to the uterus. The resistance index for each uterine artery was obtained by averaging the value of three consecutive waveforms. The average resistance index from the left and right uterine arteries was then calculated. The presence of an early diastolic notch on both sides of the uterine artery waveforms was also recorded. Resistance index values greater than 0.62 and/or the presence of a bilateral diastolic notch in the waveform profile were defined as an abnormal uterine artery velocimetric pattern. This cutoff corresponds to two standard deviations from the normal range from 20 to 37 weeks of our population. Doppler ultrasound findings of uterine artery velocimetry were masked from the consulting physician.
Maternal monitoring included blood pressure measurements (six times a day) and daily assessment of proteinuria; platelets, hematocrit, uric acid, and liver enzymes were checked twice a week. None of the patients were on antihypertensive drugs at the time of the first Doppler evaluation. Oral nifedipine (30–120 mg per day) was given if diastolic blood pressure exceeded 100 mm Hg.
Fetal monitoring included ultrasound examination for fetal biometry, amniotic fluid index, Doppler umbilical artery investigation, and nonstress test. Intrauterine growth restriction was defined when the fetal abdominal circumference was below the second standard deviation in accordance with our referral curve.16 Abnormal umbilical artery velocimetry results were defined by a pulsatility index of more than two standard deviations of our reference curve for gestational age.
After initial clinical evaluation, patients were observed at the outpatient clinic for absent proteinuria, reactive nonstress test, and normal umbilical artery velocimetry. When proteinuria was present, patients were kept under observation in the hospital.
The following outcomes were analyzed: week at delivery, neonatal weight, number of newborns with very low birth weight (less than 1500 g), number of growth-restricted fetuses, number of elective preterm deliveries at less than 34 weeks, and number of patients with abnormal umbilical artery Doppler velocimetry.
Poor pregnancy outcome was defined as the presence of growth-restricted fetuses and/or elective delivery at less than 34 weeks for maternal or fetal indication.
Pregnancy outcomes were analyzed on the basis of the presence of proteinuria (preeclampsia versus gestational hypertension) and on the basis of severity of hypertension (mild hypertension and severe hypertension), with or without proteinuria. Outcomes were subsequently evaluated in relation to uterine artery velocimetry in preeclampsia and gestational hypertension groups and in mild hypertension and severe hypertension groups.
A further statistical analysis was performed to verify which variable was more frequently associated with poor pregnancy outcomes. The following variables were considered for the study: absence or presence of significant proteinuria, mild or severe hypertension, and normal or abnormal uterine artery velocimetry.
Statistical analysis included the 
2 test to compare proportions and the nonpaired Student t test to compare continuous variables. Logistic regression was used for multivariable analysis. P values less than .05 were considered statistically significant.
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RESULTS |
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Preeclampsia was diagnosed and confirmed in 186 patients, whereas gestational hypertension was diagnosed in 158 patients. Clinical characteristics and pregnancy outcomes of the two groups are shown in Table 1
. The outcome in patients with preeclampsia was worse than the one in patients with gestational hypertension: Gestational age at delivery, mean birth weight, numbers of very low birth weight infants, and preterm deliveries at less than 34 weeks significantly differed.
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). The outcomes in patients with gestational hypertension and abnormal uterine artery velocimetry (n = 71) did not significantly differ from the outcomes in patients with preeclampsia (Table 3).
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. However, an abnormal uterine artery velocimetry identified a worse pregnancy outcome in both groups (Table 5).
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Multivariable analysis performed in the presence or absence of proteinuria, mild or severe hypertension, and normal or abnormal uterine artery velocimetry revealed that only abnormal uterine artery velocimetry was significantly associated with poor fetomaternal outcome (Table 6).
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DISCUSSION |
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In accordance with other studies, patients with hypertension without proteinuria showed better outcomes than patients with preeclampsia.
Ferrazzani et al2 reported the outcomes of pregnancy in 444 women with preeclampsia, nonproteinuric gestational hypertension, and chronic hypertension. In comparison with patients without proteinuria, preeclamptic patients showed a significantly earlier week at delivery (35.3 versus 38.6); lower birth weight (1997 versus 2922 g); and higher rates of preterm delivery (58% versus 10%), small for gestational age infants (52% versus 18%), and perinatal death (13% versus 3%). Moreover, the appearance of proteinuria in patients with chronic hypertension increased the risk of adverse perinatal outcome as in patients with pregnancy-induced hypertension.
Gofton et al3 retrospectively reviewed the maternal and neonatal outcomes of 1331 term (37–41 weeks) hypertensive pregnant women versus a control group. They found that in patients with gestational hypertension without proteinuria, although the rate of induction of labor and cesarean delivery was high, the fetoneonatal outcome was similar to that of control normotensive subjects. Only patients with preeclampsia and chronic hypertension delivered infants with lower birth weights and a higher rate of birth weight less than 2500 g than normotensive patients.
Brown and Buddle4 found a higher prevalence of maternal and fetal complications in hypertensive women with proteinuria than in women without, but even in this last group of patients they noted a significantly higher risk of maternal complications relative to controls (4–13%). The authors concluded that nonproteinuric hypertension should not always be considered a benign condition. Intensive patient surveillance is thus required not only in preeclamptic patients but also in patients with gestational hypertension.
In our study we further demonstrated that patients with gestational hypertension without proteinuria but with abnormal uterine artery velocimetry have pregnancy outcomes that do not differ significantly from the outcomes of preeclamptic patients, in terms of week at delivery, birth weight, and frequency of growth-restricted fetuses.
Other studies reported a high rate of maternal and fetal complications in subgroups of patients with gestational hypertension and no proteinuria, but the severity of hypertension was considered the important variable related to the outcome of pregnancy1 in these studies (Sibai et al5). In our study the severity of hypertension did not correlate with any significant difference in the outcomes. In both groups (mild and severe hypertension), the presence of abnormal uterine artery velocimetry identified patients with the worst outcomes. Moreover, the abnormality of uterine artery velocimetry was the only variable to be significantly associated with poor pregnancy outcome in a multivariable analysis.
Our results support the use of a simple and noninvasive technique such as uterine artery Doppler investigation in the management of hypertension in pregnancy, either with or without proteinuria, to help identify patients who need more intensive maternal–fetal surveillance.
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Footnotes |
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Received September 9, 2002. Received in revised form January 15, 2003. Accepted January 23, 2003.
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REFERENCES |
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2. Ferrazzani S, Caruso A, De Carolis S, Vercillo Martino I, Mancuso S. Proteinuria and outcome of 444 pregnancies complicated by hypertension. Am J Obstet Gynecol 1990; 162:366–71.[Medline]
3. Gofton EN, Capewell V, Natale R, Gratton RJ. Obstetrical intervention rates and maternal and neonatal outcomes of women with gestational hypertension. Am J Obstet Gynecol 2001;185:798–803.[Medline]
4. Brown MA, Buddle ML. The importance of nonproteinuric hypertension in pregnancy. Hypertens Pregnancy 1995;14:57–65.
5. Buchbinder A, Sibai BM, Caritis S, MacPherson C, Hauth J, Lindheimer MD, et al. Adverse perinatal outcomes are significantly higher in severe gestational hypertension than in mild preeclampsia. Am J Obstet Gynecol 2002;186: 66–71.[Medline]
6. North RA, Taylor RS, Shellemberg JC. Evaluation of a definition of preeclampsia. Br J Obstet Gynaecol 1999; 106:767–73.[Medline]
7. Iwata M, Matsuzaki N, Shimizu I, Mitsuda N, Nakayama M, Suehara N. Prenatal detection of ischemic changes in the placenta of the growth-retarded fetuses by Doppler flow velocimetry of the maternal uterine artery. Obstet Gynecol 1993;82:494–9.[Medline]
8. Lin S, Shimizu I, Suehara N, Nakayama M, Aono T. Uterine artery Doppler velocimetry in relation to trophoblast migration into the myometrium of the placental bed. Obstet Gynecol 1995;85:760–5.[Abstract]
9. Valensise H, Bezzeccheri V, Rizzo G, Tranquilli AL, Garzetti G, Romanini C. Doppler velocimetry of the uterine artery as a screening test for gestational hypertension. Ultrasound Obstet Gynecol 1993;3:18–22.[Medline]
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11. Bewley S, Cooper D, Campbell S. Doppler investigation of uteroplacental blood flow resistance in the second trimester: A screening study for preeclampsia and intrauterine growth retardation. Br J Obstet Gynaecol 1991;98:871–9.[Medline]
12. Albaiges G, Missfelder-Lobos H, Lees C, Parra M, Nicolaides KH. One-stage screening for pregnancy complications by color Doppler assessment of uterine arteries at 23 weeks’ gestation. Obstet Gynecol 2000;96:559–64.
13. Papageorghiou AT, Yu CKH, Bindra R, Nicolaides KH. Multicenter screening for pre-eclampsia and fetal growth restriction by transvaginal uterine artery Doppler at 23 weeks of gestation. Ultrasound Obstet Gynecol 2001;18: 441–9.[Medline]
14. Frusca T, Soregaroli M, Zanelli S, Danti L, Guandalini F, Valcamonico A. Role of uterine artery doppler investigation in pregnant women with chronic hypertension. Eur J Obstet Gynecol Reprod Biol 1998;79:47–50.[Medline]
15. National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol 2002;183:S1–22.
16. Nicolini U, Todros T, Ferrazzi E, Zorzoli A, Groli C, Zucca S, et al. Curve trasversali dell’accrescimento fetale. Studio multicentrico. Minerva Ginecol 1986;38:873.[Medline]
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