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Research Article | Volume 15 Issue 11 (November, 2025) | Pages 348 - 353
Evaluation of Uterine Artery Doppler (Mean Pulsatility Index) at 11–14 Weeks of Gestation in Primigravida Women of Singleton Pregnancy as a Predictor of Preeclampsia: A Prospective Cohort Study
 ,
 ,
 ,
1
PGT 3, Tezpur Medical College and Hospital
2
Associate Professor, Tezpur Medical College and Hospital
3
Assistant Professor, Tezpur Medical College and Hospital
4
Professor and HOD, Department of Obstetrics and Gynaecology, Tezpur Medical College and Hospital
Under a Creative Commons license
Open Access
Received
Oct. 16, 2025
Revised
Oct. 30, 2025
Accepted
Nov. 12, 2025
Published
Nov. 20, 2025
Abstract

Hypertensive disorders of pregnancy (HDP), particularly preeclampsia, remain among the leading causes of maternal and perinatal morbidity and mortality globally. Early identification of women at risk allows preventive interventions such as low-dose aspirin therapy and closer surveillance. Uterine artery Doppler velocimetry in the first trimester provides a non-invasive assessment of uteroplacental circulation and may help predict preeclampsia before clinical onset. Abnormal uterine artery pulsatility index (PI) reflects impaired trophoblastic invasion and high vascular resistance, which precede the development of HDP and adverse perinatal outcomes. Aim: To evaluate the predictive value of mean uterine artery PI measured at 11–14 weeks of gestation in primigravida women with singleton pregnancies for the development of hypertensive disorders of pregnancy and adverse perinatal outcomes. Materials and Methods: A prospective cohort study was conducted on 75 primigravida women with singleton pregnancies between 11–14 weeks of gestation attending the antenatal clinic of a Tezpur Medical College and Hospital. Mean uterine artery PI was measured by transabdominal color Doppler ultrasonography. Participants were followed up till delivery and 7 days postpartum. Based on Doppler results, women were categorized into normal PI (≤95th percentile) and abnormal PI (>95th percentile) groups. The primary outcome was the development of HDP, and secondary outcomes included preterm delivery, intrauterine growth restriction (IUGR), mode of delivery, NICU admission, and perinatal mortality. Data were analyzed using the Chi-square test for categorical variables and independent t-test for continuous variables. A p-value <0.05 was considered statistically significant. Results: Out of 75 par0ticipants, 15 (20%) had abnormal mean uterine artery PI. Preeclampsia developed in 33.3% of women with abnormal PI compared to 6.6% with normal PI (p<0.01). The abnormal PI group also showed significantly higher rates of preterm delivery (33.3% vs. 10%; p=0.04), IUGR (26.6% vs. 8.3%; p=0.045), and NICU admissions (26.6% vs. 11.6%; p=0.05). Mean birth weight was significantly lower in the abnormal PI group (2.41 ± 0.42 kg) than in the normal PI group (2.87 ± 0.36 kg). No significant difference was found in mode of delivery or perinatal mortality. Discussion: Abnormal uterine artery PI in early pregnancy was strongly associated with subsequent HDP and adverse perinatal outcomes, supporting its role as an early screening marker of placental insufficiency. These findings are consistent with those of Papageorghiou et al. [9], Gómez et al. [10], and Plasencia et al. [12], who reported significantly higher rates of preeclampsia and IUGR among women with elevated first-trimester uterine artery PI. In accordance with the ASPRE trial by O’Gorman et al. [14] and recommendations by WHO and ACOG [15,17], early identification of at-risk women can guide the initiation of low-dose aspirin prophylaxis before 16 weeks to reduce the incidence of preeclampsia and its complications. Conclusion: Mean uterine artery PI measured at 11–14 weeks of gestation is a significant early predictor of preeclampsia and adverse perinatal outcomes. Incorporating first-trimester uterine artery Doppler screening into routine antenatal care can enable early risk stratification, timely prophylaxis, and improved maternal and neonatal outcomes, particularly in primigravida women

Keywords
INTRODUCTION

Hypertensive disorders of pregnancy (HDP), particularly preeclampsia, continue to be a major cause of maternal and perinatal morbidity and mortality worldwide, especially in low- and middle-income countries where early screening and preventive strategies are often lacking [1,2]. Preeclampsia, classically defined by new-onset hypertension and proteinuria after 20 weeks of gestation, affects approximately 5–8% of pregnancies globally and contributes to nearly 15% of maternal deaths [3,4]. The condition results from abnormal placentation and inadequate trophoblastic invasion of spiral arteries, leading to high resistance and reduced uteroplacental perfusion [5]. This impaired placental perfusion triggers systemic endothelial dysfunction, resulting in hypertension, proteinuria, and multi-organ involvement [6].

Given that the clinical manifestations of preeclampsia appear only in the latter half of pregnancy, early detection of placental insufficiency during the first trimester can provide a critical window for timely intervention [7]. Among the various non-invasive methods proposed for early prediction, uterine artery Doppler velocimetry has emerged as a reliable and reproducible tool for assessing uteroplacental blood flow resistance [8]. The mean pulsatility index (PI), calculated as the average of left and right uterine artery PIs, reflects downstream impedance to blood flow. Elevated PI values during early gestation indicate poor trophoblastic remodeling and correlate with the subsequent development of preeclampsia and fetal growth restriction [9,10].

Previous studies have demonstrated that women with abnormal uterine artery PI in the first trimester are at a significantly higher risk of developing HDP and adverse perinatal outcomes [11]. Gómez et al. reported that a mean PI above the 95th percentile at 11–14 weeks was associated with a threefold increase in the risk of preeclampsia [12]. Similarly, Plasencia et al. found that abnormal Doppler indices in early gestation were linked to preterm preeclampsia and small-for-gestational-age neonates [13].

Early identification of women at high risk allows the implementation of preventive interventions such as low-dose aspirin initiated before 16 weeks of gestation. Moreover, uterine artery Doppler abnormalities not only predict preeclampsia but are also associated with an increased likelihood of preterm birth, intrauterine growth restriction (IUGR), and perinatal mortality [18].

Considering the higher prevalence of hypertensive disorders and limited access to advanced biochemical screening, evaluating the utility of mean uterine artery PI during 11–14 weeks in Indian primigravida women is particularly relevant [19]. Therefore, this study aims to assess whether mean uterine artery PI in the first trimester can effectively predict the development of preeclampsia and other adverse perinatal outcomes, thereby facilitating timely preventive strategies and improved maternal-fetal prognosis.

MATERIALS AND METHODS
  1. Study Design

This study was designed as a prospective cohort study. All eligible primigravida women with singleton pregnancies between 11–14 weeks of gestation were recruited and followed prospectively from the first trimester until delivery and 7 days postpartum. The primary objective was to determine whether mean uterine artery pulsatility index (PI) measured in the first trimester could predict the development of hypertensive disorders of pregnancy and associated adverse perinatal outcomes.

 

  1. Study Setting

The study was conducted in the Department of Obstetrics and Gynaecology, at Tezpur Medical College And Hospital and the Doppler studies were performed in the Radiology department using high-resolution ultrasound machines with color and spectral Doppler capabilities. Deliveries and follow-up of participants were carried out in the same institution, ensuring uniformity of management and data completeness.

 

  1. Study Duration

The study was carried out over a period of 12 months, from May 2024 to May 2025 which included patient recruitment, ultrasound examinations, antenatal follow-up, delivery, and postnatal monitoring up to 7 days after childbirth.

 

  1. Participants

Inclusion Criteria

  1. Primigravida women with a singleton live intrauterine pregnancy confirmed by ultrasonography.
  2. Gestational age between 11 and 14 weeks.
  3. Women willing to provide written informed consent and comply with follow-up protocols.

Exclusion Criteria

  1. Multiple gestations.
  2. Known chronic hypertension, diabetes mellitus, renal disease, or autoimmune disorders.
  3. Structural uterine anomalies or fibroids distorting uterine blood flow.
  4. History of smoking, alcohol intake, or drug abuse.
  5. Congenital fetal anomalies detected on subsequent scans.
  6. Patients lost to follow-up or with incomplete outcome data.

 

  1. Study Sampling

A non-probability consecutive sampling technique was employed. All eligible women attending the antenatal clinic during the study period who fulfilled the inclusion criteria and provided consent were enrolled sequentially until the required sample size was reached.

 

  1. Study Sample Size

The sample size was calculated based on previous literature indicating an approximate 20–25% prevalence of abnormal uterine artery PI in early pregnancy and a predicted preeclampsia incidence of 30% in that subgroup. Using a 95% confidence interval and 10% allowable error, the minimum required sample size was computed as 75 participants, which was achieved in this study.

 

  1. Study Groups

After Doppler assessment, participants were categorized into two groups based on the mean uterine artery PI values:

  • Group A (Normal PI): Mean PI ≤95th percentile for gestational age.
  • Group B (Abnormal PI): Mean PI >95th percentile for gestational age.
    The subsequent occurrence of hypertensive disorders and perinatal outcomes were compared between the two groups.
  1. Study Parameters

The main parameters assessed were:

  • Mean uterine artery PI at 11–14 weeks.
  • Maternal outcomes: development of gestational hypertension, preeclampsia, and mode of delivery.
  • Fetal and perinatal outcomes: preterm delivery (<37 weeks), intrauterine growth restriction (IUGR), birth weight, NICU admission, and pmn bvcxerinatal mortality.

 

  1. Study Procedure

Each participant underwent a detailed history and clinical examination at recruitment. Gestational age was confirmed by ultrasonography. Uterine artery Doppler studies were performed transabdominally using a 3.5–5 MHz curvilinear probe. The uterine arteries were identified at the level of the internal cervical os, and flow velocity waveforms were obtained at an insonation angle of <30°. Three uniform waveforms were recorded, and the mean PI was automatically calculated from both arteries. Abnormal mean PI was defined as a value above the 95th percentile for gestational age. Participants were followed at routine antenatal visits and at delivery for occurrence of preeclampsia and other complications.

 

  1. Study Data Collection

All relevant data including demographic profile, obstetric history, mean uterine artery PI, blood pressure recordings, gestational age at delivery, birth weight, and neonatal outcomes were recorded in a structured case record form (CRF). Data were cross-verified with hospital records to ensure accuracy.

 

  1. Data Analysis

The collected data were entered into Microsoft Excel and analyzed using Statistical Package for the Social Sciences (SPSS) version 25.0. Continuous variables were expressed as mean ± standard deviation (SD) and compared using the independent t-test. Categorical variables were presented as frequencies and percentages and compared using the Chi-square test or Fisher’s exact test where applicable. A p-value <0.05 was considered statistically significant.

 

  1. Ethical Considerations

The study protocol was reviewed and approved by the Institutional Ethics Committee prior to commencement. Written informed consent was obtained from all participants and confidentiality of patient information was strictly maintained

RESULT

A total of 75 primigravida women with singleton pregnancies were enrolled and followed up from 11–14 weeks of gestation until delivery and the early postpartum period. The results have been analyzed under the following headings.

 

Table 1: Age Distribution of Study Population

Age Group (years)

 

Number of Participants (n=75)

Percentage (%)

18–20

10

13.3

21–25

34

45.3

26–30

22

29.3

>30

9

12.0

Mean ± SD (years)

24.9 ± 3.7

Interpretation

The mean maternal age was 24.9 years, indicating a relatively young cohort, which minimizes confounding due to age-related endothelial dysfunction. No significant correlation was found between age and incidence of preeclampsia (p>0.05).

 

Table 2: Distribution According to Mean Uterine Artery PI

Mean PI Value

Number (n=75)

Percentage (%)

≤ 95th percentile (Normal)

 

60

80.0

> 95th percentile (Abnormal)

15

20.0

Total

75

100.0

Interpretation:
Twenty percent of participants had an abnormal mean uterine artery PI (>95th percentile). This aligns with international data suggesting 15–25% of early pregnancies show high resistance flow patterns before placental remodeling. These women were closely followed for adverse outcomes.

 

Table 3: Comparison of Mean Uterine Artery PI between Groups

Parameter

Normal PI (n=60)

Abnormal PI (n=15)

p-value

Mean PI

1.65 ± 0.28

2.45 ± 0.32

<0.001**

Interpretation:
The mean uterine artery PI was significantly higher among women classified as abnormal (2.45 ± 0.32) compared to those with normal PI (1.65 ± 0.28), confirming a statistically significant difference (p<0.001).

 

Table 4: Incidence of Hypertensive Disorders of Pregnancy (HDP)

Outcome

Normal PI (n=60)

Abnormal PI (n=15)

Total (n=75)

p-value

Developed HDP

4 (6.6%)

5 (33.3%)

9 (12%)

0.009**

No HDP

56 (93.4%)

10 (66.7%)

66 (88%)

 

Interpretation:
 33.3% of women with abnormal PI developed hypertensive disorders compared to those with normal PI (6.6%), with p<0.01. This establishes the strong predictive role of high uterine artery resistance for future preeclampsia.

 

Table 5: Gestational Age at Delivery

Gestational Age (weeks)

Normal PI (n=60)

Abnormal PI (n=15)

p-value

<37 (Preterm)

6 (10.0%)

5 (33.3%)

0.04*

≥37 (Term)

54 (90.0%)

10 (66.7%)

 

Mean ± SD

38.4 ± 1.6

36.9 ± 1.8

 

Interpretation:
Preterm delivery occurred in 33.3% of women with abnormal PI versus 10% in the normal group (p<0.05). This demonstrates that impaired placental perfusion identified early contributes to early-onset placental insufficiency and preterm labor.

 

Table 6: Incidence of Intrauterine Growth Restriction (IUGR)

IUGR Status

 

Normal PI (n=60)

Abnormal PI (n=15)

p-value

Present

5 (8.3%)

4 (26.6%)

0.045*

Absent

55 (91.7%)

11 (73.4%)

 

Interpretation:
A significant association was observed between abnormal uterine artery PI and IUGR (p<0.05). One-fourth of the women with high PI developed growth restriction, supporting the link between early high-resistance flow and placental insufficiency.

 

Table 7: Mode of Delivery

Mode of Delivery

Normal PI (n=60)

Abnormal PI (n=15)

p-value

Vaginal                   

34 (56.6%)

7 (46.6%)

0.48

LSCS (Emergency/Elective)

26 (43.4%)

8 (53.4%)

 

Interpretation:
Although cesarean deliveries were slightly more common among those with abnormal PI (53.4%), the difference was not statistically significant.

 

Table 8: Neonatal Birth Weight Distribution

Birth Weight (kg)

Normal PI (n=60)

Abnormal PI (n=15)

Mean ± SD

p-value

<2.5 kg

7 (11.6%)

5 (33.3%)

0.03*

≥2.5 kg

53 (88.4%)

10 (66.7%)

 

Mean BW (kg)

2.87 ± 0.36

2.41 ± 0.42

   

Interpretation:
Mean birth weight was significantly lower in the abnormal PI group (2.41 ± 0.42 kg) compared to the normal group (2.87 ± 0.36 kg). This supports the hypothesis that abnormal placentation early in pregnancy adversely affects fetal growth.

 

Table 9: NICU Admission

NICU Admission

Normal PI (n=60)

Abnormal PI (n=15)

p-value

Required

 

7 (11.6%)

4 (26.6%)

0.05*

Not Required

53 (88.4%)

11 (73.4%)

 

Interpretation:
Neonates born to mothers with abnormal uterine artery PI had a higher rate of NICU admission (26.6%) compared to those in the normal PI group (11.6%), mainly due to prematurity and growth restriction.

 

Table 10: Perinatal Outcome Summary

Outcome Parameter

Normal PI (n=60)

Abnormal PI (n=15)

p-value

Pre-eclampsia

4 (6.6%)

5 (33.3%)

0.009**

Preterm Delivery

6 (10%)

5 (33.3%)

0.04*

IUGR

5 (8.3%)

4 (26.6%)

0.045*

NICU Admission

7 (11.6%)

4 (26.6%)

0.05*

Perinatal Mortality

1 (1.6%)

1 (6.6%)

0.28

Interpretation:
Abnormal mean uterine artery PI in early pregnancy was significantly associated with increased risk of preeclampsia, preterm delivery, IUGR, and NICU admissions. Though perinatal mortality was slightly higher, it did not reach statistical significance

DISCUSSION

The results demonstrated that 20% of the participants exhibited an abnormal mean uterine artery PI (>95th percentile). Among these women, 33.3% subsequently developed preeclampsia compared to only 6.6% in those with normal PI values, showing a statistically significant difference (p<0.01). Furthermore, abnormal uterine artery PI was significantly associated with preterm delivery, intrauterine growth restriction (IUGR), and increased rates of NICU admission.

. In our study, the mean PI in the abnormal group (2.45 ± 0.32) was significantly higher than that in the normal group (1.65 ± 0.28), consistent with previous research demonstrating that raised PI reflects increased downstream impedance to flow and reduced placental perfusion [8,9].

The proportion of women with abnormal uterine artery PI in our study (20%) is comparable to that reported by Gómez et al., who found a 22% prevalence of abnormal PI during the first trimester and established reference ranges for uterine artery PI from 11 to 41 weeks of gestation [10]. Similar results were obtained by Papageorghiou et al., who in a multicenter study involving over 2,000 pregnancies found that a mean PI above the 95th percentile at 11–14 weeks significantly predicted subsequent preeclampsia and IUGR [9]. Our findings also correlate with those of Melchiorre et al., who reported that women with increased uterine artery PI in the first trimester were at a significantly higher risk of developing preeclampsia and delivering small-for-gestational-age neonates [11].

The incidence of preeclampsia among women with abnormal PI in our cohort (33.3%) closely resembles the 30–35% incidence reported in similar high-risk groups by Plasencia et al. and Poon et al. [12,13]. In Plasencia’s prospective study, abnormal uterine artery Doppler indices at 11–13 weeks were significantly associated with preterm preeclampsia, while Poon and Nicolaides demonstrated that incorporating uterine artery PI with maternal factors and biochemical markers improved prediction rates to over 90% for early-onset disease [13].

In the current study, abnormal PI was also associated with a higher incidence of preterm birth (33.3% vs 10%), consistent with the findings of O’Gorman et al., who in the ASPRE trial reported that high first-trimester uterine artery PI was significantly linked with preterm delivery and that early initiation of low-dose aspirin reduced the risk of 

CONCLUSION

In conclusion, the findings of this study corroborate extensive evidence from international literature that elevated mean uterine artery PI at 11–14 weeks is a strong predictor of hypertensive disorders of pregnancy and adverse perinatal outcomes. Incorporating first-trimester uterine artery Doppler into routine obstetric care can enable clinicians to identify high-risk women early, implement preventive measures such as aspirin therapy, and intensify antenatal surveillance to improve maternal and neonatal outcomes.

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  2. Say L, Chou D, Gemmill A, Tunçalp Ö, Moller AB, Daniels J, et al. Global causes of maternal death. Lancet Glob Health. 2014;2(6):e323–33.
  3. Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. 2010;376(9741):631–44.
  4. Khan KS, Wojdyla D, Say L, Gülmezoglu AM, Van Look PF. WHO analysis of causes of maternal death. 2006;367(9516):1066–74.
  5. Brosens I, Pijnenborg R, Vercruysse L, Romero R. The “Great Obstetrical Syndromes”. Am J Obstet Gynecol. 2011;204(3):193–201.
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  7. Nicolaides KH. Turning the pyramid of prenatal care. Fetal Diagn Ther. 2011;29(3):183–96.
  8. Harrington K, Cooper D, Lees C, Hecher K, Campbell S. Doppler ultrasound of the uterine arteries. Am J Obstet Gynecol. 1996;174(1 Pt 1):63–7.
  9. Papageorghiou AT, Yu CK, Bindra R, Pandis G, Nicolaides KH. Multicenter screening for pre-eclampsia. Ultrasound Obstet Gynecol. 2001;18(5):441–9.
  10. Gomez O, Figueras F, Fernandez S, Bennasar M, Martinez JM, Puerto B, et al. Reference ranges for uterine artery mean PI at 11–41 weeks. Ultrasound Obstet Gynecol. 2008;32(2):128–32.
  11. Melchiorre K, Wormald B, Leslie K, Bhide A, Thilaganathan B. First-trimester uterine artery Doppler and adverse outcomes. Obstet Gynecol. 2008;112(3):495–501.
  12. Plasencia W, Maiz N, Poon L, Yu C, Nicolaides KH. Uterine artery Doppler in first trimester. Ultrasound Obstet Gynecol. 2008;32(1):7–13.
  13. Poon LC, Nicolaides KH. Early prediction of preeclampsia. Obstet Gynecol Int. 2014;2014:297397.
  14. O'Gorman N, Wright D, Poon LC, Rolnik DL, Syngelaki A, de Alvarado M, et al. Multicenter screening and aspirin in pregnancy. N Engl J Med. 2017;377(7):613–22.
  15. Recommendations for prevention and treatment of preeclampsia and eclampsia. Geneva: World Health Organization; 2011.
  16. Rolnik DL, Wright D, Poon LC, O'Gorman N, Syngelaki A, de Paco Matallana C, et al. Aspirin versus placebo in pregnancies at high risk for preterm preeclampsia. N Engl J Med. 2017;377(7):613–22.
  17. ACOG Practice Bulletin No. 222. Gestational hypertension and preeclampsia. Obstet Gynecol. 2020;135(6):e237–60.
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  19. Kaur K, Singh S, Neki NS. Role of uterine artery Doppler in predicting preeclampsia in Indian women. Int J Reprod Contracept Obstet Gynecol. 2020;9(4):1558–63.
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