Preeclampsia is a hypertensive disorder of pregnancy, affecting 3–5% of pregnancies globally. ¹ This disorder is responsible for 2% to 8% of pregnancy-related complications, more than 50,000 maternal deaths, and over 500,000 foetal deaths worldwide. ² Wagner defined the diagnostic criteria for preeclampsia as a systolic blood pressure of 140 mmHg or higher or a diastolic blood pressure of 90 mmHg or higher on two separate occasions, at least 4 hours apart, with traces of protein in urine. ³ As an alternative, 110 mmHg or higher for diastolic blood pressure or 160 mmHg for systolic blood pressure with proteinuria after 20 weeks of gestation. These are consistent with the Mayo and Cleveland Clinics’ definitions of the disorder. The American College of Obstetricians and Gynaecologists and the European Society of Cardiology define preeclampsia as a pregnancy-specific disorder characterised by new-onset hypertension with end-organ dysfunction, occurring after the 20 ^th week of gestation in a previously normotensive woman. ^{4, 5} The pathophysiology of preeclampsia is multifaceted and not yet fully understood, though placental insufficiency, endothelial dysfunction, and oxidative stress are considered central mechanisms. ⁶ Although the implications of preeclampsia can be serious for the mother, it also has profound effects on foetal development, often leading to growth restriction, preterm delivery, and increased perinatal mortality.

Doppler velocimetry and foetal biometry are crucial ultrasonographic tools for assessing foetal health in preeclamptic pregnancies. These techniques provide insight into foetal growth parameters and placental blood flow, providing a window into the effects of maternal vascular dysfunction on the developing foetus. ⁷ Previous studies have established that abnormal Doppler indices, such as elevated uterine artery pulsatile index (UtA PI) and middle cerebral artery resistance index (MCA RI), are indicative of impaired placental perfusion and foetal hypoxia. ⁸ However, the extent to which these indices correlate with specific growth parameters remains an area of active investigation.

In South Africa, where socio-economic disparities influence maternal and neonatal health outcomes, understanding the impact of preeclampsia on foetal growth is critical for improving clinical care and reducing adverse outcomes. This study focuses on mother-perinate pairs who received antenatal and postnatal care at Nelson Mandela Academic Hospital in Mthatha, Eastern Cape Province. This study aims to elucidate the relationship between maternal vascular health and foetal development in preeclampsia-related preeclamptic pregnancies by evaluating foetal biometry and Doppler indices.

Ethical clearance to conduct this study was granted by the Walter Sisulu University Health Sciences Research Ethics Committee (WSU HREC 019/2025). This study was authorised by the Eastern Cape Department of Health and the Nelson Mandela Academic Hospital’s Gynaecology and Obstetrics Department. Informed written consent and assent were obtained from the mothers during recruitment. This study adhered to the principles of the Declaration of Helsinki to protect participants.

The study highlights significant differences in maternal characteristics, foetal biometry, and Doppler indices between preeclamptic and normotensive pregnancies. Women with preeclampsia had a higher prevalence of a history of preeclampsia, smoking, and alcohol consumption. Perinates in preeclamptic pregnancies were smaller and had higher uterine artery resistive indices.

The current study aligns with previous reports suggesting that a history of preeclampsia is an important contributor to the development of preeclampsia. ⁷ In fact, a retrospective study of the Swedish Birth Register from 1987–2004, in which a total of 1,430,464 deliveries were included, showed that preeclampsia occurred more commonly in women who had had preeclampsia before. The study showed a 14.7% reoccurrence rate of preeclampsia in a second pregnancy and 31.9% in a third pregnancy. ¹²

In terms of foetal biometry, foetuses from preeclamptic pregnancies exhibited significantly smaller head circumferences and lower estimated foetal weights compared to foetuses in normotensive pregnancies. These findings were consistent with studies indicating that maternal preeclampsia impedes placental function, ultimately restricting foetal growth. ¹³ This study also noted non-significant differences in abdominal circumferences, femur length, and biparietal diameter, suggesting variability in the impact of preeclampsia on foetal growth parameters. Similar studies have reported that while some foetal measurements are consistently affected by preeclampsia, others may vary depending on the severity and onset of the condition. ⁸

Doppler velocimetry revealed higher uterine artery pulsatile index (UtA PI) and middle cerebral artery pulsatile index (MCA PI) in preeclamptic pregnancies, both being statistically significant. These findings are indicative of altered blood flow dynamics in preeclampsia, which can compromise oxygen and nutrient delivery to the foetus. The elevated MCA resistance index (MCA RI) further supports the notion of increased vascular resistance in preeclampsia. ¹⁴ Increased placental vascular resistance can lead to foetal hypoxemia and potentially trigger compensatory mechanisms, where blood flow is shunted to vital organs such as the foetal brain at the expense of peripheral growth. ¹⁵ Contrasting studies have suggested that while Doppler parameters are helpful in assessing placental and foetal health, their predictive value for adverse outcomes may vary across populations. ^{16, 17}

The uterine artery pulsatile index (UtA PI) demonstrated a strong positive association with estimated foetal weight. This may be due to placental adaptation, where the placenta compensates for increased vascular resistance by enhancing nutrient transport efficiency, allowing the developing foetus to maintain or even increase its weight irrespective of compromised uteroplacental blood flow. ^{18, 19} Another mechanism that may explain this is the shunting resulting from the redistribution of blood, where the foetus prioritises blood flow to essential organs like the brain, ensuring adequate growth irrespective of placental insufficiency. ^{20, 21} The current findings are supported by Wu et al, who showed that the right UTA PI of 1.27 (95%CI: 0.84–1.63) was associated with the early onset of preeclampsia. ²² Participants in our study were diagnosed with preeclampsia before 26 weeks, even though data were only collected at 33 weeks of gestation. Furthermore, some studies have shown that higher UTA PI is associated with small for gestational age foetuses, indicating its important contribution to uteroplacental blood flow. ²³ Other contrasting findings observed no significant association between UtA PI and foetal weight in mild cases of preeclampsia, suggesting variability based on disease severity. ^{24, 25}

The relationship between UtA PI and foetal biparietal diameter (BPD) was also notable, with a positive correlation, though not statistically significant. Similar findings have been reported in studies emphasising the role of uteroplacental blood flow in determining foetal cranial growth. However, the lack of statistical significance in this study may reflect sample size limitations or variability in the impact of preeclampsia on cranial growth parameters.

Interestingly, the middle cerebral artery pulsatile index (MCA PI) correlated negatively with biparietal diameter, indicating a potential compensatory mechanism where increased cerebral blood flow prioritises brain development in response to hypoxic conditions. Elevated MCA PI reflects increased vascular resistance within foetal cerebral circulation. Over time, this can impede brain growth, sometimes reflected by reduced biparietal diameter. ²⁶ This aligns with the concept of “brain-sparing” observed in foetuses affected by preeclampsia, as reported in recent literature. ²⁷ However, the marginal significance of this finding underscores the need for further investigation to confirm its clinical relevance.

The middle cerebral artery resistive index (MCA RI) showed a strong negative correlation with BPD. Similar reports revealed that elevated vascular resistance in the foetal cerebral circulation is a compensatory response to placental insufficiency. ²⁸ However, contrasting studies have reported variability in MCA RI values, particularly in cases of late-onset preeclampsia, where cerebral haemodynamics may be less affected. ^{29, 30}

The inferential output revealed significant associations between foetal biometry and middle cerebral artery (MCA) indices, shedding light on the hemodynamic adaptations in pregnancies affected by hypertensive disorders such as preeclampsia. The negative association between the MCA resistive index (MCA RI) and biparietal diameter (BPD) suggests that increased vascular resistance in the foetal cerebral circulation may impair cranial growth. This finding aligns with the concept of “brain-sparing,” where blood flow is redistributed to prioritise vital organs under hypoxic conditions. ³¹ However, contrasting findings suggest that the degree of impact on BPD may vary depending on the severity and onset of preeclampsia, with late-onset cases enduring less severe effects. ^{32, 33}

This study demonstrates that maternal preeclampsia in a resource-limited South African setting is linked to significant reductions in foetal biometric measurements and marked alterations in placental and cerebral blood-flow indices. Doppler velocimetry’s value as an early warning tool is highlighted by showing how elevated uterine and cerebral Doppler pulsatility and resistive indices predict impaired head growth and lower estimated foetal weight. Incorporating these ultrasound metrics into routine care could enable targeted interventions to improve perinatal outcomes among high-risk pregnancies.

Not applicable.

Department of Human Biology, Walter Sisulu University, Nelson Mandela Drive, Mthatha, South Africa

Chuma Mabuto, Constance Rufaro Sewani-Rusike, Ebenezer Ackah, Ngoakoana Edna Matjuda

Department of Biological and Environmental Sciences, Walter Sisulu University, Mthatha, South Africa

Benedicta Nkeh-Chungag, Nomagugu Ndlovu, Ongeziwe Zamxaka, Yamkela Mfenyana, Roland Tiagha Akah, Jude Eteneneng Enoh

Department of Obstetrics and Gynaecology, Nelson Mandela Academic Hospital, Mthatha, South Africa

Charles Businge, Nontsikelelo Gubu-Ntaba, Nandipha Sotobe-Mbana, Malusi Madikane

Department of Obstetrics and Gynaecology, Mthatha Regional Hospital, Mthatha, South Africa

Mziwohlanga Mdondolo

Department of Obstetrics and Gynaecology, Frere Hospital, Mthatha, South Africa

Mfundo Feketshane, NP Selanto-Charman, Tandi Noah

Physiology Section, Otto Loewi Research Centre for Vascular Biology, Immunology and Inflammation, Medical University of Graz, Graz

Nandu Goswami

Corresponding authors

Correspondence to Chuma Mabuto ( 216050464@wsu.ac.za).