Fetal growth restriction (FGR) refers to the failure of the fetus to achieve its genetically determined growth potential and may result from maternal, fetal, placental, or genetic factors. Severe fetal growth restriction (sFGR) is commonly defined as an estimated fetal weight (EFW) below the third percentile [1]. The severity of FGR strongly influences perinatal outcomes, with sFGR associated with the highest rates of adverse events [2].

Gestational hypertensive disorders (GHD), including preeclampsia (PE) and gestational hypertension (GH), are leading causes of maternal and neonatal morbidity and mortality, accounting for 9–26% of maternal deaths worldwide [3]. PE, the more severe form of GHD, and FGR are both classified as “placental syndromes” and share similar pathological mechanisms, such as impaired trophoblast invasion and placental oxidative stress [4].

Although the association between PE and FGR is well established, comparative data on maternal and perinatal outcomes in sFGR cases with or without GHD remain limited. This retrospective study aims to compare the clinical characteristics and outcomes of sFGR cases, stratified by the presence of PE or GH, providing evidence to support risk stratification and guide antenatal management.

Among the 371 sFGR cases analyzed, 69 (18.6%) were complicated by PE, 15 (4.0%) by GH, and 287 (77.4%) were normotensive. A flowchart of patient selection is presented in Fig. 1.

Fig. 1.

Flowchart of sFGR cases included in the study. sFGR, severe fetal growth restriction; EFW, estimated fetal weight; AC, abdominal circumference.

Fetal growth restriction remains a major contributor to perinatal morbidity and mortality and has long-term implications for cardiovascular and metabolic health. International guidelines vary in their diagnostic criteria for FGR [8], but there is consensus that fetuses with an EFW or AC below the 3rd percentile should be classified as sFGR due to their significantly elevated risk of adverse outcomes [9, 10].

PE and sFGR share common placental pathophysiology, particularly involving abnormal spiral artery remodeling, endothelial dysfunction, and placental insufficiency [11]. It has been hypothesized that different abnormalities of trophoblastic cells resulted in different disease phenotypes [12]. Huppertz [13] suggested that malfunction of the syncytiotrophoblast may increase oxidative stress markers and compromise the integrity of the placental barrier, thereby contributing to the pathogenesis of PE. In contrast, malfunction of the cytotrophoblast can impair placental proliferation and fusion, ultimately leading to FGR [13].

Previous clinical guidelines have primarily treated FGR as a consequence of PE [14]. However, our results suggest a more complex interplay: among sFGR cases, the incidence of PE (18.80%) far exceeded that of GH. This finding may indicate a distinct pathophysiological entity rather than a linear progression from GH to PE. The global prevalence of PE has been estimated at 4.6% of deliveries [15]. The incidence of GH in FGR strongly correlated with gestational age, declining from 39–43% in early preterm cases to 4–7% in term deliveries [16]. The International Society for the Study of Hypertension in Pregnancy (ISSHP) includes FGR as a diagnostic criterion for PE [17]. However, it remains controversial that cases diagnosed as PE with hypertension and FGR alone do not show an increased incidence of adverse maternal and neonatal outcomes compared with PE with hypertension accompanied by proteinuria or organ dysfunction [18]. Consequently, to delineate their distinct effects, GH and PE were analyzed separately in the sFGR population.

Our study demonstrated that sFGR-PE and sFGR-GH were associated with significantly worse maternal and neonatal outcomes compared with normotensive sFGR. However, after adjustment for potential confounders, such as gestational age and birthweight, these associations were no longer statistically significant, indicating that these variables largely account for the adverse outcomes observed in this group. The risk of cesarean or instrumental delivery remained significantly elevated, reflecting the vulnerability of growth-restricted fetuses to intrauterine hypoxia and the limited compensatory capacity of a compromised placenta during labor [19]. The timing of delivery is a critical consideration in the management of FGR, particularly when complicated by hypertensive disorders of pregnancy. Biochemical factors, such as soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF), are increasingly incorporated into maternal evaluation [20]. In carefully selected near-term FGR fetuses without Doppler abnormalities, mechanical or pharmacological induction can be safely considered [21]. Clinicians should exercise particular caution when developing diagnostic strategies, surveillance protocols, and final recommendations for the timing of delivery of growth-restricted fetuses. While the univariable model indicated an increased likelihood of cesarean section in sFGR-PE compared with sFGR-GH, this relationship was reversed in the multivariable-adjusted model. This change, along with the large 95% CI in sFGR-GH, may be caused by the small sample size.

sFGR-PE pregnancies had significantly earlier deliveries in our study. This discrepancy may be attributed to the fact that the timing of delivery in sFGR-PE is influenced not only by fetal impairment but also by maternal conditions. Furthermore, abnormal umbilical artery Doppler waveforms appear earlier in sFGR-PE cases, which may contribute to the earlier gestational age at delivery [22]. Our study lacked data regarding the interval from disease diagnosis to delivery. Concomitant hypertensive disorders have been reported to shorten this diagnosis-to-delivery interval. However, only 24% of these deliveries were primarily due to maternal indications [23].

Compared with normotensive sFGR pregnancies, cases with coexisting GHD and PE did not show a significantly increased risk of adverse neonatal outcomes. However, poor neonatal outcomes may be influenced by prematurity. Future prospective, multicenter studies with larger sample sizes are needed to validate these findings and inform the clinical management of such pregnancies.

The data that support the findings of this study are available from the corresponding author upon reasonable request.

MY and QN designed the research study. QN performed the research. MY analyzed the data. MY and QN wrote the manuscript. Both authors contributed to editorial changes in the manuscript. Both authors read and approved the final manuscript. Both authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

The research was approved by the Ethics Committee of the Affiliated Suzhou Hospital of Nanjing Medical University (KL-2025-060-K01). Given the retrospective nature of the study, which involved only the review of existing medical records without any direct patient contact or intervention, the requirement for written informed consent was waived by the committee. All patient data were anonymized prior to analysis to ensure confidentiality. The study was carried out in accordance with the guidelines of the Declaration of Helsinki.

We acknowledged the assistance from the midwives and clinicians at Suzhou municipal hospital, the Affiliated Suzhou Hospital of Nanjing Medical University.

This research received no external funding.

The authors declare no conflict of interest.

During the preparation of this work the authors used Deepseek in order to check spell and grammar. After using this tool, the authors reviewed and edited the content as needed and takes full responsibility for the content of the publication.