Pregnancy-induced hypertension (PIH), including gestational hypertension and preeclampsia, is one of the most common and serious complications of pregnancy. It significantly contributes to maternal and perinatal morbidity and mortality worldwide [1,2]. Hypertensive disorders affect about 5–10% of pregnancies globally and remain a leading cause of maternal deaths, particularly in developing countries [3].In India, the prevalence is even higher, with estimates from various studies ranging from 7–11% [2,4]. This high burden is often linked to delayed antenatal care and socioeconomic factors, making PIH a major concern in our setting [4].The placenta is the vital organ for maternal-foetal exchange of oxygen, nutrients, and waste. In PIH, defective early placentation and incomplete remodeling of maternal spiral arteries lead to reduced uteroplacental blood flow, causing ischemia leads to placental morphological changes after delivery like reduced weight and size, infarcts, calcification, retroplacental clots, pallor of the maternal surface, and abnormal cord insertion [5,6].These gross changes are clinically important as they indicate placental insufficiency and are associated with adverse foetal outcomes such as intrauterine growth restriction (IUGR), low birth weight, and preterm delivery [1,6]. Although PIH is very common in India, there is a need for more prospective studies focusing on gross placental morphology in tertiary care hospitals. The present study aimed to evaluate the morphological and morphometric changes in placentas from PIH pregnancies compared to normotensive controls.

The present study was conducted in the Department of Anatomy in collaboration with the Department of Obstetrics and Gynecology at Government General Hospital, Kurnool for a period of 12 months. Ethical approval was obtained from the Institutional Ethics Committee, and written informed consent was taken from all participating mothers [6]. A total of 100 placentas were included: 50 from mothers diagnosed with pregnancy-induced hypertension (PIH group) and 50 from normotensive mothers (control group). PIH was defined as new-onset hypertension (blood pressure ≥140/90 mmHg on two occasions at least 4 hours apart) after 20 weeks of gestation in a previously normotensive woman [1]. Exclusion criteria included multiple gestations, chronic hypertension, diabetes mellitus, gestational diabetes, placental abruption, major foetal anomalies, intrauterine infections, or other significant maternal comorbidities [6]. Control placentas were matched as closely as possible for maternal age (20–38 years), parity, and gestational age (28–40 weeks) to minimize confounding [6].Placentas were collected immediately after vaginal or cesarean delivery, gently rinsed with normal saline to remove excess blood and clots, and examined grossly within 2 hours to avoid autolytic changes [6]. Gross morphological parameters recorded included placental weight (measured using a calibrated digital scale to the nearest 1 g), maximum diameter (in cm), thickness (in cm), presence and extent of infarcts, calcification (gritty areas), retroplacental clots or hematomas, pallor of the maternal surface, and umbilical cord insertion type (central, eccentric, marginal, or velamentous). Data were compiled and analyzed using appropriate statistical methods. Continuous variables (e.g., weight, dimensions) were expressed as mean ± standard deviation and compared between groups using Student's t-test or Mann-Whitney U test. Categorical variables (e.g., presence of infarcts, calcification) were expressed as percentages and compared using chi-square or Fisher's exact test. A p-value <0.05 was considered statistically significant[6].

A total of 100 placentas were examined: 50 from mothers with pregnancy-induced hypertension (PIH group) and 50 from normotensive mothers (control group) in the present study. The mean maternal age was comparable between the groups (26.8 ± 4.1 years in PIH vs 27.2 ± 3.8 years in controls). Parity distribution was also similar, with most women being primigravida or second gravida. Gestational age at delivery ranged from 28 to 40 weeks, but preterm deliveries (<37 weeks) were noticeably more frequent in the PIH group. Gross examination of the placentas revealed marked differences between the two groups. Placentas from PIH mothers were consistently smaller in size and weight and showed a higher frequency of visible pathological features compared to those from normotensive mothers. Placentas in the PIH group were significantly lighter and smaller in all dimensions (weight, diameter, and thickness) compared to the control group. Visible abnormalities such as infarcts (pale or haemorrhagic necrotic areas), calcification (gritty white deposits), retroplacental clots or haematomas, pallor of the maternal surface, and abnormal umbilical cord insertion (mainly eccentric or marginal) were much more common in PIH placentas. These findings indicate chronic placental ischemia and under perfusion due to pregnancy-induced hypertension [Table 1]. Newborns of mothers with PIH had significantly lower mean birth weight and higher rates of intrauterine growth restriction (IUGR), preterm delivery, and low birth weight babies. A small proportion of PIH cases also resulted in stillbirth or early neonatal death, while no such events occurred in the control group. These adverse outcomes showed a strong association with the gross placental abnormalities (smaller size, infarcts, calcification, and clots) observed in the PIH group, suggesting that placental insufficiency directly contributed to compromised foetal growth and well-being[Table 2]. All comparisons were statistically significant in the present study. Tables Table 1: Morphological and morphometric Parameters of Placenta Parameter PIH Group (n=50) Control Group (n=50) p-value Mean placental weight (g) 380 ± 45 480 ± 50 <0.001 Mean diameter (cm) 15.2 ± 2.1 18.5 ± 1.8 <0.01 Mean thickness (cm) 2.1 ± 0.4 2.8 ± 0.5 <0.001 Infarcts (%) 58% 12% <0.001 Calcification (%) 72% 18% <0.001 Retroplacental clots (%) 28% 4% <0.01 Pallor of maternal surface (%) 44% 10% <0.001 Abnormal cord insertion (%) 22% 6% <0.05 Table 2: Foetal Outcome Parameters Parameter PIH Group Control Group p-value Mean birth weight (kg) 2.4 ± 0.5 3.1 ± 0.4 <0.001 Intrauterine growth restriction (IUGR) (%) 42% 6% <0.001 Preterm delivery (<37 weeks) (%) 38% 10% <0.01 Low birth weight (<2.5 kg) (%) 48% 8% <0.001 Stillbirth / early neonatal death (%) 6% 0% <0.05

The present study demonstrates that pregnancy-induced hypertension (PIH) leads to significant gross morphological changes in the placenta compared to normotensive pregnancies. These changes contribute to placental insufficiency and result in adverse foetal outcomes. In our study, placentas from PIH mothers had markedly lower mean weight (380 ± 45 g vs 480 ± 50 g in controls), smaller diameter (15.2 ± 2.1 cm vs 18.5 ± 1.8 cm), and reduced thickness (2.1 ± 0.4 cm vs 2.8 ± 0.5 cm). Visible abnormalities were more frequent: infarcts in 58% (vs 12%), calcification in 72% (vs 18%), retroplacental clots in 28% (vs 4%), pallor of maternal surface in 44% (vs 10%), and abnormal cord insertion in 22% (vs 6%). These gross features indicate chronic ischemia and poor uteroplacental perfusion due to PIH.These observations are consistent with previous Indian studies. Majumdar and Dasgupta reported smaller placental size, reduced weight, pallor, and clots in hypertensive pregnancies [6]. Salmani et al. found reduced placental weight and dimensions along with more infarcts and calcification in PIH cases [7]. Narasimha and Vasudeva described similar gross changes, including lower weight and frequent infarcts in preeclampsia [8]. Kambale et al. noted smaller placentas with infarcts and clots in PIH, linking them to foetal implications [9]. Recent studies also confirm reduced placental weight and increased infarcts/calcification in hypertensive disorders [10,11].The pathophysiological basis involves defective trophoblast invasion and incomplete spiral artery remodeling, leading to persistent high-resistance flow and placental hypoxia [5]. This results in gross lesions like infarcts (from ischemic necrosis) and calcification (dystrophic response to chronic damage) [3,6]. These visible changes correlate well with poorer foetal outcomes in our study: lower mean birth weight (2.4 ± 0.5 kg vs 3.1 ± 0.4 kg), higher IUGR (42% vs 6%), preterm delivery (38% vs 10%), low birth weight (48% vs 8%), and rare stillbirth/neonatal death (6% vs 0%). Similar associations between gross placental pathology and IUGR/low birth weight have been reported in Indian settings [12].In India, where PIH prevalence remains high (around 7–11%) [2,4], routine gross placental examination is a simple, cost-effective tool for assessing disease impact, especially in resource-limited areas. Our findings align with the two-stage model of preeclampsia, where early placental ischemia manifests as gross changes and affects foetal growth [5]. Overall, this study highlights that PIH causes prominent gross placental alterations, which explain the increased perinatal risks observed. These results support the need for placental evaluation in hypertensive pregnancies to better understand and manage complications.

Pregnancy-induced hypertension induces significant gross morphological changes in the placenta, including reduced weight and size, infarcts, calcification, retroplacental clots, pallor, and abnormal cord insertion. These alterations reflect placental ischemia and insufficiency, leading to adverse foetal outcomes such as low birth weight, IUGR, and preterm delivery. Routine gross examination of the placenta in PIH cases is valuable for predicting perinatal risks and improving maternal-foetal care.

1. Say L, Chou D, Gemmill A, Tunçalp Ö, Moller AB, Daniels J, et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health. 2014;2(6):e323-33. 2. Dhinwa M, Gawande K, Jha N, Anjali M, Bhadoria AS, Sinha S. Prevalence of Hypertensive disorders of pregnancy in India: a systematic review and meta-analysis. J Med Evid. 2021;2(2):10-7. 3. Burton GJ, Redman CW, Roberts JM, Moffett A. Pre-eclampsia: pathophysiology and clinical implications. BMJ. 2019;366:l2381. 4. Dhinwa M, Gawande K, Jha N, Anjali M, Bhadoria AS, Sinha S. Prevalence of Hypertensive disorders of pregnancy in India: a systematic review and meta-analysis. J Med Evid. 2021;2(2):10-7. 5. Roberts JM, Hubel CA. The two stage model of preeclampsia: variations on the theme. Placenta. 2009;30 Suppl A:S32-7. 6. Majumdar S, Dasgupta H. A study of placenta in normal and hypertensive pregnancies. J Anat Soc India. 2005;54(1):1-9. 7. Salmani D, Purushothaman S, Somashekara SC, Gnanagurudasan E, Sumangaladevi K, Harikishan R, et al. Study of structural changes in placenta in pregnancy-induced hypertension. J Nat Sci Biol Med. 2014;5(2):352-5. 8. Narasimha AP, Vasudeva DS. Spectrum of changes in placenta in pregnancies complicated by preeclampsia. J Clin Diagn Res. 2014;8(11):FC04-8. 9. Kambale T, Iqbal B, Ramraje S, Swaimul K, Salve S. Placental morphology and foetal implications in pregnancies complicated by pregnancy-induced hypertension. Med J Dr DY Patil Univ. 2016;9(3):341-7. 10. Singh P, Kumar R, Rani A. Morphometric and histopathological evaluation of placenta in pregnancy-induced hypertension. Int J Reprod Med. 2022;2022:8372961. 11. Tripathi S, Varma K, Gupta S, Chaurasia A, Misra V. Placental morphological and histopathological changes in preeclampsia and eclampsia: a prospective case-control study using an objective scoring system. Int J Reprod Contracept Obstet Gynecol. 2025; (in press, cited from recent publication). 12. Vinnakota A, Uma S. Study of histopathological changes in placenta in pregnancy-induced hypertension. Int J Reprod Contracept Obstet Gynecol. 2019;8(3):1025-30.