Spectrum of Morphological Changes in the Placenta of Women with Preeclampsia/Eclampsia and Correlation with Neonatal Morbidity

Spectrum of Morphological Changes in the Placenta of Women with Preeclampsia/Eclampsia and Correlation with Neonatal Morbidity | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Spectrum of Morphological Changes in the Placenta of Women with Preeclampsia/Eclampsia and Correlation with Neonatal Morbidity Folaranmi Olaleke Oluwasegun, Buhari Mikhail Olayinka, Ibrahim Olatunde Kazeem, and 4 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4695829/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Preeclampsia/eclampsia is a leading cause of maternal and perinatal mortality; the prevailing theory is that it is a consequence of disordered placentation with the resultant underperfusion of the placenta triggering release of cytokines and vascular factors which cause widespread endothelial damage. The placental changes are manifested as vascular and villous abnormalities with consequences in the developing foetus. The objective of this study was to compare the gross and microscopic changes in the placentas of women with preeclampsia/eclampsia and healthy mothers. Methods 146 pregnant women were recruited; 73 were normotensive (control group) while 73 were diagnosed with preeclampsia/eclampsia (study group). The macroscopic and microscopic placental changes in the two groups were further examined. Results 34% of the women in the study group had mild-moderate preeclampsia, 44% had severe preeclampsia and 22% had eclampsia. The placental weights were lower in the study group than the controls (556.82 grams ± 169.72 vs. 649.93 grams ± 116.38, p < 0.001). The major pathologic lesions with strong associations with preeclampsia/eclampsia in this study were decidual vasculopathy, infarction, increased syncytial knots (Tenney-Parker changes), accelerated villi maturity, stromal fibrosis and microcalcifications (p < 0.001). There was also a strong association between disease severity and Apgar scores in the 1st minute. The study group had 11% neonatal mortality. Conclusion There were distinct microscopic changes consistent with maternal vascular malperfusion changes in the placentas of mothers with preeclampsia/eclampsia and demonstrable neonatal morbidity depicted by high incidence of preterm birth and low birth weights. Placenta Preeclampsia Morphological changes Neonatal morbidity Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9 Figure 10 Figure 11 BACKGROUND Preeclampsia/eclampsia is a pregnancy-specific syndrome characterized by new-onset hypertension and proteinuria. 1 It has been recognized as a significant contributor to maternal and foetal mortality and morbidity for over 100 years. It was in the late nineteenth century that it was recognized that eclampsia, which had been considered a convulsive disorder of pregnancy for almost a thousand years, was preceded by increased maternal blood pressure and proteinuria, hence preeclampsia. Not long after these observations, it was evident that even without seizures, preeclampsia indicated a potentially fatal disease for mothers and babies. 2 The overall prevalence in the United States is 3-8% with higher incidence in specific ethnic subpopulations, notably African-Americans. 3 Studies done in Nigeria have recorded varying values ranging from 5-7.6%. 4-7 Despite being one of the leading causes of maternal death and a major contributor to maternal and perinatal morbidity, the pathogenesis of preeclampsia/eclampsia has not been fully unravelled. Hypertension associated with preeclampsia develops during pregnancy and remits after delivery, implicating the placenta as a central culprit in the pathogenic process. 1 An initiating event in preeclampsia has been postulated to be reduced placental perfusion that leads to widespread dysfunction of the maternal vascular endothelium and hypertension by mechanisms that remain to be defined. 1,3,8 Histopathological and microbiological examination of the placenta can reveal the aetiology of many conditions, such as stillbirth, pre-term delivery, intrauterine growth restrictions (IUGR), and neurological impairment. 9 Placental examination reveals abnormal findings in almost all cases of foetal death, and the pathology report can diagnose the cause of death in about one-third of the cases in which it could not be determined clinically. 10 Furthermore, medical conditions that can recur can be recognized, providing information to manage or treat subsequent pregnancies. 10-12 The data from a placental examination may also offer essential evidence in medical liability cases. They may provide defence against allegations of malpractice when the findings indicate that foetal or placental disease contributed to adverse pregnancy outcomes independent of the clinical care provided. 10,11 Many studies have established the pathological changes in the placenta of preeclamptic mothers, which include gross findings of smaller placentas with foci of calcification, infarction, and microscopic findings of increased syncytial knot formation, fibrinoid necrosis, stromal fibrosis, hyalinised villi, altered villous vascularity, cytotrophoblastic cell proliferation, increased villi vascularisation and branching, intervillous haemorrhage and basement membrane thickening. 13-19 There is paucity of such data in this environment; the placenta is handed to the mother or relatives almost immediately after birth most times without examination due to social and cultural beliefs that the placenta can be used for diabolical purposes. In 1997, the College of American Pathologists (CAP) published practical guidelines for placental pathological examination following delivery. 12 In recent times, institutions have published modifications based on the original guidelines; the recommendations are for underlying maternal disease, pregnancy complications, foetal/ neonatal conditions, or placental indications. 20 Since the use of Apgar scores more than 50 years ago, it has served as a globally acceptable method of assessing the physical status of the newborn in the immediate post-natal life and also as a predictor of infant morbidity and mortality. 21 This research aimed to study the pathological changes in the placenta of preeclamptic/eclamptic mothers and the impact on newborn morbidity and mortality. Methods 146 booked pregnant women diagnosed at the clinic, labour ward, or at the Emergency Room of University of Ilorin Teaching hospital Nigeria were recruited for this study. The sample size was calculated as reported by Goyal 2013 22 . Informed consents were taken from the recruited patients. Inclusion criteria: Study group 1. Maternal age from 18-40 years. 2. Gestational age from viability (28 weeks) to term (not beyond 41 weeks, 6 days). 3. Diagnosed cases of preeclampsia. 4. Willingness to participate and signing of the informed consent after explaining the aim of the study Control group 1. Maternal age from 18-40 years. 2. Gestational age from viability (28 weeks) to expected date of delivery (not beyond 41 weeks, 6 days). 3. Normal clinical and laboratory parameters 3. Willingness to participate and signing of the informed consent after explaining the aim of the study. Exclusion criteria: 1. Presence of other maternal diseases such as chronic renal diseases, diabetes mellitus, sickle cell disease, autoimmune disorders and coagulopathies. 2. Evidence of gross foetal anomalies (in utero and post-delivery). 3. Post term pregnancies (gestational age ≥ 42 weeks). 4. Unwillingness to participate in the study. The diagnosis of preeclampsia was based on findings of new onset hypertension and or proteinuria occurring after 20 weeks of gestation with significant proteinuria (i.e., ≥300 mg per 24 hours, protein to creatinine ratio ≥0.3 day or 1+ urinary protein dipstick reading) 23 The study group participants were further stratified into those with: Mild-Moderate Preeclampsia: Patients with systolic BP >140mmHg but ˂160mmHg and Diastolic˂110mmHg, proteinuria >0.3g/24 hours or 1+ on dipstick Severe preeclampsia: Patients with any of these: (a)Systolic BP ≥160mmHg or diastolic BP >110mmHg on two occasions at least 4 hours apart, proteinuria >5g/24 hours or >3+ on dipstick. (b) Thrombocytopenia (platelet count <100,000). (c) Impaired liver function (d) New development of renal insufficiency. (e) Pulmonary oedema. (f) New-onset cerebral or visual disturbances. 3. Eclampsia: Preeclamptic patient with onset of seizures before, during or after delivery. Immediately after delivery, the newborns’ weights and Apgar scores were recorded. The placentas were washed to remove blood clots, weighed. They were examined for completeness, and gross abnormalities in the umbilical cord, foetal membranes, and placenta disc. Full-thickness sections were taken from the central areas, grossly abnormal areas, and the membrane roll. The sections were fixed for 24 hours in 10% neutral-buffered formalin, processed for paraffin sections using a carousel-type automatic tissue processor. Masson’s Trichrome and Periodic Acid Schiff (PAS) were used to demonstrate the presence of fibrosis, and the basement membranes of placental/villous vessels respectively. The stained slides were reviewed to evaluate the pathologic changes and the pathologic findings were correlated to the birth weights and Apgar scores of the newborns. Statistical analysis was done with the Statistical Package for the Social Science (SPSS) version 22.0 (SPSS Inc., Chicago, IL, USA). Descriptive analysis was reported as means and standard deviations. Pearson’s chi-squared test and Student’s t-test were used to analyze the observed differences in the study and control groups. The level of significance was established at a p value of ≤ 0.05. Results Demographic characteristics of study group A total of 1,575 women had their deliveries taken at the Department of Obstetrics and Gynaecology of the University of Ilorin Teaching Hospital, Ilorin during the period of study. 5.14% of the women had preeclampsia-eclampsia. 60.3% of the preeclampsia/eclampsia patients had mild-moderate preeclampsia, 17.8% had severe preeclampsia and 21.9% had eclampsia. 23% had a history of hypertension in pregnancy without proteinuria (PIH), and 16.4% had a history of chronic hypertension (Fig. 1 ). The mean ages of the participants (study vs. control) were 30.04 ± 4.67 and 29.86 ± 4.81 with both groups having ages ranging from 21–40 years. The mean gestational age at which the diagnosis of preeclampsia-eclampsia was made was 35.21 ± 3.85 weeks. The means of the gestational age at delivery for the study and control groups were 37.04 ± 2.32 weeks and 38.48 ± 1.28 weeks respectively. There is a remarkable increase in the rate of caesarean section in those with preeclampsia/eclampsia (41.1%) compared to the control group (2.7%) with 97.3% of the control group having vaginal delivery compared to 58.9% for the study group. Foetal weight and Apgar score The mean birth weights of the study and control group were 2.66 ± 0.77kg and 3.21 ± 0.43kg respectively, 41.1% and 5.5% of the neonates in the study group had low birth weights and very low birth weights respectively compared to 9.6% in the control group who had low birth weights. The control group had no neonate in the very low birth weight category. 53.4% of the study group had normal birth weights, compared to 90.4% in the control group. The mean Apgar scores in the 5th minute in the study group and control group were 7.07 ± 2.75 and 8.71 ± 0.48 respectively. Placental parameters in the participants (Study vs. Control). Gross changes: Gross findings of infarction were seen in 16.4% of the placentas in the study group (66.7% were seen in mothers with severe preeclampsia, 25% eclampsia and 8.3% mild-moderate preeclampsia), while none was observed in the placentas of the control group. The mean placental weights in the study vs. control group were 556.82g ± 169.72g vs. 649.93g ± 116.38g. All the 3 placentas that weighed less than 300g were from mothers with severe preeclampsia. 71.4% of those weighing between 300-399g were from women with severe preeclampsia and 28.6% mild-moderate preeclampsia. 29 placentas weighed above 600g, out of which 51.7% were from mothers with mild-moderate preeclampsia, 31% severe preeclampsia, and 17.2% eclampsia. Microscopic changes: The pathologic findings seen include decidual arteriopathy, infarction, increased syncytial knots, abnormal vascular remodelling, terminal villous hypoplasia, accelerated villi maturation, villi immaturity, stromal fibrosis, acute chorioamnionitis, and chorangiosis. Comparison of microscopic abnormalities in the study and control groups demonstrated statistical significance (with most showing strong association), Table 1 , in all of the microscopic features except for chorangiosis (Fig. 2) and acute chorioamnionitis (Fig. 3) in which there were no significant differences between the two groups (p = 0.085 and p = 0.698). Table 1 Comparison of microscopic placental parameters (Study vs. Control). Microscopic parameters Study group n (%) Control n (%) χ 2 ρ Yes No Yes No Decidual arteriopathy 11 (15.1) 62 (84.9) 0 (0.0) 73 (100.0) 11.896 0.001* Infarction 22 (30.1) 51 (69.9) 0 (0.0) 73 (100.0) 25.903 < 0.001* Increased syncytial knots 48 (65.8) 25 (34.2) 0 (0.0) 73 (100.0) 71.510 < 0.001* Incomplete vascular remodelling 9 (12.3) 64 (87.7) 0 (0.0) 73 (100.0) 9.591 0.002* Chorangiosis 7 (9.6) 66 (90.4) 2 (2.7) 71 (97.3) 2.960 0.085 Terminal villous hypoplasia 4 (5.5) 69 (94.5) 0 (0.0) 73 (100.0) 4.113 0.043* Accelerated villi maturity 11 (15.1) 62 (84.9) 0 (0.0) 73 (100.0) 11.896 0.001* Villi immaturity 11 (15.1) 62 (84.9) 3 (4.1) 70 (95.9) 5.056 0.025* Stromal fibrosis 50 (68.5) 23 (31.5) 0 (0.0) 73 (100.0) 76.042 < 0.001* Acute chorioamnionitis 3 (4.1) 70 (95.9) 4 (5.5) 69 (94.5) 0.150 0.698 Microcalcifications 54 (74.0) 19 (26.0) 24 (32.9) 49 (67.1) 24.774 < 0.001* χ 2 : Chi Square test. *= p < 0.050 (statistically significant) Decidual arteriopathy (Fig. 4) was seen in 15.1% of the placentas in the study group as against none in the control group (p = 0.001) and infarction (Fig. 5) was seen in 30.1% of the placentas in the study group as against none in the control group (p < 0.001). 65.8% showed increased syncytial knotting (Fig. 6) while none was seen in the control group (p < 0.001). Incomplete vascular remodelling (Fig. 7) was seen in 12.3% of the placentas in the study group but none was observed in the control group (p = 0.002). 5.5% in the study group showed terminal villous hypoplasia (Fig. 8) versus none in the control group (p = 0.043). 15.1% showed accelerated maturity (Fig. 9) in premature neonates in the study group while none was recorded in the control group (p = 0.001). 15.1% of placentas showed villi immaturity (Fig. 9) in the study group as against 4.1% in the control group (p = 0.025). Stromal fibrosis (Fig. 10) was seen in 68.5% of the placentas while none was seen in the control group. 74% in the study group showed microcalcifications (Fig. 11) (p < 0.001). By comparison, 32.9% placentas in the control group showed microcalcifications (p < 0.001). Microscopic placental findings, severity of preeclapsia/eclampsia and foetal outcome. The total number of placentas with features of incomplete vascular modelling was 9, 55.6% were seen in mothers with severe preeclampsia and 44.4% were seen in those with eclampsia. Villi immaturity was seen in 11 placentas, 54.5% in mothers with severe preeclampsia, and 45.5% in eclampsia. 54 placentas showed microcalcifications, 50% were seen in mothers with severe preeclampsia, 25.9% mild-moderate preeclampsia, and 24.1% were seen in those with eclampsia (Table 2 ). Infarction was seen in 40.9% of those with severe preeclampsia, 31.8% eclampsia, and 27.3% mild-moderate preeclampsia. Microscopic findings of accelerated villi maturity had no statistical significance but were observed to be more common in the placenta of patients with severe disease with 36.4% in severe preeclampsia 45.5% in eclampsia and 18.2% in mild-moderate preeclampsia. Table 2 Association between microscopic finding and severity of disease Severity of disease Microscopy Mild/ moderate (%) Severe preeclampsia (%) Eclampsia (%) Total χ 2 ρ Presence of decidual vasculopathy 1 (9.1) 6 (54.5) 4 (36.4) 11 3.965 0.138 Infarction 6 (27.3) 9 (40.9) 7 (31.8) 22 1.917 0.383 Increased syncytial knots 16 (33.3) 21 (43.8) 11 (22.9) 48 0.098 0.952 Incomplete vascular remodelling 0 (0.0) 5 (55.6) 4 (44.4) 9 6.214 0.045 Chorangiosis 2 (28.6) 5 (71.4) 0 (0.0) 7 3.115 0.211 Terminal villous hypoplasia 2 (50.0) 2 (50.0) 0 (0.0) 4 1.271 0.530 Accelerated villi maturity in preterm 2 (18.2) 4 (36.4) 5 (45.5) 11 4.415 0.110 Villi immaturity 0 (0.0) 6 (54.5) 5 (45.5) 11 8.048 0.018 Stromal fibrosis 15 (30.0) 22 (44.00) 13 (26.0) 50 2.043 0.360 Acute chorioamnionitis 3 (100.0) 0 (0.0) 0 (0.0) 3 6.007 0.050 Microcalcifications 14 (25.9) 27 (50.0) 13 (24.1) 54 6.433 0.040 χ 2 : Chi Square test. *= p < 0.050 (statistically significant) 11 placentas showed features of decidual arteriopathy, 63.6% were in neonates who survived and 36.4% were seen in neonates who died. Nine placentas showed incomplete vascular remodelling with 55.6% in neonates who survived and 44.4% in those who died. Eleven placentas showed accelerated villi maturity with 63.6% in neonates that survived and 36.4% in those that died. Features of acute chorioamnionitis were seen in 3 placentas, and the neonates died. 54 placentas showed microcalcifications with 94.4% seen in neonates that survived while 5.6% were seen in those that died. Microscopic findings of infarction, increased syncytial knots, chorangiosis, terminal villous hypoplasia, villi immaturity, and stromal fibrosis were seen more predominantly in neonates that survived, with chorangiosis and terminal villous being exclusive findings to this group. Discussion Preeclampsia-eclampsia is a pregnancy-specific disease hence its historic name “Toxaemia of pregnancy”. 24 It is characterized by new onset hypertension and/or proteinuria differentiating it from chronic hypertension (hypertension before 20 weeks of gestation) and gestational hypertension also referred to as pregnancy-induced hypertension (PIH) which lacks proteinuria. The placenta has been identified as the root cause of preeclampsia resulting from disordered implantation, poor perfusion of the placenta leading to release of cytokines, and vascular factors which cause widespread endothelial injury. A common pattern of placental injury associated with altered uterine and intervillous blood flow is maternal vascular malperfusion of the placenta. Maternal vascular malperfusion is defined by a group of pathology findings observed in the maternal decidual vessels, which reflect unusual spiral artery remodeling and villous parenchyma abnormalities relating to oxygenation and flow dynamics within the intervillous space of the placenta. 25 The prevalence of preeclampsia in this study is similar to a work done by Adedoyin and Adetoro 4 in the late 80s on pregnancy outcomes in teenage mothers in Ilorin. They reported a prevalence rate of 5%. 4 . This might suggest that there had been no change in the prevalence of this disease within this locality. The prevalence of the disease varies widely all over the world and even within regions. Studies done in other parts of Nigeria have also shown regional variation; Singh et al 7 reported a prevalence of 6% in Sokoto, Northwest Nigeria, Yakasai et al 26 reported a prevalence of 8% in Kano, Ezeigwe et al reported 5.44% in Nnewi, Anambra state. 27 while Onyiriuka et al 5 recorded 5.6% in Benin-city. However, a lower prevalence rate of 1.2% was reported by Kooffreh et al in Calabar 28 , and 3.3% by Sotunsa et al in Ogun state. 29 The reasons for these interregional differences are not known but could be due to sociocultural practices and geographical factors. The percentages of women with a past obstetric history of preeclampsia/eclampsia and/or chronic hypertension in previous pregnancies were 17.8% and 16.4% respectively. This implies recurrence in this group of patients. A large study done in the UK noted higher risks of recurrence in Asians and Blacks and also highlighted chronic hypertension as an established risk factor for preeclampsia with data showing up to 22% of women with chronic hypertension having subsequent preeclampsia. 30 In this study, the gestational age at delivery in the study group was significantly lower than in the control group hence prematurity was one of the major perinatal complications seen. The increased rate of Caesarean delivery seen in the study group showed that preeclamptic mothers had over 13 times the risk of having surgical obstetric intervention than normotensive patients due to the precarious states the mothers present in. The high prevalence of low-birth-weight newborns seen in the study group implied that preeclampsia imposes a 5x risk of low birth weight in preeclamptic mothers compared to the control group. The high incidence of low birth weight in the neonates born to preeclamptic mothers in this study is a reflection of the high incidence of prematurity (49.3%), as prematurity was the major adverse perinatal outcome. The overall mean placental weights in those with preeclampsia in this study were significantly lower than those of the normotensive control group. Similar weights were reported by Ezeigwe et al 27 in Southeast Nigeria, Sankar et al 18 and Kambale et al 31 in India, Kos et al 15 in Croatia where comparisons were also made between preeclamptic and normal groups. A previous work in this centre by Adesina et al recorded a mean placental weight of 580.8 grams. 32 . The mean foeto-placental weight ratios in the study and the control group were 4.87 and 5.01. The foeto-placental weight was slightly lower in the study group but had no statistical differences between these groups. The study concluded that babies born to preeclamptic mothers had similar growth patterns to those born to normotensive women. A higher incidence of abnormal cord insertion was recorded in the study group. The incidence of marginal cord insertion was 10 times higher in the study group compared to the control group. However, abnormal cord insertions are not considered specific for preeclampsia. Gross infarcts were appreciated in only 16% of the placentas from the preeclamptic group compared to none seen in the normotensive group. Other studies have recorded higher incidences. Placental infarcts are common but when they are multiple or occupy more than 5% of the placental volume, they are considered pathologic. The microscopic placental lesions exclusively seen in the preeclampsia/eclampsia group (in decreasing frequency) in this study were stromal fibrosis, increased syncytial knotting, infarction, decidual arteriopathy, accelerated villi maturity and incomplete vascular remodelling. The incidence of villous/vascular lesions was 4–7 folds higher in the placentas of the preeclampsia group compared to the normotensive groups. These findings were comparable to early work by Moldenhauer et al 33 who reported that decidual arteriolopathy, villi hypermaturity, intervillous thrombi, and central infarction were significantly higher in the placentas of women with preeclampsia than in normotensive patients. 33 Similar findings were reported by Falcon et al 34 in which 8 studies of histopathological changes in preeclampsia in only English language literature and human studies were reviewed. The study noted that villous lesions account for 48.2% of preeclamptic pregnancies and 11.6% of normal pregnancies while vascular lesions were recorded in 37.3% of preeclamptic pregnancies and 8.1% of normal pregnancies. This review concluded that the incidence of villous/vascular lesions was 4–7 folds higher in the placentas of the preeclampsia group compared to the normotensive groups. 34 The significant microscopic findings in the placentas of preeclamptic women in the study by Ezeigwe et al 27 were decidual arteriopathy, accelerated villous maturation, and cytotrophoblastic proliferation while stromal fibrosis, stromal oedema and syncytial knots were recorded as insignificant findings. 27 These findings were partly comparable to our own findings as stromal fibrosis and increased syncytial knots were prominent findings in our study. Ezeigwe et al employed only routine Haematoxylin/Eosin staining in its histological assessment of the placenta with no additional histochemical staining. This could explain the low incidence of stromal fibrosis recorded in that study. Although chorangiosis was seen more in placentas of those with severe preeclampsia, there was no strong association with maternal disease severity in this study. While some studies have linked chorangiosis to preeclampsia and diabetes suggesting that it is a sequel to placental insufficiency. 19 , 35 Hargitai et al 36 and Roberts 37 pointed out that chorangiosis is an adaptive feature developing as a result of maternal hypoxaemia which could be due to cardiopulmonary diseases or high altitude and not necessarily placental insufficiency or ischaemia. On the other hand, villous immaturity was unexpectedly a significant finding; it is not usually associated with hypertensive diseases, in fact, some studies have reported this finding in cases of maternal diabetes, some cases of foetal growth restriction, and chronic cord obstruction. 36 , 38 This study found associations between vascular and villous abnormalities in the placentas of preeclamptic mothers and Apgar scores at the 5th minute. These same observations were made in the association between the aforementioned vascular and villi abnormalities and foetal outcome but with much stronger statistical significance. Stevens et al 39 examined the association between decidual arteriopathy and worse clinical outcomes and found a striking linear correlation between the numbers of vessels showing fibrinoid necrosis and/or thrombosis in the placental bed (decidua basalis) and increased perinatal mortality. 39 There were strong associations between disease severity and microscopic findings of incomplete vascular remodelling, villi immaturity, and calcifications in the placenta. These lesions were seen mostly in patients with severe preeclampsia and eclampsia. The absence of incomplete vascular remodelling in the placentas of normotensive women and those with mild diseases implied the specificity of this finding in the severe spectrum of preeclampsia, It was seen in 11% of the preeclamptic group and 4.1% of the normotensive group and with a strong association with severe disease. It is usually seen in mothers with metabolic diseases; obesity, excessive weight gain during pregnancy, impaired glucose tolerance, and diabetes We recorded 11% neonatal mortality in the study group but none in the control group. This is corroborated by a similar finding by Randriamahavonjy et al 40 in Madagascar which reported intrauterine mortality and perinatal mortality of 11.34%. 40 Placental insufficiency is often described as the cause of perinatal mortality in preeclampsia. It is defined as the inability of the poorly adaptive placental tissue to deliver adequate perfusion to the growing foetus in utero. A secondary analysis by the World Health Organization (WHO) on the adverse outcomes of preeclampsia/eclampsia in Low-Medium Income countries (LMICs) found that preeclampsia was a predominant risk factor for maternal/perinatal mortality, preterm birth and low birth weight. Also, there was an inverse linear relationship between perinatal mortality and increasing gestation age up to 40 weeks Conclusion The major pathologic lesions in the placenta with a strong association with preeclampsia/eclampsia were acute atherosis, infarction, increased syncytial knots (Tenney-Parker changes), accelerated villi maturity, stromal fibrosis, and microcalcifications. There is a strong association between disease severity and Apgar scores in the 1st minute. There were distinct pathological changes in the placentas of mothers with preeclampsia and demonstrable neonatal morbidity depicted by a high incidence of preterm birth, low birth weights, and low Apgar scores in the 1st minute. The vascular lesions are more of a consequence of the initiating placental pathology in preeclampsia/eclampsia rather than the direct cause of morbidity. Declarations Ethics approval and consent to participate The study was approved by the University of Ilorin Teaching Hospital Ethical Research Committee, Approval number ERC PAN/2017/01/1625. Both study and control group participants showed willingness to participate and signing of the informed consent after explaining the aim of the study. Signing of consent form was part of the inclusion criteria. Consent for publication Not applicable Availability of data and materials The datasets used and analysed during this current study are available from the corresponding author on reasonable request. Competing interest The authors declare that they have no competing interests. Funding Not applicable Authors contribution FOO, BKO, IOK conceptualized and designed this project, FOO collected and analysed the data. FOO, IKM, FIO, IAS and AL wrote the manuscript. All authors proofread the manuscript. Acknowledgement Not applicable References Palei AC, Spradley FT, Warrington JP, George EM, Granger JP. Pathophysiology of hypertension in pre-eclampsia: a lesson in integrative physiology. Acta Physiol (Oxf). 2013 Jul;208(3):224–33. Roberts JM, Bell MJ. If we know so much about preeclampsia, why haven’t we cured the disease? J Reprod Immunol. 2013 Sep;99(1–2):1–9. Warrington JP, George EM, Palei AC, Spradley FT, Granger JP. Recent advances in the understanding of the pathophysiology of preeclampsia. Hypertension. 2013 Oct;62(4):666–73. Adedoyin MA, Adetoro O. Pregnancy and its outcome among teenage mothers in Ilorin, Nigeria. East Afr Med J. 1989;66(7):448–52. Onyiriuka AN, Okolo AA. Perinatal Outcome in Patients With Pre-Eclampsia in Benin City, Nigeria. Trop J Obstet Gynaecol. 2005 Feb 10;21(2):148–52. Ogunlaja OA, Fawole AA, Adesina KT, Akande HJ, Adeniran AS, Ogunlaja IP. Amniotic Fluid Parameters And Perinatal Outcome in Preeclaampsia at Term. Int J Res Med Heal Sci. 2014;4(2):30–5. Singh S, Ekele BA, Shehu CE, Nwobodo EI. Hypertensive disorders in pregnancy among pregnant women in a Nigerian Teaching Hospital. Niger Med J. 2014;55(5):384. Xiong X, Xu H, Wei SQ, Fraser WD. Impact of preeclampsia on placental weight and fetal growth: Preterm versus term births. Journal of Maternal-Fetal and Neonatal Medicine. Informa Healthcare; 2010. p. 201. (22nd European Congress of Perinatal Medicine, 2010 Granada Spain. Conference Start: 20100526 Conference End: 20100529; vol. 23). Placenta: indications for Histopathological and Microbiological Examination. Clinical Guidelines: Obstetrics and Gynaecology. Perth Western Australia: Government of Western Australia, Department of Health; 2015. Phelan ST, Ianus VD, Carpenter Jr RJ, Popek EJ. Point-Counterpoint: Placental examination. Contemp Ob Gyn. 2014;59(2):52–8. Spencer MK, Khong TY. Conformity to guidelines for pathologic examination of the placenta. Arch Pathol Lab Med. 2003 Mar;127(2):205–7. Sills A, Steigman C, Ounpraseuth ST, Odibo I, Sandlin AT, Magann EF, et al. Pathologic examination of the placenta: recommended versus observed practice in a university hospital. Int J Womens Health. 2013;5:309–12. Dahlstrøm B, Romundstad P, Øian P, Vatten LJ, Eskild A. Placenta weight in pre-eclampsia. Acta Obstet Gynecol Scand. 2008 Jan;87(6):608–11. Motwani R, Sontakke Y, Goyal M. Effects of pregnancy induced hypertension on human placenta. J Evol Med Dent Sci. 2013;2(33):6275–82. Kos M, Czernobilsky B, Hlupic L, Kunjko K. Pathological changes in placentas from pregnancies with preeclampsia and eclampsia with emphasis on persistence of endovascular trophoblastic plugs. Croat Med J. 2005 Jun;46(3):404–9. Narasimha A, Vasudeva DS. Spectrum of changes in placenta in toxemia of pregnancy. Indian J Pathol Microbiol. 2011 Jan 1;54(1):15–20. Rani N, Dhingra R, Arya DS, Bhatla N, Kumar R. Morphological and histological changes in placentas of preeclamptic patients. Ann Natl Acad Med Sci. 2009;3(45):221–32. Sankar KD, Bhanu PS, Ramalingam K, Kiran S, Ramakrishna BA. Histomorphological and morphometrical changes of placental terminal villi of normotensive and preeclamptic mothers. Anat Cell Biol. 2013 Dec;46(4):285–90. Sudeshna M, Sharmitha B, Skeikh AA, Hasi D, Abhijit B, Chiranjib B, et al. Changes in the Placenta of a Hypertensive and Diabetic Mother. Indian J Basic Appl Med Res. 2013;1(3):6–11. Zuccollo J. A practical approach to placental examination. O&G Mag R Aust New Zeal Coll Obstet Gynaecol. 2010;12(4):39–41. Jepson HA, Talashek ML, Tichy AM. The Apgar score: evolution, limitations, and scoring guidelines. Birth. 1991;18(2):83–92. Goyal RC. Determination of Sample Size. In: Research Methodology for Health Professionals. 1st ed. Wardha, Maharashtra, India: New Delhi; Jaypee Brothers Medical Publishers Ltd; 2013. p. 119–28.. ACOG Committee on Practice Bulletins--Obstetrics. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Number 33, January 2002. Obstet Gynecol. 2002;99(1):159–67. Nelson DB, Ziadie MS, McIntire DD, Rogers BB, Leveno KJ. Placental pathology suggesting that preeclampsia is more than one disease. Am J Obstet Gynecol. 2014 Jan 1;210(1):66.e1-66.e7. Ernst LM. Maternal vascular malperfusion of the placental bed. APMIS 2018; 126: 551–560. Yakasai IA, Morhason-Bello IO. Risk factors for pre-eclampsia among women at antenatal booking in Kano, Northern Nigeria. Healthc Low-resource Settings. 2013;1(1):12. Ezeigwe CO, Okafor CI, Eleje GU, Udigwe GO, Anyiam DC. Placental Peripartum Pathologies in Women with Preeclampsia and Eclampsia. 2018;2018. Kooffreh M, Ekott M, Ekpoudom D. The prevalence of pre-eclampsia among pregnant women in the University of Calabar Teaching Hospital, Calabar. Saudi J Heal Sci. 2014;3(3):133. Sotunsa J, Sharma S, Imaralu J, Lee T, Vidler M, Adepoju A, et al. The hypertensive disorders of pregnancy in Ogun state, Nigeria. Pregnancy Hypertens An Int J Women’s Cardiovasc Heal. 2016 Jul 1;6(3):209. Bramham K, Briley AL, Seed P, Poston L, Shennan AH, Chappell LC. Adverse maternal and perinatal outcomes in women with previous preeclampsia: a prospective study. Am J Obstet Gynecol. 2011;204(6):512.e1-512.e9. Kambale T, Iqbal B, Ramraje S, Swaimul K, Salve S. Placental morphology and fetal implications in pregnancies complicated by pregnancy-induced hypertension. Med J Dr DY Patil Univ. 2016;9(3):341. Adesina, Ogunlaja OO, Aboyeji AP, Akande HJ, Adeniran AS, Olarinoye A, et al. Relationship between gross placental characteristics and perinatal outcome of low-risk singleton deliveries. Niger Postgrad Med J. 2016;23(4):191. Moldenhauer JS, Stanek J, Warshak C, Khoury J, Sibai B. The frequency and severity of placental findings in women with preeclampsia are gestational age dependent. Am J Obstet Gynecol. 2003;189(4):1173–7. Falco ML, Sivanathan J, Laoreti A, Thilaganathan B, Khalil A. Placental histopathology associated with pre-eclampsia : systematic review and meta-analysis. 2017;(April):295–301. Gupta R, Nigam S, Arora P, Khurana N, Batra S, Mandal AK. Clinico-pathological profile of 12 cases of chorangiosis. Arch Gynecol Obstet. 2006;274(1):50–3. Hargitai B. Best practice No 178: Examination of the human placenta. J Clin Pathol. 2004;57(8):785–92. Roberts DJ. Placental pathology, a survival guide. Arch Pathol Lab Med. 2008 Apr;132(4):641–51. Redline RW. Classification of placental lesions. Vol. 213, American Journal of Obstetrics and Gynecology. 2015. Stevens DU, Al-Nasiry S, Bulten J, Spaanderman MEA. Decidual vasculopathy in preeclampsia: Lesion characteristics relate to disease severity and perinatal outcome. Placenta. 2013;34(9):805–9. Randriamahavonjy R, Tsifiregna RL, Andrianirina ZZ, Andrianampanalinarivo HR. Materno-fetal outcomes in pre eclampsia in a rural hospital of Antananarivo Madagascar. 2018;6(4):1064–7. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-4695829","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":333546041,"identity":"33ce3096-57ab-498a-8046-0f3ec4ee5496","order_by":0,"name":"Folaranmi Olaleke Oluwasegun","email":"","orcid":"","institution":"University of Ilorin Teaching Hospital","correspondingAuthor":false,"prefix":"","firstName":"Folaranmi","middleName":"Olaleke","lastName":"Oluwasegun","suffix":""},{"id":333546042,"identity":"3b47f655-dda7-4775-9c2b-3a84fbe16e9d","order_by":1,"name":"Buhari Mikhail Olayinka","email":"","orcid":"","institution":"University of Ilorin Teaching Hospital","correspondingAuthor":false,"prefix":"","firstName":"Buhari","middleName":"Mikhail","lastName":"Olayinka","suffix":""},{"id":333546043,"identity":"4df91c9b-99d3-46b4-bea9-8be5c0dff287","order_by":2,"name":"Ibrahim Olatunde Kazeem","email":"","orcid":"","institution":"University of Ilorin Teaching Hospital","correspondingAuthor":false,"prefix":"","firstName":"Ibrahim","middleName":"Olatunde","lastName":"Kazeem","suffix":""},{"id":333546044,"identity":"36e39363-6a83-467d-996d-70beffc2627e","order_by":3,"name":"Ibiyeye Kehinde Muibat","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABD0lEQVRIie2QMWsCMRTHX0i5KXrrOyLpV0i5wYriZzkRdLHgdLMgxMVZrrj0Uzif3CrneuCiS2e7iIPS5gRR4VI7FsxvSfLP+5H3AmCx/EMcJIPTBoHGAPIVgJ7yPylOoBW8r+jS88rk1fEXpcyHCr9UA7zJYsf7fRTVUSmGbZhA1f0obqwyV9676gDnbzMeSfQrSTkgUZpALVobZmkpXlIJiFxhElsRZZLmicxis3JU31rpfV6U4z2FqFg31nMuCsmV5cA0y7A2TtvMm3b8ulZ81Mp8nHaZzIp/7Hk62mT7sClw1d6s2KEh0F28rPdhXchlcWOaJyQOsJsor2WAgUmhWzgUXrjGVywWi+Wx+AHvlVErnbMC1wAAAABJRU5ErkJggg==","orcid":"","institution":"University of Ilorin","correspondingAuthor":true,"prefix":"","firstName":"Ibiyeye","middleName":"Kehinde","lastName":"Muibat","suffix":""},{"id":333546045,"identity":"6bc17797-932c-452f-8191-283bea032a97","order_by":4,"name":"Fodeke Isreal Olayinka","email":"","orcid":"","institution":"University of Ilorin Teaching Hospital","correspondingAuthor":false,"prefix":"","firstName":"Fodeke","middleName":"Isreal","lastName":"Olayinka","suffix":""},{"id":333546046,"identity":"776192b6-7b50-4019-a9a8-722df4110174","order_by":5,"name":"Isa Abdulazeez Salman","email":"","orcid":"","institution":"University of Ilorin Teaching Hospital","correspondingAuthor":false,"prefix":"","firstName":"Isa","middleName":"Abdulazeez","lastName":"Salman","suffix":""},{"id":333546047,"identity":"afad5a83-3a8d-4ae9-b7cd-19b050f74977","order_by":6,"name":"Abdulkadir Lukman","email":"","orcid":"","institution":"University of Ilorin Teaching Hospital","correspondingAuthor":false,"prefix":"","firstName":"Abdulkadir","middleName":"","lastName":"Lukman","suffix":""}],"badges":[],"createdAt":"2024-07-06 08:36:02","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-4695829/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-4695829/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":62139691,"identity":"ef3f5a5e-9530-445f-ade1-805754554a7f","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":25860,"visible":true,"origin":"","legend":"\u003cp\u003ePie chart showing the distribution of preeclampsia cases.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/61883a7e1e4e80f9e2055f9f.png"},{"id":62139692,"identity":"a519ccbc-1d9f-4d13-a315-a03e6fdbfec8","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":480628,"visible":true,"origin":"","legend":"\u003cp\u003eChorangiosis: Photomicrograph showing increased villous capillaries and congestion. H\u0026amp;E. A x100, B x400\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/88446a56146f0e9f2389f03e.png"},{"id":62140312,"identity":"1b74f874-f62c-4c3e-92bc-5aba8e3efca2","added_by":"auto","created_at":"2024-08-09 17:03:20","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":226762,"visible":true,"origin":"","legend":"\u003cp\u003eAcute chorioamnionitis showing neutrophilic infiltrates in the chorionic plate.\u003c/p\u003e\n\u003cp\u003eH\u0026amp;E x400\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/86f64cd5e18d1a1b4276320f.png"},{"id":62140311,"identity":"53d2927d-16af-4479-9399-1c15f464ff16","added_by":"auto","created_at":"2024-08-09 17:03:20","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":417855,"visible":true,"origin":"","legend":"\u003cp\u003eA. Photomicrograph showing advanced decidual arteriopathy with acute atherosis and fibronoid necrosis. H\u0026amp;E x100.\u003c/p\u003e\n\u003cp\u003eB. Advanced decidual arteriopathy with marked fibrinoid necrosis of decidual vessels. x400\u003c/p\u003e","description":"","filename":"4.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/0e2028b342520d5c5ac81789.png"},{"id":62139694,"identity":"d49ce52d-7286-49db-892c-cf9cacfbf5e6","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":455654,"visible":true,"origin":"","legend":"\u003cp\u003eA. Photomicrograph of placental infarction with collapse of the intervillous space, loss of nuclear basophilia in the villi (few pockets of viable villi in the left upper part). H\u0026amp;E x100.\u003c/p\u003e\n\u003cp\u003eB. Fibrin deposition (intense pink) around necrotic villi (pale pink), loss of basophilia and loss of intervillous space. PAS x100\u003c/p\u003e","description":"","filename":"5.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/2a84a10b10ea8dd9df1ed3bb.png"},{"id":62139702,"identity":"f02f3923-4b5e-4312-b7ef-e05d4dad38eb","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":6,"title":"Figure 6","display":"","copyAsset":false,"role":"figure","size":279367,"visible":true,"origin":"","legend":"\u003cp\u003eTenney Parker” changes: Increased syncytial knots in the intermediate and terminal villi. H\u0026amp;E x100\u003c/p\u003e","description":"","filename":"6.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/4292ec8da135fa617a3fcc90.png"},{"id":62139698,"identity":"16ad061d-bf20-4b48-aa94-b2a032bc7e7c","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":7,"title":"Figure 7","display":"","copyAsset":false,"role":"figure","size":346607,"visible":true,"origin":"","legend":"\u003cp\u003eA. Basal plate showing an arteriole with persistent muscularised arterioles (abnormal vascular remodelling). H\u0026amp;E x100\u003c/p\u003e\n\u003cp\u003eB. Masson’s Trichrome (MT) x100\u003c/p\u003e","description":"","filename":"7.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/217edf63e9f4fb749ad128c6.png"},{"id":62139696,"identity":"ff1ec46a-34bc-43e1-b074-5cd275a97e6a","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":8,"title":"Figure 8","display":"","copyAsset":false,"role":"figure","size":265751,"visible":true,"origin":"","legend":"\u003cp\u003eVillous hypoplasia: Term placenta characterized by long, slender, minimal branching terminal villi and unusually wide intervillous spaces. H\u0026amp;E x100.\u003c/p\u003e","description":"","filename":"8.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/27727b17bef6305062a2c9e0.png"},{"id":62139700,"identity":"caa05a07-4247-4501-be91-09e75082146e","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":9,"title":"Figure 9","display":"","copyAsset":false,"role":"figure","size":286565,"visible":true,"origin":"","legend":"\u003cp\u003eVilli immaturity. Placental section showing predominantly immature intermediate villi (larger), few mature intermediate villi and few terminal villi. H\u0026amp;E x 100\u003c/p\u003e","description":"","filename":"9.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/0930d8f980a1a171b60515ef.png"},{"id":62139699,"identity":"2615e8ef-5b21-4c32-bfa6-3d12e21ab00f","added_by":"auto","created_at":"2024-08-09 16:55:20","extension":"png","order_by":10,"title":"Figure 10","display":"","copyAsset":false,"role":"figure","size":278791,"visible":true,"origin":"","legend":"\u003cp\u003eStromal fibrosis: Terminal villi showing increased collagen and reduced vasculature. MT x100\u003c/p\u003e","description":"","filename":"10.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/1ddad8c704a1fea23b14cc17.png"},{"id":62140313,"identity":"9c7afba3-0106-416c-9794-d783aa7f62e7","added_by":"auto","created_at":"2024-08-09 17:03:20","extension":"png","order_by":11,"title":"Figure 11","display":"","copyAsset":false,"role":"figure","size":257282,"visible":true,"origin":"","legend":"\u003cp\u003eFigure 12. Microcalcifications (dark blue) in a term placenta. H\u0026amp;E x40\u003c/p\u003e","description":"","filename":"11.png","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/3d419be6d76ae7b39799e3d0.png"},{"id":77399124,"identity":"ca5f95ec-a885-4056-93e8-db8ee3051807","added_by":"auto","created_at":"2025-02-28 08:09:12","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":4007404,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4695829/v1/f3018bd7-030e-4480-90de-bd3868159fbc.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Spectrum of Morphological Changes in the Placenta of Women with Preeclampsia/Eclampsia and Correlation with Neonatal Morbidity","fulltext":[{"header":"BACKGROUND","content":"\u003cp\u003ePreeclampsia/eclampsia is a pregnancy-specific syndrome characterized by new-onset hypertension and proteinuria.\u003csup\u003e1\u003c/sup\u003e It has been recognized as a significant contributor to maternal and foetal mortality and morbidity for over 100 years. It was in the late nineteenth century that it was recognized that eclampsia, which had been considered a convulsive disorder of pregnancy for almost a thousand years, was preceded by increased maternal blood pressure and proteinuria, hence preeclampsia. Not long after these observations, it was evident that even without seizures, preeclampsia indicated a potentially fatal disease for mothers and babies.\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eThe overall prevalence in the United States is 3-8% with higher incidence in specific ethnic subpopulations, notably African-Americans.\u003csup\u003e3\u003c/sup\u003e Studies done in Nigeria have recorded varying values ranging from 5-7.6%.\u003csup\u003e4-7\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eDespite being one of the leading causes of maternal death and a major contributor to maternal and perinatal morbidity, the pathogenesis of preeclampsia/eclampsia has not been fully unravelled. Hypertension associated with preeclampsia develops during pregnancy and remits after delivery, implicating the placenta as a central culprit in the pathogenic process.\u003csup\u003e1\u003c/sup\u003e An initiating event in preeclampsia has been postulated to be reduced placental perfusion that leads to widespread dysfunction of the maternal vascular endothelium and hypertension by mechanisms that remain to be defined.\u003csup\u003e1,3,8\u003c/sup\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eHistopathological and microbiological examination of the placenta can reveal the aetiology of many conditions, such as stillbirth, pre-term delivery, intrauterine growth restrictions (IUGR), and neurological impairment.\u003csup\u003e9\u003c/sup\u003e Placental examination reveals abnormal findings in almost all cases of foetal death, and the pathology report can diagnose the cause of death in about one-third of the cases in which it could not be determined clinically.\u003csup\u003e10\u003c/sup\u003e Furthermore, medical conditions that can recur can be recognized, providing information to manage or treat subsequent pregnancies.\u003csup\u003e10-12\u003c/sup\u003e The data from a placental examination may also offer essential evidence in medical liability cases. They may provide defence against allegations of malpractice when the findings indicate that foetal or placental disease contributed to adverse pregnancy outcomes independent of the clinical care provided.\u003csup\u003e10,11\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eMany studies have established the pathological changes in the placenta of preeclamptic mothers, which include gross findings of smaller placentas with foci of calcification, infarction, and microscopic findings of increased syncytial knot formation, fibrinoid necrosis, stromal fibrosis, hyalinised villi, altered villous vascularity, cytotrophoblastic cell proliferation, increased villi vascularisation and branching, intervillous haemorrhage and basement membrane thickening.\u003csup\u003e13-19\u0026nbsp;\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eThere is paucity of such data in this environment; the placenta is handed to the mother or relatives almost immediately after birth most times without examination due to social and cultural beliefs that the placenta can be used for diabolical purposes.\u003c/p\u003e\n\u003cp\u003eIn 1997, the College of American Pathologists (CAP) published practical guidelines for placental pathological examination following delivery.\u003csup\u003e12\u003c/sup\u003e In recent times, institutions have published modifications based on the original guidelines; the recommendations are for underlying maternal disease, pregnancy complications, foetal/ neonatal conditions, or placental indications.\u003csup\u003e20\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eSince the use of Apgar scores more than 50 years ago, it has served as a globally acceptable method of assessing the physical status of the newborn in the immediate post-natal life and also as a predictor of infant morbidity and mortality.\u003csup\u003e21\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eThis research aimed to study the pathological changes in the placenta of preeclamptic/eclamptic mothers and the impact on newborn morbidity and mortality.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003e146 booked pregnant women diagnosed at the clinic, labour ward, or at the Emergency Room of University of Ilorin Teaching hospital Nigeria were recruited for this study. \u0026nbsp;The sample size was calculated as reported by Goyal 2013\u003csup\u003e22\u003c/sup\u003e. Informed consents were taken from the recruited patients.\u003c/p\u003e\n\u003cp\u003eInclusion criteria:\u003c/p\u003e\n\u003cp\u003eStudy group\u003c/p\u003e\n\u003cp\u003e1. Maternal age from 18-40 years.\u003c/p\u003e\n\u003cp\u003e2. Gestational age from viability (28 weeks) to term (not beyond 41 weeks, 6 days).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e3. Diagnosed cases of preeclampsia.\u003c/p\u003e\n\u003cp\u003e4. Willingness to participate and signing of the informed consent after explaining the aim of the study\u003c/p\u003e\n\u003cp\u003eControl group\u003c/p\u003e\n\u003cp\u003e1. Maternal age from 18-40 years.\u003c/p\u003e\n\u003cp\u003e2. Gestational age from viability (28 weeks) to expected date of delivery (not beyond 41 weeks, 6 days).\u003c/p\u003e\n\u003cp\u003e3. Normal clinical and laboratory parameters\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e3. Willingness to participate and signing of the informed consent after explaining the aim of the study.\u003c/p\u003e\n\u003cp\u003eExclusion criteria:\u003c/p\u003e\n\u003cp\u003e1. Presence of other maternal diseases such as chronic renal diseases, diabetes mellitus, sickle cell disease, autoimmune disorders and coagulopathies.\u003c/p\u003e\n\u003cp\u003e2. Evidence of gross foetal anomalies (in utero and post-delivery).\u003c/p\u003e\n\u003cp\u003e3. Post term pregnancies (gestational age \u0026ge; 42 weeks).\u003c/p\u003e\n\u003cp\u003e4. Unwillingness to participate in the study.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe diagnosis of preeclampsia was based on findings of new onset hypertension and or proteinuria occurring after 20 weeks of gestation with significant proteinuria (i.e., \u0026ge;300 mg per 24 hours, protein to creatinine ratio \u0026ge;0.3 day or 1+ urinary protein dipstick reading)\u003csup\u003e23\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eThe study group participants were further stratified into those with:\u003c/p\u003e\n\u003col\u003e\n \u003cli\u003eMild-Moderate Preeclampsia: Patients with systolic BP \u0026gt;140mmHg but ˂160mmHg and Diastolic˂110mmHg, proteinuria \u0026gt;0.3g/24 hours or 1+ on dipstick\u003c/li\u003e\n \u003cli\u003eSevere preeclampsia: Patients with any of these:\u003c/li\u003e\n\u003c/ol\u003e\n\u003cp\u003e(a)Systolic BP \u0026ge;160mmHg or diastolic BP \u0026gt;110mmHg on two occasions at least 4 hours apart, proteinuria \u0026gt;5g/24 hours or \u0026gt;3+ on dipstick.\u003c/p\u003e\n\u003cp\u003e(b) Thrombocytopenia (platelet count \u0026lt;100,000).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e(c) Impaired liver function\u003c/p\u003e\n\u003cp\u003e(d) New development of renal insufficiency.\u003c/p\u003e\n\u003cp\u003e(e) Pulmonary oedema.\u003c/p\u003e\n\u003cp\u003e(f) New-onset cerebral or visual disturbances.\u003c/p\u003e\n\u003cp\u003e3. \u0026nbsp; Eclampsia: Preeclamptic patient with onset of seizures before, during or after delivery.\u003c/p\u003e\n\u003cp\u003eImmediately after delivery, the newborns\u0026rsquo; weights and Apgar scores were recorded. The placentas were washed to remove blood clots, weighed. They were examined for completeness, and gross abnormalities in the umbilical cord, foetal membranes, and placenta disc.\u003c/p\u003e\n\u003cp\u003eFull-thickness sections were taken from the central areas, grossly abnormal areas, and the membrane roll. The sections were fixed for 24 hours in 10% neutral-buffered formalin, processed for paraffin sections using a carousel-type automatic tissue processor. Masson\u0026rsquo;s Trichrome and Periodic Acid Schiff (PAS) were used to demonstrate the presence of fibrosis, and the basement membranes of placental/villous vessels respectively. The stained slides were reviewed to evaluate the pathologic changes and the pathologic findings were correlated to the birth weights and Apgar scores of the newborns.\u003c/p\u003e\n\u003cp\u003eStatistical analysis was done with the Statistical Package for the Social Science (SPSS) version 22.0 (SPSS Inc., Chicago, IL, USA). \u0026nbsp;Descriptive analysis was reported as means and standard deviations. Pearson\u0026rsquo;s chi-squared test and Student\u0026rsquo;s t-test were used to analyze the observed differences in the study and control groups. The level of significance was established at a p value of \u0026le; 0.05.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eDemographic characteristics of study group\u003c/p\u003e \u003cp\u003eA total of 1,575 women had their deliveries taken at the Department of Obstetrics and Gynaecology of the University of Ilorin Teaching Hospital, Ilorin during the period of study. 5.14% of the women had preeclampsia-eclampsia. 60.3% of the preeclampsia/eclampsia patients had mild-moderate preeclampsia, 17.8% had severe preeclampsia and 21.9% had eclampsia. 23% had a history of hypertension in pregnancy without proteinuria (PIH), and 16.4% had a history of chronic hypertension (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). The mean ages of the participants (study vs. control) were 30.04\u0026thinsp;\u0026plusmn;\u0026thinsp;4.67 and 29.86\u0026thinsp;\u0026plusmn;\u0026thinsp;4.81 with both groups having ages ranging from 21\u0026ndash;40 years. The mean gestational age at which the diagnosis of preeclampsia-eclampsia was made was 35.21\u0026thinsp;\u0026plusmn;\u0026thinsp;3.85 weeks. The means of the gestational age at delivery for the study and control groups were 37.04\u0026thinsp;\u0026plusmn;\u0026thinsp;2.32 weeks and 38.48\u0026thinsp;\u0026plusmn;\u0026thinsp;1.28 weeks respectively. There is a remarkable increase in the rate of caesarean section in those with preeclampsia/eclampsia (41.1%) compared to the control group (2.7%) with 97.3% of the control group having vaginal delivery compared to 58.9% for the study group.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eFoetal weight and Apgar score\u003c/p\u003e \u003cp\u003eThe mean birth weights of the study and control group were 2.66\u0026thinsp;\u0026plusmn;\u0026thinsp;0.77kg and 3.21\u0026thinsp;\u0026plusmn;\u0026thinsp;0.43kg respectively, 41.1% and 5.5% of the neonates in the study group had low birth weights and very low birth weights respectively compared to 9.6% in the control group who had low birth weights. The control group had no neonate in the very low birth weight category. 53.4% of the study group had normal birth weights, compared to 90.4% in the control group.\u003c/p\u003e \u003cp\u003eThe mean Apgar scores in the 5th minute in the study group and control group were 7.07\u0026thinsp;\u0026plusmn;\u0026thinsp;2.75 and 8.71\u0026thinsp;\u0026plusmn;\u0026thinsp;0.48 respectively.\u003c/p\u003e \u003cp\u003ePlacental parameters in the participants (Study vs. Control).\u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eGross changes:\u003c/h2\u003e \u003cp\u003eGross findings of infarction were seen in 16.4% of the placentas in the study group (66.7% were seen in mothers with severe preeclampsia, 25% eclampsia and 8.3% mild-moderate preeclampsia), while none was observed in the placentas of the control group.\u003c/p\u003e \u003cp\u003eThe mean placental weights in the study vs. control group were 556.82g\u0026thinsp;\u0026plusmn;\u0026thinsp;169.72g vs. 649.93g\u0026thinsp;\u0026plusmn;\u0026thinsp;116.38g. All the 3 placentas that weighed less than 300g were from mothers with severe preeclampsia. 71.4% of those weighing between 300-399g were from women with severe preeclampsia and 28.6% mild-moderate preeclampsia. 29 placentas weighed above 600g, out of which 51.7% were from mothers with mild-moderate preeclampsia, 31% severe preeclampsia, and 17.2% eclampsia.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec4\" class=\"Section2\"\u003e \u003ch2\u003eMicroscopic changes:\u003c/h2\u003e \u003cp\u003eThe pathologic findings seen include decidual arteriopathy, infarction, increased syncytial knots, abnormal vascular remodelling, terminal villous hypoplasia, accelerated villi maturation, villi immaturity, stromal fibrosis, acute chorioamnionitis, and chorangiosis.\u003c/p\u003e \u003cp\u003eComparison of microscopic abnormalities in the study and control groups demonstrated statistical significance (with most showing strong association), Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, in all of the microscopic features except for chorangiosis (Fig.\u0026nbsp;2) and acute chorioamnionitis (Fig.\u0026nbsp;3) in which there were no significant differences between the two groups (p\u0026thinsp;=\u0026thinsp;0.085 and p\u0026thinsp;=\u0026thinsp;0.698).\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eComparison of microscopic placental parameters (Study vs. Control).\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"7\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMicroscopic parameters\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colspan=\"2\" nameend=\"c3\" namest=\"c2\"\u003e \u003cp\u003eStudy group n (%)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colspan=\"2\" nameend=\"c5\" namest=\"c4\"\u003e \u003cp\u003eControl n (%)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eχ\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e \u003cp\u003eρ\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eYes\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eYes\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDecidual arteriopathy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e11 (15.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e62 (84.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e73 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e11.896\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.001*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInfarction\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e22 (30.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e51 (69.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e73 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e25.903\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e\u0026lt;\u0026thinsp;0.001*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIncreased syncytial knots\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e48 (65.8)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e25 (34.2)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e73 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e71.510\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e\u0026lt;\u0026thinsp;0.001*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIncomplete vascular remodelling\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e9 (12.3)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e64 (87.7)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e73 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e9.591\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.002*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eChorangiosis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e7 (9.6)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e66 (90.4)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2 (2.7)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e71 (97.3)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e2.960\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e0.085\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTerminal villous hypoplasia\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e4 (5.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e69 (94.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e73 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e4.113\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.043*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAccelerated villi maturity\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e11 (15.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e62 (84.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e73 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e11.896\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.001*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVilli immaturity\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e11 (15.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e62 (84.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e3 (4.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e70 (95.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e5.056\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.025*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eStromal fibrosis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e50 (68.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e23 (31.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e73 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e76.042\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e\u0026lt;\u0026thinsp;0.001*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAcute chorioamnionitis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e3 (4.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e70 (95.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e4 (5.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e69 (94.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e0.150\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e0.698\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMicrocalcifications\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e54 (74.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e19 (26.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e24 (32.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e49 (67.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c6\"\u003e \u003cp\u003e24.774\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e\u0026lt;\u0026thinsp;0.001*\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"7\"\u003eχ\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e: Chi Square test. *= p\u0026thinsp;\u0026lt;\u0026thinsp;0.050 (statistically significant)\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eDecidual arteriopathy (Fig.\u0026nbsp;4) was seen in 15.1% of the placentas in the study group as against none in the control group (p\u0026thinsp;=\u0026thinsp;0.001) and infarction (Fig.\u0026nbsp;5) was seen in 30.1% of the placentas in the study group as against none in the control group (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). 65.8% showed increased syncytial knotting (Fig.\u0026nbsp;6) while none was seen in the control group (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). Incomplete vascular remodelling (Fig.\u0026nbsp;7) was seen in 12.3% of the placentas in the study group but none was observed in the control group (p\u0026thinsp;=\u0026thinsp;0.002). 5.5% in the study group showed terminal villous hypoplasia (Fig.\u0026nbsp;8) versus none in the control group (p\u0026thinsp;=\u0026thinsp;0.043). 15.1% showed accelerated maturity (Fig.\u0026nbsp;9) in premature neonates in the study group while none was recorded in the control group (p\u0026thinsp;=\u0026thinsp;0.001). 15.1% of placentas showed villi immaturity (Fig.\u0026nbsp;9) in the study group as against 4.1% in the control group (p\u0026thinsp;=\u0026thinsp;0.025). Stromal fibrosis (Fig.\u0026nbsp;10) was seen in 68.5% of the placentas while none was seen in the control group. 74% in the study group showed microcalcifications (Fig.\u0026nbsp;11) (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). By comparison, 32.9% placentas in the control group showed microcalcifications (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001).\u003c/p\u003e \u003cp\u003eMicroscopic placental findings, severity of preeclapsia/eclampsia and foetal outcome.\u003c/p\u003e \u003cp\u003eThe total number of placentas with features of incomplete vascular modelling was 9, 55.6% were seen in mothers with severe preeclampsia and 44.4% were seen in those with eclampsia. Villi immaturity was seen in 11 placentas, 54.5% in mothers with severe preeclampsia, and 45.5% in eclampsia. 54 placentas showed microcalcifications, 50% were seen in mothers with severe preeclampsia, 25.9% mild-moderate preeclampsia, and 24.1% were seen in those with eclampsia (Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eInfarction was seen in 40.9% of those with severe preeclampsia, 31.8% eclampsia, and 27.3% mild-moderate preeclampsia. Microscopic findings of accelerated villi maturity had no statistical significance but were observed to be more common in the placenta of patients with severe disease with 36.4% in severe preeclampsia 45.5% in eclampsia and 18.2% in mild-moderate preeclampsia.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eAssociation between microscopic finding and severity of disease\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"7\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colspan=\"3\" nameend=\"c4\" namest=\"c2\"\u003e \u003cp\u003eSeverity of disease\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMicroscopy\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eMild/ moderate (%)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eSevere preeclampsia (%)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eEclampsia (%)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eTotal\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eχ\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e \u003cp\u003eρ\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of decidual vasculopathy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (9.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6 (54.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4 (36.4)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e3.965\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.138\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInfarction\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6 (27.3)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e9 (40.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e7 (31.8)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e22\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1.917\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.383\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIncreased syncytial knots\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e16 (33.3)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e21 (43.8)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11 (22.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e48\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.098\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.952\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIncomplete vascular remodelling\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5 (55.6)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4 (44.4)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e6.214\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.045\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eChorangiosis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2 (28.6)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5 (71.4)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e3.115\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.211\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTerminal villous hypoplasia\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2 (50.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2 (50.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1.271\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.530\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAccelerated villi maturity in preterm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2 (18.2)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e4 (36.4)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e5 (45.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e4.415\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.110\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVilli immaturity\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6 (54.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e5 (45.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e11\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e8.048\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.018\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eStromal fibrosis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e15 (30.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e22 (44.00)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e13 (26.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e50\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e2.043\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.360\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAcute chorioamnionitis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3 (100.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0 (0.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e6.007\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e0.050\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMicrocalcifications\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e14 (25.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e27 (50.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e13 (24.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e54\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e6.433\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e\u003cb\u003e0.040\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"7\"\u003eχ\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e: Chi Square test. *= p\u0026thinsp;\u0026lt;\u0026thinsp;0.050 (statistically significant)\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e11 placentas showed features of decidual arteriopathy, 63.6% were in neonates who survived and 36.4% were seen in neonates who died. Nine placentas showed incomplete vascular remodelling with 55.6% in neonates who survived and 44.4% in those who died. Eleven placentas showed accelerated villi maturity with 63.6% in neonates that survived and 36.4% in those that died. Features of acute chorioamnionitis were seen in 3 placentas, and the neonates died. 54 placentas showed microcalcifications with 94.4% seen in neonates that survived while 5.6% were seen in those that died. Microscopic findings of infarction, increased syncytial knots, chorangiosis, terminal villous hypoplasia, villi immaturity, and stromal fibrosis were seen more predominantly in neonates that survived, with chorangiosis and terminal villous being exclusive findings to this group.\u003c/p\u003e \u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003ePreeclampsia-eclampsia is a pregnancy-specific disease hence its historic name \u0026ldquo;Toxaemia of pregnancy\u0026rdquo;.\u003csup\u003e\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e\u003c/sup\u003e It is characterized by new onset hypertension and/or proteinuria differentiating it from chronic hypertension (hypertension before 20 weeks of gestation) and gestational hypertension also referred to as pregnancy-induced hypertension (PIH) which lacks proteinuria. The placenta has been identified as the root cause of preeclampsia resulting from disordered implantation, poor perfusion of the placenta leading to release of cytokines, and vascular factors which cause widespread endothelial injury. A common pattern of placental injury associated with altered uterine and intervillous blood flow is maternal vascular malperfusion of the placenta. Maternal vascular malperfusion is defined by a group of pathology findings observed in the maternal decidual vessels, which reflect unusual spiral artery remodeling and villous parenchyma abnormalities relating to oxygenation and flow dynamics within the intervillous space of the placenta.\u003csup\u003e\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eThe prevalence of preeclampsia in this study is similar to a work done by Adedoyin and Adetoro\u003csup\u003e\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u003c/sup\u003e in the late 80s on pregnancy outcomes in teenage mothers in Ilorin. They reported a prevalence rate of 5%.\u003csup\u003e4\u003c/sup\u003e. This might suggest that there had been no change in the prevalence of this disease within this locality. The prevalence of the disease varies widely all over the world and even within regions. Studies done in other parts of Nigeria have also shown regional variation; Singh et al\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e reported a prevalence of 6% in Sokoto, Northwest Nigeria, Yakasai et al\u003csup\u003e\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e\u003c/sup\u003e reported a prevalence of 8% in Kano, Ezeigwe et al reported 5.44% in Nnewi, Anambra state.\u003csup\u003e\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e\u003c/sup\u003e while Onyiriuka et al\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e recorded 5.6% in Benin-city. However, a lower prevalence rate of 1.2% was reported by Kooffreh et al in Calabar\u003csup\u003e\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e\u003c/sup\u003e, and 3.3% by Sotunsa et al in Ogun state.\u003csup\u003e\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e\u003c/sup\u003e The reasons for these interregional differences are not known but could be due to sociocultural practices and geographical factors.\u003c/p\u003e \u003cp\u003eThe percentages of women with a past obstetric history of preeclampsia/eclampsia and/or chronic hypertension in previous pregnancies were 17.8% and 16.4% respectively. This implies recurrence in this group of patients. A large study done in the UK noted higher risks of recurrence in Asians and Blacks and also highlighted chronic hypertension as an established risk factor for preeclampsia with data showing up to 22% of women with chronic hypertension having subsequent preeclampsia.\u003csup\u003e\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eIn this study, the gestational age at delivery in the study group was significantly lower than in the control group hence prematurity was one of the major perinatal complications seen. The increased rate of Caesarean delivery seen in the study group showed that preeclamptic mothers had over 13 times the risk of having surgical obstetric intervention than normotensive patients due to the precarious states the mothers present in. The high prevalence of low-birth-weight newborns seen in the study group implied that preeclampsia imposes a 5x risk of low birth weight in preeclamptic mothers compared to the control group. The high incidence of low birth weight in the neonates born to preeclamptic mothers in this study is a reflection of the high incidence of prematurity (49.3%), as prematurity was the major adverse perinatal outcome.\u003c/p\u003e \u003cp\u003eThe overall mean placental weights in those with preeclampsia in this study were significantly lower than those of the normotensive control group. Similar weights were reported by Ezeigwe et al\u003csup\u003e\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e\u003c/sup\u003e in Southeast Nigeria, Sankar et al\u003csup\u003e\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e\u003c/sup\u003e and Kambale et al\u003csup\u003e\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e\u003c/sup\u003e in India, Kos et al\u003csup\u003e\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u003c/sup\u003e in Croatia where comparisons were also made between preeclamptic and normal groups. A previous work in this centre by Adesina et al recorded a mean placental weight of 580.8 grams.\u003csup\u003e\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e\u003c/sup\u003e. The mean foeto-placental weight ratios in the study and the control group were 4.87 and 5.01. The foeto-placental weight was slightly lower in the study group but had no statistical differences between these groups. The study concluded that babies born to preeclamptic mothers had similar growth patterns to those born to normotensive women. A higher incidence of abnormal cord insertion was recorded in the study group. The incidence of marginal cord insertion was 10 times higher in the study group compared to the control group. However, abnormal cord insertions are not considered specific for preeclampsia. Gross infarcts were appreciated in only 16% of the placentas from the preeclamptic group compared to none seen in the normotensive group. Other studies have recorded higher incidences. Placental infarcts are common but when they are multiple or occupy more than 5% of the placental volume, they are considered pathologic.\u003c/p\u003e \u003cp\u003eThe microscopic placental lesions exclusively seen in the preeclampsia/eclampsia group (in decreasing frequency) in this study were stromal fibrosis, increased syncytial knotting, infarction, decidual arteriopathy, accelerated villi maturity and incomplete vascular remodelling. The incidence of villous/vascular lesions was 4\u0026ndash;7 folds higher in the placentas of the preeclampsia group compared to the normotensive groups. These findings were comparable to early work by Moldenhauer et al\u003csup\u003e\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e\u003c/sup\u003e who reported that decidual arteriolopathy, villi hypermaturity, intervillous thrombi, and central infarction were significantly higher in the placentas of women with preeclampsia than in normotensive patients.\u003csup\u003e\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e\u003c/sup\u003e Similar findings were reported by Falcon et al\u003csup\u003e\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e\u003c/sup\u003e in which 8 studies of histopathological changes in preeclampsia in only English language literature and human studies were reviewed. The study noted that villous lesions account for 48.2% of preeclamptic pregnancies and 11.6% of normal pregnancies while vascular lesions were recorded in 37.3% of preeclamptic pregnancies and 8.1% of normal pregnancies. This review concluded that the incidence of villous/vascular lesions was 4\u0026ndash;7 folds higher in the placentas of the preeclampsia group compared to the normotensive groups.\u003csup\u003e\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e\u003c/sup\u003e The significant microscopic findings in the placentas of preeclamptic women in the study by Ezeigwe et al\u003csup\u003e\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e\u003c/sup\u003e were decidual arteriopathy, accelerated villous maturation, and cytotrophoblastic proliferation while stromal fibrosis, stromal oedema and syncytial knots were recorded as insignificant findings.\u003csup\u003e\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e\u003c/sup\u003e These findings were partly comparable to our own findings as stromal fibrosis and increased syncytial knots were prominent findings in our study. Ezeigwe et al employed only routine Haematoxylin/Eosin staining in its histological assessment of the placenta with no additional histochemical staining. This could explain the low incidence of stromal fibrosis recorded in that study.\u003c/p\u003e \u003cp\u003eAlthough chorangiosis was seen more in placentas of those with severe preeclampsia, there was no strong association with maternal disease severity in this study. While some studies have linked chorangiosis to preeclampsia and diabetes suggesting that it is a sequel to placental insufficiency.\u003csup\u003e\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e,\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e\u003c/sup\u003e Hargitai et al\u003csup\u003e\u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e\u003c/sup\u003e and Roberts\u003csup\u003e\u003cspan citationid=\"CR37\" class=\"CitationRef\"\u003e37\u003c/span\u003e\u003c/sup\u003e pointed out that chorangiosis is an adaptive feature developing as a result of maternal hypoxaemia which could be due to cardiopulmonary diseases or high altitude and not necessarily placental insufficiency or ischaemia. On the other hand, villous immaturity was unexpectedly a significant finding; it is not usually associated with hypertensive diseases, in fact, some studies have reported this finding in cases of maternal diabetes, some cases of foetal growth restriction, and chronic cord obstruction.\u003csup\u003e\u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e,\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eThis study found associations between vascular and villous abnormalities in the placentas of preeclamptic mothers and Apgar scores at the 5th minute. These same observations were made in the association between the aforementioned vascular and villi abnormalities and foetal outcome but with much stronger statistical significance. Stevens et al\u003csup\u003e\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e\u003c/sup\u003e examined the association between decidual arteriopathy and worse clinical outcomes and found a striking linear correlation between the numbers of vessels showing fibrinoid necrosis and/or thrombosis in the placental bed (decidua basalis) and increased perinatal mortality.\u003csup\u003e\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eThere were strong associations between disease severity and microscopic findings of incomplete vascular remodelling, villi immaturity, and calcifications in the placenta. These lesions were seen mostly in patients with severe preeclampsia and eclampsia. The absence of incomplete vascular remodelling in the placentas of normotensive women and those with mild diseases implied the specificity of this finding in the severe spectrum of preeclampsia, It was seen in 11% of the preeclamptic group and 4.1% of the normotensive group and with a strong association with severe disease. It is usually seen in mothers with metabolic diseases; obesity, excessive weight gain during pregnancy, impaired glucose tolerance, and diabetes\u003c/p\u003e \u003cp\u003eWe recorded 11% neonatal mortality in the study group but none in the control group. This is corroborated by a similar finding by Randriamahavonjy et al\u003csup\u003e\u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e\u003c/sup\u003e in Madagascar which reported intrauterine mortality and perinatal mortality of 11.34%.\u003csup\u003e40\u003c/sup\u003e Placental insufficiency is often described as the cause of perinatal mortality in preeclampsia. It is defined as the inability of the poorly adaptive placental tissue to deliver adequate perfusion to the growing foetus in utero. A secondary analysis by the World Health Organization (WHO) on the adverse outcomes of preeclampsia/eclampsia in Low-Medium Income countries (LMICs) found that preeclampsia was a predominant risk factor for maternal/perinatal mortality, preterm birth and low birth weight. Also, there was an inverse linear relationship between perinatal mortality and increasing gestation age up to 40 weeks\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThe major pathologic lesions in the placenta with a strong association with preeclampsia/eclampsia were acute atherosis, infarction, increased syncytial knots (Tenney-Parker changes), accelerated villi maturity, stromal fibrosis, and microcalcifications. There is a strong association between disease severity and Apgar scores in the 1st minute. There were distinct pathological changes in the placentas of mothers with preeclampsia and demonstrable neonatal morbidity depicted by a high incidence of preterm birth, low birth weights, and low Apgar scores in the 1st minute. The vascular lesions are more of a consequence of the initiating placental pathology in preeclampsia/eclampsia rather than the direct cause of morbidity.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eEthics approval and consent\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003eto participate\u003c/p\u003e\n\u003cp\u003eThe study was approved by the University of Ilorin Teaching Hospital Ethical Research Committee, Approval number ERC PAN/2017/01/1625. Both study and control group participants showed willingness to participate and signing of the informed consent after explaining the aim of the study. Signing of consent form was part of the inclusion criteria.\u003c/p\u003e\n\u003cp\u003eConsent for publication\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials\u003c/p\u003e\n\u003cp\u003eThe datasets used and analysed during this current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003eCompeting interest\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003eFunding\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e\n\u003cp\u003eAuthors contribution\u003c/p\u003e\n\u003cp\u003eFOO, BKO, IOK conceptualized and designed this project, FOO collected and analysed the data.\u003c/p\u003e\n\u003cp\u003eFOO, IKM, FIO, IAS and AL wrote the manuscript. All authors proofread the manuscript.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAcknowledgement\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003ePalei AC, Spradley FT, Warrington JP, George EM, Granger JP. Pathophysiology of hypertension in pre-eclampsia: a lesson in integrative physiology. Acta Physiol (Oxf). 2013 Jul;208(3):224\u0026ndash;33. \u003c/li\u003e\n\u003cli\u003eRoberts JM, Bell MJ. If we know so much about preeclampsia, why haven\u0026rsquo;t we cured the disease? J Reprod Immunol. 2013 Sep;99(1\u0026ndash;2):1\u0026ndash;9. \u003c/li\u003e\n\u003cli\u003eWarrington JP, George EM, Palei AC, Spradley FT, Granger JP. Recent advances in the understanding of the pathophysiology of preeclampsia. Hypertension. 2013 Oct;62(4):666\u0026ndash;73. \u003c/li\u003e\n\u003cli\u003eAdedoyin MA, Adetoro O. Pregnancy and its outcome among teenage mothers in Ilorin, Nigeria. East Afr Med J. 1989;66(7):448\u0026ndash;52. \u003c/li\u003e\n\u003cli\u003eOnyiriuka AN, Okolo AA. Perinatal Outcome in Patients With Pre-Eclampsia in Benin City, Nigeria. Trop J Obstet Gynaecol. 2005 Feb 10;21(2):148\u0026ndash;52. \u003c/li\u003e\n\u003cli\u003eOgunlaja OA, Fawole AA, Adesina KT, Akande HJ, Adeniran AS, Ogunlaja IP. Amniotic Fluid Parameters And Perinatal Outcome in Preeclaampsia at Term. Int J Res Med Heal Sci. 2014;4(2):30\u0026ndash;5. \u003c/li\u003e\n\u003cli\u003eSingh S, Ekele BA, Shehu CE, Nwobodo EI. Hypertensive disorders in pregnancy among pregnant women in a Nigerian Teaching Hospital. Niger Med J. 2014;55(5):384. \u003c/li\u003e\n\u003cli\u003eXiong X, Xu H, Wei SQ, Fraser WD. Impact of preeclampsia on placental weight and fetal growth: Preterm versus term births. Journal of Maternal-Fetal and Neonatal Medicine. Informa Healthcare; 2010. p. 201. (22nd European Congress of Perinatal Medicine, 2010 Granada Spain. Conference Start: 20100526 Conference End: 20100529; vol. 23). \u003c/li\u003e\n\u003cli\u003ePlacenta: indications for Histopathological and Microbiological Examination. Clinical Guidelines: Obstetrics and Gynaecology. Perth Western Australia: Government of Western Australia, Department of Health; 2015. \u003c/li\u003e\n\u003cli\u003ePhelan ST, Ianus VD, Carpenter Jr RJ, Popek EJ. Point-Counterpoint: Placental examination. Contemp Ob Gyn. 2014;59(2):52\u0026ndash;8. \u003c/li\u003e\n\u003cli\u003eSpencer MK, Khong TY. Conformity to guidelines for pathologic examination of the placenta. Arch Pathol Lab Med. 2003 Mar;127(2):205\u0026ndash;7. \u003c/li\u003e\n\u003cli\u003eSills A, Steigman C, Ounpraseuth ST, Odibo I, Sandlin AT, Magann EF, et al. Pathologic examination of the placenta: recommended versus observed practice in a university hospital. Int J Womens Health. 2013;5:309\u0026ndash;12. \u003c/li\u003e\n\u003cli\u003eDahlstr\u0026oslash;m B, Romundstad P, \u0026Oslash;ian P, Vatten LJ, Eskild A. Placenta weight in pre-eclampsia. Acta Obstet Gynecol Scand. 2008 Jan;87(6):608\u0026ndash;11. \u003c/li\u003e\n\u003cli\u003eMotwani R, Sontakke Y, Goyal M. Effects of pregnancy induced hypertension on human placenta. J Evol Med Dent Sci. 2013;2(33):6275\u0026ndash;82. \u003c/li\u003e\n\u003cli\u003eKos M, Czernobilsky B, Hlupic L, Kunjko K. Pathological changes in placentas from pregnancies with preeclampsia and eclampsia with emphasis on persistence of endovascular trophoblastic plugs. Croat Med J. 2005 Jun;46(3):404\u0026ndash;9. \u003c/li\u003e\n\u003cli\u003eNarasimha A, Vasudeva DS. Spectrum of changes in placenta in toxemia of pregnancy. Indian J Pathol Microbiol. 2011 Jan 1;54(1):15\u0026ndash;20. \u003c/li\u003e\n\u003cli\u003eRani N, Dhingra R, Arya DS, Bhatla N, Kumar R. Morphological and histological changes in placentas of preeclamptic patients. Ann Natl Acad Med Sci. 2009;3(45):221\u0026ndash;32. \u003c/li\u003e\n\u003cli\u003eSankar KD, Bhanu PS, Ramalingam K, Kiran S, Ramakrishna BA. Histomorphological and morphometrical changes of placental terminal villi of normotensive and preeclamptic mothers. Anat Cell Biol. 2013 Dec;46(4):285\u0026ndash;90. \u003c/li\u003e\n\u003cli\u003eSudeshna M, Sharmitha B, Skeikh AA, Hasi D, Abhijit B, Chiranjib B, et al. Changes in the Placenta of a Hypertensive and Diabetic Mother. Indian J Basic Appl Med Res. 2013;1(3):6\u0026ndash;11. \u003c/li\u003e\n\u003cli\u003eZuccollo J. A practical approach to placental examination. O\u0026amp;G Mag R Aust New Zeal Coll Obstet Gynaecol. 2010;12(4):39\u0026ndash;41. \u003c/li\u003e\n\u003cli\u003eJepson HA, Talashek ML, Tichy AM. The Apgar score: evolution, limitations, and scoring guidelines. Birth. 1991;18(2):83\u0026ndash;92. \u003c/li\u003e\n\u003cli\u003eGoyal RC. Determination of Sample Size. In: Research Methodology for Health Professionals. 1st ed. Wardha, Maharashtra, India: New Delhi; Jaypee Brothers Medical Publishers Ltd; 2013. p. 119\u0026ndash;28.. \u003c/li\u003e\n\u003cli\u003eACOG Committee on Practice Bulletins--Obstetrics. ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Number 33, January 2002. Obstet Gynecol. 2002;99(1):159\u0026ndash;67.\u003c/li\u003e\n\u003cli\u003eNelson DB, Ziadie MS, McIntire DD, Rogers BB, Leveno KJ. Placental pathology suggesting that preeclampsia is more than one disease. Am J Obstet Gynecol. 2014 Jan 1;210(1):66.e1-66.e7. \u003c/li\u003e\n\u003cli\u003eErnst LM. Maternal vascular malperfusion of the placental bed. APMIS 2018; 126: 551\u0026ndash;560. \u003c/li\u003e\n\u003cli\u003eYakasai IA, Morhason-Bello IO. Risk factors for pre-eclampsia among women at antenatal booking in Kano, Northern Nigeria. Healthc Low-resource Settings. 2013;1(1):12. \u003c/li\u003e\n\u003cli\u003eEzeigwe CO, Okafor CI, Eleje GU, Udigwe GO, Anyiam DC. Placental Peripartum Pathologies in Women with Preeclampsia and Eclampsia. 2018;2018.\u003c/li\u003e\n\u003cli\u003eKooffreh M, Ekott M, Ekpoudom D. The prevalence of pre-eclampsia among pregnant women in the University of Calabar Teaching Hospital, Calabar. Saudi J Heal Sci. 2014;3(3):133.\u003c/li\u003e\n\u003cli\u003eSotunsa J, Sharma S, Imaralu J, Lee T, Vidler M, Adepoju A, et al. The hypertensive disorders of pregnancy in Ogun state, Nigeria. Pregnancy Hypertens An Int J Women\u0026rsquo;s Cardiovasc Heal. 2016 Jul 1;6(3):209.\u003c/li\u003e\n\u003cli\u003eBramham K, Briley AL, Seed P, Poston L, Shennan AH, Chappell LC. Adverse maternal and perinatal outcomes in women with previous preeclampsia: a prospective study. Am J Obstet Gynecol. 2011;204(6):512.e1-512.e9. \u003c/li\u003e\n\u003cli\u003eKambale T, Iqbal B, Ramraje S, Swaimul K, Salve S. Placental morphology and fetal implications in pregnancies complicated by pregnancy-induced hypertension. Med J Dr DY Patil Univ. 2016;9(3):341.\u003c/li\u003e\n\u003cli\u003eAdesina, Ogunlaja OO, Aboyeji AP, Akande HJ, Adeniran AS, Olarinoye A, et al. Relationship between gross placental characteristics and perinatal outcome of low-risk singleton deliveries. Niger Postgrad Med J. 2016;23(4):191.\u003c/li\u003e\n\u003cli\u003eMoldenhauer JS, Stanek J, Warshak C, Khoury J, Sibai B. The frequency and severity of placental findings in women with preeclampsia are gestational age dependent. Am J Obstet Gynecol. 2003;189(4):1173\u0026ndash;7.\u003c/li\u003e\n\u003cli\u003eFalco ML, Sivanathan J, Laoreti A, Thilaganathan B, Khalil A. Placental histopathology associated with pre-eclampsia : systematic review and meta-analysis. 2017;(April):295\u0026ndash;301. \u003c/li\u003e\n\u003cli\u003eGupta R, Nigam S, Arora P, Khurana N, Batra S, Mandal AK. Clinico-pathological profile of 12 cases of chorangiosis. Arch Gynecol Obstet. 2006;274(1):50\u0026ndash;3. \u003c/li\u003e\n\u003cli\u003eHargitai B. Best practice No 178: Examination of the human placenta. J Clin Pathol. 2004;57(8):785\u0026ndash;92. \u003c/li\u003e\n\u003cli\u003eRoberts DJ. Placental pathology, a survival guide. Arch Pathol Lab Med. 2008 Apr;132(4):641\u0026ndash;51. \u003c/li\u003e\n\u003cli\u003eRedline RW. Classification of placental lesions. Vol. 213, American Journal of Obstetrics and Gynecology. 2015. \u003c/li\u003e\n\u003cli\u003eStevens DU, Al-Nasiry S, Bulten J, Spaanderman MEA. Decidual vasculopathy in preeclampsia: Lesion characteristics relate to disease severity and perinatal outcome. Placenta. 2013;34(9):805\u0026ndash;9. \u003c/li\u003e\n\u003cli\u003eRandriamahavonjy R, Tsifiregna RL, Andrianirina ZZ, Andrianampanalinarivo HR. Materno-fetal outcomes in pre eclampsia in a rural hospital of Antananarivo Madagascar. 2018;6(4):1064\u0026ndash;7.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Placenta, Preeclampsia, Morphological changes, Neonatal morbidity","lastPublishedDoi":"10.21203/rs.3.rs-4695829/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4695829/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003ePreeclampsia/eclampsia is a leading cause of maternal and perinatal mortality; the prevailing theory is that it is a consequence of disordered placentation with the resultant underperfusion of the placenta triggering release of cytokines and vascular factors which cause widespread endothelial damage. The placental changes are manifested as vascular and villous abnormalities with consequences in the developing foetus. The objective of this study was to compare the gross and microscopic changes in the placentas of women with preeclampsia/eclampsia and healthy mothers.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003e146 pregnant women were recruited; 73 were normotensive (control group) while 73 were diagnosed with preeclampsia/eclampsia (study group). The macroscopic and microscopic placental changes in the two groups were further examined.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003e34% of the women in the study group had mild-moderate preeclampsia, 44% had severe preeclampsia and 22% had eclampsia. The placental weights were lower in the study group than the controls (556.82 grams\u0026thinsp;\u0026plusmn;\u0026thinsp;169.72 vs. 649.93 grams\u0026thinsp;\u0026plusmn;\u0026thinsp;116.38, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). The major pathologic lesions with strong associations with preeclampsia/eclampsia in this study were decidual vasculopathy, infarction, increased syncytial knots (Tenney-Parker changes), accelerated villi maturity, stromal fibrosis and microcalcifications (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001). There was also a strong association between disease severity and Apgar scores in the 1st minute. The study group had 11% neonatal mortality.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThere were distinct microscopic changes consistent with maternal vascular malperfusion changes in the placentas of mothers with preeclampsia/eclampsia and demonstrable neonatal morbidity depicted by high incidence of preterm birth and low birth weights.\u003c/p\u003e","manuscriptTitle":"Spectrum of Morphological Changes in the Placenta of Women with Preeclampsia/Eclampsia and Correlation with Neonatal Morbidity","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-08-09 16:55:15","doi":"10.21203/rs.3.rs-4695829/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"6268c5b9-c49a-4e65-8423-57f94b1f5daa","owner":[],"postedDate":"August 9th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-02-28T08:08:40+00:00","versionOfRecord":[],"versionCreatedAt":"2024-08-09 16:55:15","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-4695829","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4695829","identity":"rs-4695829","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}