Placental Infarction Research Articles

Тромботические события при редких формах генетических тромбофилий

Цель исследования: изучить лабораторный фенотип редких мутаций Лейдена [FVL А(1961)A] и гена протромбина [FII А(20210)A] при их клинической реализации в виде тромбозов. Материалы и методы. Проведено многоцентровое проспективное наблюдательное исследование, включающее 80 носителей редких генетических форм тромбофилий: FVL А(1961)A (n = 31), FII А(20210)A (n = 10) и компаунд FII G(20210)A + FVL G(1691)A (n = 39). У всех пациентов исследована резистентность фактора Va к активированному протеину С (APC-R) по нормализованному отношению (НО) и уровень активности протромбина в плазме крови в состоянии физического здоровья и в случае эпизода тромботического события. Результаты. Определена ассоциативная связь развития тромботических событий со снижением НО при оценке APC-R как у гомозиготных носителей мутации Лейден (Ме = 0,35; 95% ДИ = 0,31–0,37 по НО), так и гетерозиготных компаундов (Ме = 0,43; 95% ДИ = 0,42–0,45 по НО). Заключение. Лабораторный мониторинг пациентов с редкими формами генетических тромбофилий позволяет выделить группу высокого тромбогенного риска, нуждающуюся в пролонгированной тромбопрофилактике. Objectives: to study the laboratory phenotype of rare Leiden mutation [FVL A(1961)A] and the prothrombin gene mutation [FII А(20210)A] implementating clinically as thrombosis. Patients / Methods. A multicenter prospective observational study included 80 carriers of rare genetic kinds of thrombophilia: FVL A(1961)A (n = 31), prothrombin FII А(20210)A (n = 10) and the compound FII G(20210)A + FVL G(1691)A (n = 39). All patients were tested for the factor Va resistance to activated protein C (APC-R), normalized ratio (NR), and the plasma prothrombin activity (%) in healthy conditions and in the case of thrombotic event. Results. An associative relation between the development of thrombotic events and a decrease in NR was determined when assessing APC-R, both in homozygous carriers of the Leiden mutation (Me = 0.35; 95% CI = 0.31–0.37 in NR) and heterozygous compounds (Me = 0.43; 95% СI = 0.42–0.45 in NR). Conclusions. Laboratory follow up for patients with rare kinds of genetic thrombophilias allows to identify a group at high thrombogenic risk requiring prolonged thromboprophylaxis.

The global antiphospholipid syndrome score in women with systemic lupus erythematosus and adverse pregnancy outcomes.

To validate the global antiphospholipid syndrome score (GAPSS) in a cohort of women with systemic lupus erythematosus (SLE) and antiphospholipid antibodies (aPL). This retrospective study included 143 women ever pregnant with SLE who presented in our outpatient clinic were included. Data on cardiovascular risk factors and aPL status were retrospectively collected and their individual GAPSS score was calculated. Significantly higher GAPSS values were found in women with any placental medicated complication (such as foetal death, placental abruption, prematurity, pre-eclampsia or intrauterine growth restriction (IUGR)) (GAPSS 8.2±3.0 vs. 3.5±3.0, p<0.001). Significantly higher GAPSS values were also found in those with recurrent miscarriages (RM) <10 weeks, foetal death, placental abruption, prematurity, pre-eclampsia or IUGR) (GAPSS 8.3±4.5 vs. 3.2±2.6, p<0.001). Patients with 3 or more consecutive early miscarriages (<10 weeks), foetal death, miscarriage <10 weeks' gestation, premature birth (<34 weeks), pre-eclampsia (<34 weeks), stillbirth, and placental infarction had significantly higher GAPSS values compared to those without previous pregnancy complications. The odds ratio of having any pregnancy morbidity when having a GAPSS value ≥8 was 20 compared to those with a GAPSS of ≤1 (p<0.001). Women with a history of aPL-related pregnancy complications had higher GAPSS values in this retrospective cohort compared to women without pregnancy complications. This study is the first step to assess the clinical utility of the GAPSS score in pregnancy. A prospective validation is needed.

Prevalence and Clinical Significance of Factor V Leiden Mutation in Egyptian Preeclamptic Women

Background: Factor V [Leiden] mutation, also known as activated protein-C resistance, is the most common of the inherited thrombophilias. Aim of the work: The present study aimed to ass the prevalence of factor V Leiden mutation in a group of Egyptian pregnant women and its relation to maternal and neonatal outcomes. Patients and methods: The present prospective study included 130 preeclamptic women with a singleton pregnancy in the 3rd trimester. Blood samples were obtained for DNA analysis to assay factor V Leiden mutation. Transabdominal obstetric ultrasound examination was performed to confirm the fetal number, viability, presentation, estimated fetal weight, position & grade of the placenta, amount of liquor, biophysical profile, and gestational age. This was achieved through the measurements of the biparietal diameter, head circumference, abdominal circumference, and femur length. Flow velocity waveforms were obtained from each uterine artery. Results: Factor V Leiden [FVL] mutation was identified in 20 patients [15.4 %]. Comparison between women with FVL and women without revealed a significantly higher frequency of intrauterine growth restriction [IUGR], intrauterine fetal death [IUFD], small for gestational age [SGA], preterm labor, and intensive care unit [ICU] admission among women with FVL mutation. They also have a significantly higher frequency of abnormal Doppler findings, abruptio placenta, and placental infarction. Conclusion: The present study suggested that maternal and neonatal complications in PE patients may be related to FVL, abnormal uterine artery Doppler findings, and placental infarction.

Prevalence, placenta development, and perinatal outcomes of women with hypertensive disorders of pregnancy at Komfo Anokye Teaching Hospital.

BackgroundOne of the most common medical problems associated with pregnancy is hypertension. Hypertensive disorders of pregnancy (HDP), which has been attributable to abnormal placentation may have adverse effects on both mother and foetus if left unchecked. The objective of this study was to determine the prevalence of this condition and its effect on placental morphology as well as maternal and perinatal outcomes.Materials and methodsThis was a prospective case-control study, conducted at Komfo Anokye Teaching Hospital (KATH), Ghana between February 2018 and July 2018. The progression of pregnancy in normotensive and hypertensive pregnant women, and the eventual perinatal outcomes were closely followed. Statistical analysis was performed using IMB-SPSS version 23. Associations were considered significant at p values of ≤ 0.05.ResultsFrom a total of 214 deliveries recorded during the period of study, 84 (39.25%) were hypertensives. Forty four (52%) of the hypertensives had preeclampsia, 28 (33.3%) had gestational hypertension, 6 (7.1%) had eclampsia, 4 (4.8%) had chronic hypertension, and 2 (2.4%) had preeclampsia superimposed on chronic hypertension. The frequency of placental haematoma, placental infarction, and placental calcification in the normotensives were significantly (p = 0.001) lower than that of the hypertensives. The mean placental weight (p = 0.01), placental volume (p = 0.001), placental diameter (p = 0.03), and placental thickness (p = 0.001) of the normotensives were significantly higher than those of the hypertensives. The number of normotensives in whom labour was induced, who had their babies delivered by caesarean section, and who were admitted after they had given birth were significantly (p = 0.001) lower than that of hypertensives who underwent similar procedures. No stillbirths were recorded in the normotensives compared with four in the hypertensives. The number of babies delivered to the normotensives who were admitted to the NICU was significantly (p = 0.001) lower than those delivered by hypertensives.ConclusionThere was a high prevalence of hypertensive disorders of pregnancy in the study site. Pregnant women who developed HDP are at a risk of developing placental abnormalities that adversely affected perinatal outcomes. These adverse effects can be curtailed by embarking on a vigorous health education drive.

VP37.13: Clinical value of TEI index as an adjunct to Doppler velocimetry in diagnosis, surveillance and management of fetal growth restriction: a case report

A 31-year-old G2P0 (0100) was noted at 30 weeks gestation to have fetal growth lag on prenatal sonography. Cerebroplacental ratio was abnormal. Placental infarcts were noted. Placental mapping further revealed a Battledore placenta. At this time, TEI index was normal at 0.35. The patient was non-diabetic and non-hypertensive. She had a previous stillbirth at 28 weeks in her previous pregnancy. Anomaly scan was reviewed, infectious disease screening was carried out and results were unremarkable. Work-up for antiphospholipid antibody syndrome was suggested but patient was unable to comply. The patient was given antenatal steroids. Close fetal surveillance was carried out, with daily CTG, BPP twice weekly and weekly Doppler velocimetry. At 32 weeks, umbilical artery Doppler showed intermittent absent end diastolic flow with elevated pusatility index (PI). MCA PI was decreased, with an abnormal cerebroplacental ratio of 0.6. TEI index was 0.53. Family conference was done, with the decision to push as near to term as possible. At 33 weeks of gestation, absent end diastolic flow in the umbilical artery was noted, with deepening A-wave of the ductus venosus, and an elevated TEI index of 0.59. NST revealed persistently minimal variability. Thus intervention was done and patient delivered a livebaby boy weighing 1.7kg. Grossly, the placenta was small weighing 300 grams and the cord was thin, measuring 1cm, inserted at the placental edge. Histopathology report revealed placenta with infarcts and umbilical cord with venous thrombosis. Both mother and baby had unremarkable postpartum course and were discharged well. This case shows how TEI index can be used to augment findings on Doppler velocimetry in the surveillance and management of preterm fetuses with IUGR, secondary to uteroplacental insufficiency. Results from these investigations can guide the clinicians in making decisions regarding the timing of delivery to ensure the best maternal and fetal outcomes.

Fetal Autopsy-Categories and Causes of Death at a Tertiary Care Center.

A fetus is defined from 8 weeks after conception until term while in the uterus. Fetal death is defined as death of the fetus before the complete expulsion or extraction from the mother, irrespective of the duration of pregnancy that is not an induced termination of pregnancy. The causes of fetal death determined after fetal autopsy can be categorized according to the classification proposed by Cunningham and Hollier as fetal, placental, and maternal. All fetuses dying in utero, that is, prior to birth, regardless of the gestational age, to the mothers admitted in the Department of Obstetrics and Gynecology along with the respective placentas were received in the Department of Pathology, MGM Medical College, Aurangabad, after an informed and written consent from October 26, 2017, to October 30, 2019, and were included in this study. Clinical details along with obstetric history and antenatal ultrasonographic findings were also recorded. Anthropometric examination of the fetus was performed and evisceration was then done using the Rokitansky technique. Representative sections from each of the organs were taken and kept in tissue cassettes and processed for routine hematoxylin and eosin staining. This study was done on 33 cases of fetal death. Most fetal deaths occurred in the gestational age between 15 and 19 weeks (14 cases [42.42%]) and the least amount during 35 to 39 weeks (2 cases [6.06%]). The cause of death could not be ascertained in 6 cases (18.18%), whereas the maximum cases had fetal factor as the cause of death (15 cases [45.45%]). Maternal causes were seen in only 4 cases (12.12%). Gestational hypertension was seen to be the most common maternal factor associated with fetal death, which comprised 24.24% of cases (8 of 33). Thirteen of the total 33 cases did not have any associated obstetric complication. Of the total 33 fetal deaths, only 7 had associated placental defects on gross examination. Twenty-six placentas did not show any gross abnormality. Of these 7 cases, 5 were seen to have placental infarction. Fetal autopsy is a valuable and cost-effective modality for the confirmation of cause of fetal death. Fetal autopsy can also prove beneficial to the parents in planning for future pregnancies. Fetal autopsy can serve as the ultimate tool in diagnosing cause of fetal death in cases where no other diagnostic clue is available. Therefore, it should be encouraged and couples to be counseled regarding its importance and clinical utility.

Update on the gestational effects of maternal hyperthermia.

I plan to review the types of defects caused by gestational hyperthermia. Hyperthermia-induced malformations in animals and humans involve many organs and structures, particularly the central nervous system, as well as other defects. The type of defect is related to the timing of the hyperthermic insult, and the underlying mechanisms include cell death, membrane disruption, vascular disruption, and placental infarction. Review of recent epidemiologic studies (2005-2020) has confirmed an association between gestational hyperthermia and birth defects. There are strong associations between neural tube defects and maternal fever, and other studies have demonstrated associations between first trimester hyperthermia and an increased risk for cardiovascular defects, oral clefts, isolated congenital ear defects, cataracts, hypospadias, renal anomalies, possibly anorectal malformations, and congenital anomalies in general, suggesting that this association between maternal hyperthermia and birth defects in humans is causal. The first prospective evaluation of maternal fever was reported in 1998, and this study confirmed findings from previous case-control studies and case series regarding the magnitude and duration of elevated maternal body temperature in relation to an increased risk for neural tube defects as well as a specific pattern of malformation. The consistency of findings across these different study designs supports the causal nature of the relationship between maternal fever and specific birth defects. This review summarizes the recent human evidence documenting the gestational effects of maternal hyperthermia.

Placental histopathological features of fetoscopic laser photocoagulation for monoaminotic diamniotic twin pregnancies

IntroductionThis study aimed to compare the histopathological placental features of monochorionic diamniotic (MCDA) twins who did and did not undergo fetoscopic laser photocoagulation (FLP). MethodsThis was a retrospective single-institution cohort study on MCDA twins who underwent FLP between October 2010 and December 2018. The control group included MCDA twins who did not undergo FLP and were delivered during the same period in the institute. The incidence of chorioamnionitis (CAM), funisitis, and other pathological findings was compared between the FLP and control groups after matching by gestational age at delivery. ResultsIn total, 292 MCDA pregnant women who underwent FLP and 356 controls gave birth during the study period. After matching the two groups in the ratio 1:1 by gestational age at delivery, each group comprised 194 subjects. The incidence of histological CAM with Blanc association (stage I, 6.2% vs. 3.1%, crude odds ratio (cOR) = 3.1, P = 0.052; stage II, 7.2% vs. 5.7%, cOR = 1.6, P = 0.30; stage III, 2.1% vs. 2.6%, cOR = 0.66, P = 0.52) and funisitis (artery, 5.2% vs. 3.6%, cOR = 1.3, P = 0.63; vein 7.2% vs. 4.1%, cOR = 1.6, P = 0.29) was not statistically significant difference between the FLP and control groups. The FLP group demonstrated a higher incidence of partial placental infarction than the control group (10.3% vs. 3.1%, cOR = 4.3, P = 0.004, adjusted OR = 2.8, P = 0.031). DiscussionFLP did not appear to increase the incidence of histological CAM or funisitis in subjects matched by gestational age at delivery. The FLP group demonstrated a higher incidence of partial placental infarction than the control group.

Aplasia cutis congenita in Korea: Single center experience and literature review.

Aplasia cutis congenita (ACC) is a rare congenital malformation characterized by a localized absence of skin. which most commonly affects the scalp. We performed the present study to elucidate the basic clinical data regarding ACC in Korea, including demographics, clinical features, radiological and therapeutic results. Fifty-nine patients (70 lesions) with ACC (35 from our department and 24 from a Koreamed database search) were enrolled. We assessed demographics, family and obstetrical histories, clinical features (multiplicity, subtype, size, shape, hair collar sign, location, and Frieden's classification), and radiologic and therapeutic results. The mean age of patients was 2.62years, with a male-to-female ratio of 1.03. A minority of patients had a family history (three patients), birth trauma (one patient), maternal drug use (two patients), or human immunodeficiency virus infection (one patient) during pregnancy, and fetus papyraceus of placental infarcts (two patients). Six patients (6/59, 10.17%) had multiple lesions. Scarring was the most common manifestation (39/70, 55.71%). The scalp was the most commonly affected site (50 cases, 71.43%). Thirty-nine patients (66.10%) met Frieden's type I classification (scalp ACC without multiple anomalies). Radiological investigations were performed in 30 patients (30/59, 50.85%) with abnormal findings in eight patients. Twenty-five patients (42.37%) were managed conservatively, and 17 patients (28.81%) were treated with local wound care. This is the first and largest study assessing the basic clinical data of ACC in Korea. The results of the present study could be useful for pediatricians and dermatologists who routinely manage ACC.

Placental infarcts in the collaborative perinatal project: Variable associations infer variable constructs

PurposeReproducible diagnoses of placental infarcts may permit more accurate assessment of their clinical significance. Using data across the 12 study sites of the National Collaborative Perinatal Project, we investigated the consistency of associations between infarct features with birthweight, placental weight and measures of placental “efficiency.” MethodsAll delivered infants, live or stillborn, single or multiple, regardless of gestational age, were included. Pathologists scored infarcts by color (tan-white or “old” or pink-red “more recent”), size (cm), location (marginal or central), and total number. ResultsIncidence of any infarcts and distributions of specific features such as size, color (indicating age), locations and total numbers of infarcts were highly variable across sites, as were their associations with birthweight and placental efficiency. The most stable associations (consistent results across sites) of placental infarct scores were with placental size and/or other placental shape variables and with birthweight, but the number of significant associations ranged from 13 to 1. ConclusionGiven the extremes of infarct incidence within each site plus the variable correlations of infarct features with other placental and birth outcome measures, CPP infarct scores cannot be used as indicative of an underlying shared pathophysiologic construct. However, given the accumulating evidence that intrauterine stressors have the potential for lifelong impact on health, we propose that the infarct features and distinctions proposed are neither complex nor should they be jettisoned. Rather these measures should be clarified and refined. Only then can we understand the reported associations of placental infarcts with child and adult health outcomes.

SIGNIFICANCE OF PLACENTAL HISTOPATHOLOGICAL FINDINGS IN PRETERM/TERM BIRTH

Background: This study is cross-sectional, observational and comparative study, at Index Medical College, Hospital &amp; Research Centre, Indore, Madhya Pradesh from July 2017 to July 2019 with sample size 100 placentae.&#x0D; Method: The placenta received was evaluated blinded of maternal pregnancy outcome. The pattern of morphology was evaluated both qualitatively (type of lesion) and quantitatively (number of lesions).&#x0D; Result: In Present study 79% of the deliveries were term deliveries and 21% were preterm deliveries. On placental macroscopy, placenta weight was significantly low among the neonates of preterm deliveries (370.00±60.49) as compared to term deliveries (440.89±55.22). Preterm placenta had higher number of abnormal placental lesion compared to term pregnancies.&#x0D; Conclusion: The uteroplacental insufficiency defined as placental infarct, fibrosis of chorionic villi, thickening of blood vessels, and poor vascularity of chorionic villi. Placental histopathological lesions are strongly associated with maternal under perfusion and uteroplacental insufficiency. These are the reasons for preterm birth. Thus, knowledge of the etiological factor can be use to reduce maternal and neonatal morbidity and mortility.&#x0D; Keywords: Placenta, Term &amp; Preterm.

Human TLR8 Adversely Affects Placental Development and Induces Spontaneous Pregnancy Loss in a model of Systemic Lupus Erythematosus

Abstract SLE is associated with adverse pregnancy outcomes, particularly in the presence of antiphospholipid antibodies (aPL). Pathogenic mechanisms damaging the fetal-maternal unit, however, remain poorly understood. A role for endosomal TLR8 was recently hypothesized in aPL induced placental damage. The role of TLR8 in systemic autoimmunity has remained elusive as TLR8 function differs from mouse to man. We investigated the effect of human (hu)TLR8 expression on pregnancy outcomes in Sle1 mice that develop aPL antibodies. huTLR8 transgenic(tg) Sle1 mice were generated and huTLR8 DNA copy number and mRNA expression was confirmed by qDigital- and qRT-PCR. Pregnancies were closely followed and terminal C-sections performed at signs of dystocia/prolonged labor. Pup and placental weight was assessed. Placental tissues were characterized by H&amp;E and Myeloperoxidase (MPO) staining and inflammatory cytokine expression was assessed in placental tissue. Splenic and bone marrow immune populations were analyzed using flow cytometry. Female Sle1.huTLR8tg mice developed aPL and sm/RNP autoantibodies earlier than Sle1 controls and ±50% loss of litters was observed, compared to 0% in controls. IL-6, TNFa and MPO mRNA expression was significantly increased in placentas of affected litters and negatively correlated with placental weight. Abnormal placental morphology included placental infarcts, loss of placental lakes, arterial wall thickening and increased netting neutrophils. Here we identify a new model to study adverse pregnancy complications in SLE. In the presence of both Sle1 and huTLR8, we observed early onset of aPS autoantibodies and pregnancy loss attributed to placental developmental abnormalities, infarcts and inflammation.

The Burden of Placental Histopathology in Stillbirths Associated With Maternal Obesity.

Obesity is an increasing health problem that has become a common medical disorder among women of childbearing age, representing worldwide a risk factor for stillbirth. The aim of the study is to evaluate the association between placental histopathologic findings and obesity in stillbirth. Placentas were analyzed according to the Amsterdam consensus statement. Histologic findings in stillbirth from obese and lean mothers were analyzed and compared with those observed in liveborn controls. Stillbirth in obese mothers displayed placental pathology in all gestational ages, mostly at term of pregnancy. The most observed placental lesions were those consistent with maternal vascular malperfusion of the placental bed. Decidual arteriopathy and placental infarcts appeared specifically associated with maternal obesity. Moreover, obese women with stillbirth showed the highest cumulative number of placental lesions. Considering the significant association between stillbirth, maternal obesity, and placental histopathologic findings, health care providers should be aware about the importance of placental examination in obese women, especially in stillborn cases. The high prevalence of lesions consistent with vascular malperfusion of the placental bed suggests that stillbirth prevention strategies in obese women should rely on the development of tools to study and improve decidual artery functioning early in pregnancy.

Prediction of outcome in fetal autoimmune complete heart block.

Retrospective cohort review of CAVB pregnancies, excluding fetuses with significant cardiac anomalies. CAVBs are in 17 fetuses, diagnosed at mean gestational age of 23 ± 5 weeks. Overall mortality is 18%: 1 termination, 1 fetal demise (intrauterine fetal demise [IUFD]), and 1 postnatal death. Both mortalities had intrauterine growth restriction; IUFD had placental infarction. Presenting CVP 8.7 ± 1. No fetus had CVP <7; the score correlated with increased risk of perinatal death. The 2 mortalities had initial CVP scores of 8 and 9; both increased to 10 on subsequent exams. 30% of fetuses had low middle cerebral artery pulsatility (MCA-PI) on the last study. All had high umbilical artery pulsatility (UA-PI) throughout gestation. The 2 deaths had the lowest MCA-PI. Despite low heart rates, high CVP scores in our cohort remained high and were not predictive of mortality. Abnormalities in MCA flow reflects fetal cerebral vasodilation that may indicate altered hemodynamics and be predictive of outcomes, but data is limited. Abnormal umbilical artery (UA) flow suggests that perinatal mortality may also be related to placental disease.

Placental histopathology in late preterm infants: clinical implications.

BackgroundThe etiopathogenesis of late preterm (LPT) birth is undetermined. Placental histopathology, which reflects an adverse intrauterine environment and is reportedly associated with preterm labor and neonatal morbidities, has not been studied in LPT infants.PurposeWe investigated placental pathological lesion as markers of an adverse intrauterine environment during LPT labor.MethodsThis retrospective case-control study compared placental histopathological and clinical variables between LPT and term neonates. Placental variables included chorioamnionitis, funisitis, hemorrhage, abruption, infarction, calcification, and syncytial knots. Maternal variables included age, substance abuse, pregnancyassociated diabetes mellitus and hypertension, duration of rupture of membrane, antibiotic use, and magnesium sulfate, whereas, those of neonates included gestational age, birth weight, race, sex, and Apgar scores. Standard statistical proedures were applied to analyze the data.ResultsChorioamnionitis (50% vs. 17.8%, P<0.001) and funisitis (20% vs. 4.4%, P=0.002) were more common in term infants. Placental infarction rate was insignificantly higher in LPT infants (25.6% vs. 14.3%, P=0.08). The mothers in the LPT group were older (30.4 years vs. 28.1 years, P=0.05; odds ratio [OR], 1.06; 95% confidence interval [CI], 0.998–1.12, P=0.056) and more often suffered from hypertension (28.9 vs. 12.9 %, P=0.02), and received magnesium sulfate (48.9 vs. 20%, P< 0.001; OR, 2.86; 95% CI, 1.12–7.29, P<0.05). Duration of rupture of membrane was higher in term infants (13.6 hours vs. 9.1 hours, P<0.001). Chorioamnionitis (OR, 0.33; 95% CI, 0.13–0.79; P<0.05) was associated with a lower risk of LPT delivery.ConclusionPlacental infection is not a risk factor for LPT births. There is a nonsignificant predominance of vascular anomalies in LPT placentas. Higher maternal age, magnesium sulfate therapy, and maternal hypertension are clinical risk factors for LPT labor.

Evaluation of placental vascularization in thrombophilia and intrauterine growth restriction (IUGR).

The placenta is an essential organ in the proper development of pregnancy, and it can present a lot of structural and vascular lesions that can affect fetal development. One of the pathologies associated with pregnancy, which can change the placental structure is thrombophilia (TPh), and this can be correlated with an intrauterine growth restriction (IUGR) of the fetus. Maternal clinical aspects (age, weight) can be correlated with fetal ones (weight, gender), but also with the structural and vascular aspect of the placenta. The placental structure associated with TPh and IUGR shows macroscopic changes, such as fibrin deposition, calcifications and placental infarctions, but microscopic lesions are best highlighted by classical staining techniques: Hematoxylin–Eosin (HE), Masson’s trichrome (MT) and Periodic Acid–Schiff (PAS)–Hematoxylin, but also by immunohistochemistry technique with the help of anti-cluster of differentiation 34 (CD34) antibody that could make it possible to quantify vascular density depending on the pathology. Microscopic changes were massive infarcts caused by vascular ischemia, intravenous and extravillous fibrin deposits, calcifications, and vascular thrombosis. All these clinical, morphological and morphopathological data are interconnected and may vary in the presence of TPh and IUGR.

Perinatal Risk Factor and Morbidity in Term Large-for-Gestational-Age Infants according to Classification by Ponderal Index

Objective: Large-for-gestational-age (LGA, birth weight ≥90th percentile) infants have increased risks of adverse perinatal outcomes. Further classification within the LGA group enables identification of infants at highest risk for neonatal morbidity. The objective of the study is to investigate the difference of perinatal risk factors and morbidity in LGA infants born at 37-41 weeks of gestation according to classification by the ponderal index (PI). Methods: 195 LGA infants between January 2016 and December 2018, were enrolled in this retrospective study. They were divided into two groups base on PI; symmetric LGA (PI ≤90th percentile) and asymmetric LGA (PI >90th percentile). Neonatal and maternal demographics with clinical characteristics, and neonatal morbidity were compared between two groups. Results: The gestational age of term LGA infants was 38.6±1.2 weeks and birth weight was 3,963±326 g. Maternal pre-pregnancy body mass index was 25.8±6.6 kg/m2 and diabetes mellitus was 23.6%. Maternal diabetes mellitus and placental infarction were also significantly higher in the asymmetric LGA infants. Asymmetric LGA infants had higher incidence of hypoglycemia, clavicle or humerus fracture and had higher initial hemoglobin and hematocrit levels than the symmetric LGA infants. Conclusion: In the asymmetric LGA group, maternal diabetes and neonatal morbidity such as clavicle or humerus fracture and hypoglycemia were higher than in the symmetric group. Early identification of fetuses for being the asymmetric LGA gives a chance to optimize management of these newborns associated with increased morbidity. Thus, the combination of birth weight and PI helps a more appropriate parameter than birth weight alone.

The influence of gestational diabetes mellitus (GDM) and gestational hypertension (GH) on placental morphological changes.

Gestational diabetes mellitus (GDM) and gestational hypertension (GH) are some of the most common medical conditions associated with pregnancy. These can be correlated with placental morphopathological changes and implicitly can influence good fetal development. The age and weight of the mother can be correlated directly proportionally with those of the fetus but also with histoarchitecture and placental vascularization. The placental appearance associated with GDM and GH reveals macroscopic features, such as calcifications, fibrin deposits and placental infarcts, but the most relevant pathological features are the microscopic ones, highlighted by the classical staining techniques: Hematoxylin–Eosin (HE), Periodic Acid–Schiff (PAS)–Hematoxylin and Masson’s trichrome (MT), but also by immunohistochemical technique with the help of the anti-cluster of differentiation 34 (CD34) antibody that labeled the capital endothelium in the structure of the placental terminal villi and thus we were able to quantify the vascular density according to the associated medical pathology. The microscopic changes identified were represented by intravillous and extravillous fibrin depositions, massive placental infarctions caused by vascular suppression due to various causes, such as thrombosis, but also placental calcifications. All these macroscopic and microscopic morphopathological changes, together with the clinical data of the mother and the newborn, we have demonstrated that they are interconnected and that they can vary depending on the pathology, GH or GDM.

Morphological and histopathological changes in placentas of pregnancies with intrauterine growth restriction.

Aim: The definition of fetal growth restriction (FGR) refers to the incapability of a fetus to achieve the appropriate estimated growth, with expected fetal weight below the 10th percentile calculated for its gestational age. Placental factors and hypoxemia are considered to be essential elements with influence on intrauterine growth restriction (IUGR) and fetal death. The purpose of the present study was to investigate the macroscopic and microscopic pathological findings regarding the placentas in pregnancies complicated by influence on IUGR. Patients, Materials and Methods: Our study included 42 third-trimester pregnant patients admitted to the Cuza Vodă Hospital of Obstetrics and Gynecology, Iaşi, Romania, in the last three years. Soon after delivery, the 42 placentas were collected and analyzed; 32 placentas came from cases previously diagnosed with influence on IUGR and were included in our study group. Ten other placentas included in the control group were selected from uncomplicated pregnancies. Standard Hematoxylin–Eosin (HE) staining method, as well as Periodic Acid–Schiff (PAS) staining, and immunohistochemical techniques for cluster of differentiation 31 (CD31) and collagen IV were used in order to highlight the morphological features of the studied placentas. Results: Our study revealed that reduced placental dimensions and eccentric umbilical cord insertion are correlated with the birthweight of the fetuses with IUGR (p<0.05). The most common histological finding in our study group was placental infarction later correlated with IUGR, but a certain causality could not be demonstrated, as this finding was also present in normal pregnancies. Other histopathological findings were also present in the influence on IUGR group, such as fibrin deposits, diffuse calcification, chronic villitis, avascular chronical villi, with no significant statistical correlations. CD31 was strongly immunoexpressed in the villous endothelial cells. Collagen IV presented a strong immunoreaction in the basement membrane and mesenchyme of the placental villi. Conclusions: Our study revealed a correlation between the dimensions of the diameters and volume of the maternal placenta and the presence of influence on IUGR. Moreover, it confirms the available data suggesting that the place of insertion of the umbilical cord is correlated with the weight of the fetus. Further studies with extended panel antibodies are needed in order to determine and complete the role of these morphological changes in the development of influence on IUGR.

Frequency of placental infarcts in patients with severe placental abruption.

Introduction: Peripheral infarcts on maternal side are relatively common and are not thought to be clinically sig­nificant. However those that occupy more than 5% of the placental mass or are more than 3cm in di­ameter in size are associated with perinatal mortality and morbidity. Objectives: To determine the frequency of placental infracts and its different severity grades among women with severe placental abruption. Study Design: Cross sectional descriptive study. Setting: Department of Obstetrics &amp; Gynaecology, Postgraduate Medical Institute, Lady Reading Hospital Peshawar. Period: January 2016 to July 2016. Material and Methods: Patients admitted in hypovolemic shock or intrauterine fetal death was considered as severe abruption. Placenta of the subject was collected from labour room of the wards and was fixed in 10% formalin. Gross examination of placenta performed and then the section of placenta was stained with hematoxylin &amp; eosin stain. The consultant pathologist reviewed the slides. All the data was recorded on predesigned Performa and analyzed through SPSS version 11.0. Results: Among 124 cases, majority of women (41.93%) were in the age group 30-40 years and presented at gestation age more than 37 weeks. 21.77% of patients were having placental infarcts of less than 3 cm and 18.54% of cases were having placental infarcts of more than 3 cm. 79.03% of babies born alive, 41.12% were preterm and stillbirth was a finding in 20.96% of cases. Overall frequency of placenta infarcts in patients was 40.32%. Conclusion: Placental infarcts were seen in about 40.32% placentae of women with placental abruption. Association between placental infarcts and preterm babies and stillbirths was also significant.