CONTEXT.—:A severe third wave of COVID-19 disease affected Ireland in the first 3 months of 2021. In this wave, 1 second-trimester miscarriage and 6 stillbirths were observed in the Irish population because of placental insufficiency as a result of SARS-CoV-2 placentitis. This observation was at odds with the country's previous experience with COVID-19 disease in pregnant mothers.OBJECTIVE.—:To describe the clinical and pathologic features of these pregnancy losses.DESIGN.—:Retrospective review of clinical and pathologic data of cases of second-trimester miscarriage, stillbirth, or neonatal death identified by perinatal pathologists as being due to SARS-CoV-2 placentitis during the third wave of COVID-19 in Ireland.RESULTS.—:Clinical and pathologic data were available for review in 6 pregnancies. Sequencing or genotyping of the virus identified SARS-CoV-2 alpha (B.1.1.7) in all cases. Three of the 6 cases had maternal thrombocytopenia, and fetal growth restriction was not prominent, suggesting a rapidly progressive placental disease.CONCLUSIONS.—:The identification of SARS-CoV-2 alpha in all these cases suggests that the emergence of the variant was associated with an increased risk of fetal death due to SARS-CoV-2 placentitis when compared with the original virus. Maternal thrombocytopenia may have potential as a clinical marker of placentitis, but other inflammatory markers need investigation. Three of the 6 women had been assessed for reduced fetal movements in hospital some days before the fetal deaths actually occurred; this could suggest that there may be a window for intervention in some cases.

CONTEXT:-The value of placental examination in investigations of adverse pregnancy outcomes may be compromised by sampling and definition differences between laboratories.OBJECTIVE:-To establish an agreed-upon protocol for sampling the placenta, and for diagnostic criteria for placental lesions. Recommendations would cover reporting placentas in tertiary centers as well as in community hospitals and district general hospitals, and are also relevant to the scientific research community.DATA SOURCES:-Areas of controversy or uncertainty were explored prior to a 1-day meeting where placental and perinatal pathologists, and maternal-fetal medicine specialists discussed available evidence and subsequently reached consensus where possible.CONCLUSIONS:-The group agreed on sets of uniform sampling criteria, placental gross descriptors, pathologic terminologies, and diagnostic criteria. The terminology and microscopic descriptions for maternal vascular malperfusion, fetal vascular malperfusion, delayed villous maturation, patterns of ascending intrauterine infection, and villitis of unknown etiology were agreed upon. Topics requiring further discussion were highlighted. Ongoing developments in our understanding of the pathology of the placenta, scientific bases of the maternofetoplacental triad, and evolution of the clinical significance of defined lesions may necessitate further refinements of these consensus guidelines. The proposed structure will assist in international comparability of clinicopathologic and scientific studies and assist in refining the significance of lesions associated with adverse pregnancy and later health outcomes.

The existence of placental AVS has remained illusive. Microscopy of small infarcts offers an insight. Placental infarction results from cessation of both the fetal and maternal blood supply. Survival of the mainstem villus in the centre of an area of infarction indicates that the vascular supply which is selectively maintaining the viability of the mainstem villus, is being diverted within the villus, and away from the terminal villi. This diversion must occur via an AVS. Our aim was to review the viability of mainstem villi in small infarcts to determine the incidence of AVS. Routine placental pathology reports from December '10 to July '11 were reviewed to identify minor infarction=/< 1.0 cm in diameter. Cases were identified and collected prospectively. The haematoxylin and eosin stained slides were reviewed. The status of the mainstem villi regarding necrosis or viability was recorded. The study was confined to simple infarctions only. Infarcts complicated by intervillus haemorrhage were excluded. In total 102 infarcts fulfilling the inclusion criteria (from a total of 147 lesions) were examined. The mean maximum diameter of the infarcts was 7.8mm. The mainstem villi were viable/non-infarcted in 82 infarcts (80%), and necrotic/ infracted in 20 (20%). The 80% incidence of viable mainstem villi within placental infarcts is highly significant and strongly supports the likelihood that AVS exist in the mainstem villi. The presence of AVS may significantly influence the interpretation of both physiological and pathophysiological settings in the placenta.

Aim: To determine the association, if any, between placental architecture findings assessed ultrasonographically at 22 and 36 weeks and placental histology.Methods: There was prospective recruitment of 1011 low-risk primigravids from the antenatal clinic at the Rotunda Hospital, Dublin, Ireland. Ultrasound of the placenta was performed at 22 and 36 weeks and histological assessment was made of the placenta of all participants.Results: Complete data pertaining to ultrasound and placental histology was available for 810 women (80%). Placental calcification on ultrasound in the third trimester was associated with a higher incidence of placental infarction identified following placental histology (80.0% vs. 21.5%; P = 0.009: r = 0.115). The placental thickness on ultrasound in the second trimester was less in cases complicated by chorioamnionitis (2.62 cm vs. 3.07 cm; P = 0.039: r = -0.176). Chronic villitis was associated with a statistically significant increased incidence of antenatal placental infarction identified on ultrasound in the third trimester (10.7% vs. 1.9%; P = 0.020: r = 0.113). Intervillous thrombi occurred more frequently in cases with reduced placental thickness on ultrasound in the second trimester (3.0 cm vs. 3.3 cm; P = 0.035: r = -0.171).Conclusions: Antenatal ultrasound of the placenta may aid detection of placental disease, particularly in the identification of placental infarction.

We aimed to compare the changes in factor VIII:C, antithrombin, protein C, protein S and fibrinogen in a cohort of low-risk primigravida who developed maternal or fetal complications to those who had uncomplicated pregnancies and to correlate these findings with placental pathology. This is a case-control study of 170 cases and 122 controls selected from a prospective cohort of 1,011 low-risk primigravida. Significantly elevated levels of factor VIII:C and significantly decreased levels of antithrombin were seen in women who developed pre-eclampsia (p < 0.001), placental infarction (p < 0.001) or had infants with a birth weight <3rd centile (p < 0.001). Placental villous dysmaturity was significantly associated with raised factor VIII:C (p < 0.001). Women who developed pre-eclampsia showed elevated fibrinogen at 14 weeks (p = 0.03). Significantly higher than normal pregnancy levels of factor VIII:C, in tandem with significantly lower antithrombin levels associated with certain adverse pregnancy outcomes, may be related to underlying placental insufficiency. This is supported by associated placental findings.

Hypercoiling of the umbilical cord (HCUC) has been recognised since the 17th century. Many have considered it as an accentuation of normal coiling, but clinicians have been slow to give it credibility as a significant diagnosis. Recent studies, however, have linked fetal distress with hypercoiling, and have introduced an umbilical coiling index by which the degree of coiling may be judged. This study aims to determine the significance of HCUC as a risk factor for intrapartum adverse events. Cases of HCUC were identified retrospectively from placental pathology reports recording umbilical coiling indexes >0.3. Cases with additional significant placental pathology were excluded. The control group were normal placentas with normal coiling indexes (0.1-0.3). A chart review of all identified cases was conducted. 50 HCUCs and 32 controls were retrieved. Significant differences identified between the two groups are shown in the table. This study identifies HCUC as an independent risk factor for fetal distress and fetal acidosis in labour, requiring obstetric intervention.Tabled 1 Open table in a new tab

Society for Pediatric Pathology Fall Meeting, Houston, Texas, October 11–14, 2012 1. TLE1 Immunohistochemistry for Diagnosis of Pediatric Synovial Sarcomas. AF Lee, CH Lee, LM Sullivan, O Popescu. University of British Columbia, Vancouver General Hospital, and Children’s and Women’s Hospital of British Columbia, Vancouver, BC; The Children’s Hospital of Philadelphia, Philadelphia, PA. Background: Synovial sarcoma (SS), a high-grade sarcoma seen in young adults and adolescents, is characterized by t(X;18)(p11.2;q11.2). SS can be monophasic or biphasic in appearance. The monophasic variant has a histologic differential including a wide range of spindle and small round blue cell neoplasms. TLE1 was found in gene-expression profiling studies to be highly upregulated in SS and initial reports showed it was a sensitive and specific marker for SS. However, a subset of rhabdomyosarcoma (RMS) and peripheral nerve sheath tumors are also immunoreactive. Its expression in pediatric tumors is not fully characterized. We therefore performed TLE1 immunohistochemistry on various pediatric spindle/round cell tumors to address TLE1 immunoreactivity in this patient population. Design: Pathology files at Children’s and Women’s Hospital of BC, Vancouver General Hospital, and The Children’s Hospital of Philadelphia were searched for formalin-fixed, paraffin embedded pediatric tumors to create 3 tissue microarrays containing 24 SS (19 molecularly confirmed), 83 RMS, 21 Ewing sarcoma, 4 infantile fibrosarcoma, 17 desmoid fibromatosis, 6 digital fibromatosis, 9 fibrous hamartoma of infancy, 3 fibromatosis colli, 13 hepatoblastoma, 7 myofibroma/myofibromatosis, 11 neuroblastoma, 5 superficial fibromatosis, and 25 Wilms tumor. Whole mount sections from 5 cases of molecularly confirmed SS were also obtained. All cases and an external positive control (molecularly confirmed adult SS), were stained concurrently with anti-TLE1 antibody. Immunostaining was scored as 0 (no nuclear staining); 1+ (weak-moderate staining in , 50% of tumor nuclei); 2+ (weak-moderate staining in 50% or greater of tumor nuclei) and 3+ (strong staining in . 10% of tumor nuclei). Cases with 2+ or 3+ TLE1 staining were considered positive. Results: TLE1 was negative in infantile fibrosarcoma, desmoid fibromatosis, digital fibromatosis, fibrous hamartoma of infancy, fibromatosis colli, hepatoblastoma, neuroblastoma, myofibroma/myofibromatosis, superficial fibromatosis and Wilms tumor. Conclusions: TLE1 identifies the majority of pediatric SS with 3+ staining, but at a lower rate than reported for adult SS. While 2+ staining was occasionally observed in alveolar/embryonal RMS and Ewing sarcoma, it appears that 3+ staining is preferentially seen in SS. TLE1 staining may be useful in cases where tissue is limited. Rare alveolar/ embryonal RMS also show 3+ staining, which is an important pitfall of TLE1 staining that must be recognized in the pediatric population. 2. Prevalence of Hepatic Steatosis in Stillborns Delivered to Women with Diabetes Mellitus. K Patel (1), F White (1), G Deutsch (2). (1) Department of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO; (2) Department of Pathology, University of Washington and Seattle Children’s Hospital, Seattle, MO. Background: Maternal diabetes is a known risk factor for pregnancy complications including stillbirth, fetal macrosomia and congenital anomalies. We have observed prominent hepatic steatosis in stillbirth autopsies complicated by maternal diabetes, a finding not previously reported. In this case review we aim to determine if hepatic steatosis is associated with maternal diabetes. Design: Autopsy reports (2005-present) from both institutions were searched for cases of stillbirth occurring in the setting of maternal diabetes including: late onset diabetes mellitus (DM), early onset insulin dependent diabetes Table 1. Pediatric mesenchymal tumors with positive TLE1 immunoreactivity. Diagnosis 2+ or 3+ Staining 3+ Staining Only

To evaluate the correlation of placental examination findings with abnormal umbilical artery (UA) Doppler velocimetries in monochorionic (MC) and dichorionic (DC) twin pregnancies. Structurally and chromosomally normal diamniotic twin pregnancies were prospectively evaluated in a multicentre observational study. Serial sonographic surveillance included evaluation of UA Doppler indices. Doppler abnormalities were defined as a pulsatility index >90th centile or absent/reversed end diastolic flow. Placentas were examined for evidence of histological abnormalities and cord insertion site was recorded. The association between abnormal UA Doppler velocimetries at final sonogram before delivery and abnormal findings at placental examination was evaluated. Results were stratified by chorionicity. 668 twin pairs had complete placental and sonographic data available for comparison. 79.1% (n=528) were DC and 20.9% (n=140) MC. Abnormalities on histological examination were significantly more frequent in MC than DC twin placentas (42.1% vs 32.8%, p=0.003). MC twins were also more likely to have an abnormal UA Doppler on antenatal sonogram (16.4% vs 9.9%, p=0.003). Abnormal UA Doppler at final examination correlated significantly with placental disease in the dichorionic but not the monochorionic cohort (p=0.002 and 0.09 respectively). A non-central cord insertion, present in 30.9% and 16.9% of MC and DC twins respectively (p<0.0001 for difference), did not correlate with UA Doppler indices in either group (p=0.11 and 0.09 respectively). In a large prospectively assessed cohort of twins UA Doppler abnormalities were associated with underlying placental disease in DC twins but not MC twins. This may imply that Doppler abnormalities and growth abnormalities in MC twins reflect gross structural and vascular abberations in the placenta.

Introduction Placenta praevia complicates 0.4% of pregnancies and is associated with adverse maternal and neonatal outcome. Implantation over the cervix may differ from placentation implantation in the uterine corpus as the cervix differs in both composition and blood flow. Our hypothesis is that placenta praevia may predispose to placental disease secondary to impaired maternal placental perfusion. Aim To determine the incidence of placental ischemic disease and fetal hypoxia in cases complicated by placenta praevia. Methods Retrospective review of all cases of placenta praevia in singleton pregnancies between January 1st 2005 to December 31st 2010 in the Rotunda Hospital, Dublin 1. Cases were identified from the computerised maternity records. Maternal placental ischemic disease was defined as uteroplacental insufficiency (UPI), which is the presence of accelerated villous maturation (AVM) or placental infarction. Histological evidence of fetal hypoxia was defined as the presence of nucleated erythroblasts or chorionic villous haemorrhage. Maternal age, ethnicity, parity, previous sections, gestation at delivery, obstetric and neonatal outcome were reviewed. Results 112 cases of placenta praevia were reviewed. There were 12 multiple pregnancies and these were excluded. Histology was available in 71%. Accelerated villous maturation was present in 38%. This is seven times higher than the reported incidence of AVM in population studies. Placental infarction occurred in 15.5%. Fetal hypoxia was present in 21.1% (15/71). Conclusion Placenta praevia is associated with increased rates of maternal placental ischaemic disease with further negative implications for fetal wellbeing.

Background: Sudden infant death syndrome (SIDS) is postulated to be a developmental disorder originating during fetal life in utero. Knowledge regarding the intrauterine environment in which SIDS infants develop is, however, inadequate and how the placenta develops prior to a SIDS event has not been studied.Aim: To investigate the morphological development of the placenta obtained from full-term infants who subsequently succumbed to SIDS.Study design: To estimate the percentage and total volumes of the chorionic villi and villous trophoblast membrane using stereological techniques.Subjects: Placentas were obtained retrospectively from normal birthweight (SIDS-NBW n = 18) and small-for-gestational age (SIDS-SGA, n = 14) infants who had succumbed to SIDS, and compared to either control (n = 8) or SGA placentas (n = 7), respectively.Results: SIDS-NBW placentas displayed evidence of augmented villous growth shown by significantly greater volumes of placental chorionic villi (gas-exchanging (GE) villi) in comparison to controls: this was not observed for SIDS-SGA placentas. However, both SIDS-NBW and SIDS-SGA placentas displayed significantly greater volumes of the cytotrophoblast (CT) (SIDS-NBW only), syncytiotrophoblast (SIDS-SGA only) and syncytial knots (SCT-K) and those displaying apoptotic syncytial nuclei (AP SCT-K). In contrast, SGA placentas displayed significantly reduced volumes of chorionic villi, GE villi and the villous trophoblast indicating a SIDS-specific effect associated with augmented placental growth.Conclusions: Our findings provide initial evidence that placental abnormality, although not necessarily causative, may precede a subset of SIDS cases supporting the hypothesis that the origins of SIDS begin during fetal life in utero. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

OBJECTIVE: We sought to evaluate the association between placental histological abnormalities and birthweight discordance and growth restriction in twin pregnancies.STUDY DESIGN: We performed a multicenter, prospective study of twin pregnancies. Placentas were examined for evidence of infarction, retroplacental hemorrhage, chorangioma, subchorial fibrin, or abnormal villus maturation. Association of placental lesions with chorionicity, birthweight discordance, and growth restriction were assessed.RESULTS: In all, 668 twin pairs were studied, 21.1% monochorionic and 78.9% dichorionic. Histological abnormalities were more frequent in placentas of smaller twins of birthweight discordant pairs (P = .02) and in placentas of small for gestational age infants (P = .0001) when compared to controls. The association of placental abnormalities with both birthweight discordance and small for gestational age was significant for dichorionic twins (P = .01 and .0001, respectively). No such association was seen in monochorionic twins.CONCLUSION: In a large, prospective, multicenter study, we observed a strong relationship between abnormalities of placental histology and birthweight discordance and growth restriction in dichorionic, but not monochorionic, twin pregnancies.

Our objective was to compare Ponderal index (PI) with birth weight centiles as predictors of perinatal morbidity and to determine which best reflects the presence of placental disease. We prospectively recruited 1,011 low-risk primigravidas and calculated PI and birth weight centiles following delivery. Perinatal morbidity was defined as: pre-term birth (PTB); fetal acidosis; an Apgar score <7 at 5 min or neonatal resuscitation. Placental disease was defined as chronic uteroplacental insufficiency (CUPI); villous dysmaturity; infection or vascular pathology. Ponderal index was statistically reduced (25.33 vs 27.79 p =0.001) and the incidence of infant birth weight <9th centile was statistically higher (11.1% vs 5.1%; p =0.004) in cases with PTB and in CUPI (26.23 vs 27.84; p =0.001 and 28.2.1% vs 10.4%; p =0.002). Both PI and infant birth weight centile <9th centile for gestational age correlate with PTB, however overall, both are poor predictors of neonatal and placental disease.

Stereological evaluation of accelerated villous maturation associated with birth weight (BW) discordance in dichorionic twins. Twin placentas were examined to establish chorionicity and the incidence of accelerated villous maturation in one or both twins. 42/154 (27%) dichorionic twins demonstrated accelerated villous maturation. This was associated with a ≥20% BW discordance profile in 27/42 (43%) cases. Stereology was performed on coded dichorionic twin placentas with ≥20% BW discordance and accelerated villous maturation in one twin only; 3 cohorts of controls comprising: (i) 10 twins with ≤10% BW discordance and normal terminal villi in both twins; (ii) 10 singleton placentas from gestational-age matched normal pregnancies and (iii) 10 preeclampsia-associated IUGR singleton placentas as positive controls for CUPI IUGR. Stereology was used to quantify the terminal villous interface and internal vasculature by measurement of surface area and volume fraction. Stereological evaluation of the Surface Area in terminal villi and capillaries were significantly decreased when compared with their co-twins (p=0.04; p=0.049 respectively). Volume Fraction of terminal villi was significantly reduced when compared to their co-twins (p=0.02), although capillary volume fraction was reduced when compared to co-twins this was not quite significant (p=0.06). This profile was similar to the contrast observed between the preeclampsia-associated IUGR and normal control cohorts. Our results demonstrate that chronic uteroplacental insufficiency affects a significant number of discordant dichorionic twin pregnancies. Stereology has confirmed the histological finding of chorionic villi demonstrating accelerated villous maturation. In contrast to maternal conditions, which necessarily affect both twins, accelerated villous maturation affecting one twin suggests a primary disorder of the non-villous trophoblast causing impaired physiological adaptation of maternal vessels in these pregnancies.

Aims: To evaluate the impact of umbilical and uterine artery Doppler in the second and third trimester on antenatal course, labor and delivery in a low-risk primigravid population.Methods: Prospective recruitment of 1011 low-risk primigravidas with uterine and umbilical artery Doppler assessment at 22-24 weeks and 36 weeks. All mothers and infants were reviewed postnatally with a retrospective analysis of ultrasound and clinical outcome data.Results: Elevated uterine artery indices were associated with increased rates of threatened miscarriage, higher rates of preeclampsia (PET) and a higher incidence of fetal birth weight < 2(nd) and 9(th) centile for gestation. Uterine artery pulsatility index (PI) > 95(th) centile for gestation was associated with statistically higher rates of small-for-gestational age (SGA) infants. Elevated umbilical artery indices were associated with higher rates of induction of labor and a higher incidence of fetal birth weight infants < 2(nd) and 9(th) centile for gestation. Umbilical artery PI > 95(th) centile for gestation was associated with statistically higher rates of SGA infants.Conclusion: Elevated uterine and umbilical artery indices are associated with higher rates of maternal and fetal disease.

Accelerated Villus Maturation is classically associated with chronic uteroplacental insufficiency (CUPI) of placental chorionic villi e.g. pre-eclampsia with IUGR (PET-IUGR), thrombophilia and smoking. These small sized villi represent a reduced fetomaternal interface for both nutrient absorption and gas exchange. Our group have studied accelerated villus maturation associated with normal birth weight in both singleton and twin placentas. Case selection: Histopathological examination of placentas from 800 low risk singleton pregnancies and 154 dichorionic twin gestations allowed selection of the study cohorts. 4 cohorts of 10 placentas were examined, these comprised :- i) singleton accelerated villus maturation associated with normal birth weight; ii) twin gestation with accelerated villus maturation in one placenta (and normal co-twin); iii) PET-IUGR and iv) normal term singleton pregnancies. Stereological examination of terminal villous surface area and volume and that of the fetal vasculature was carried out. 53 (6.7%) of singleton placentas and 10 of 154 (6.5%) dichorionic twins had accelerated villus maturation associated with normal birth weight (in one twin placenta only). When examined by Stereology, the CUPI normal birth weight placenta from both singleton and twin placentas had a reduced capillary volume fraction (p=0.006; p=0.005 respectively) and surface area (p=0.0008; p=0.005 respectively) when compared to their respective controls, but had a normal villous surface area. The PET-IUGR capillary surface area was significantly reduced compared to normal controls (p=0.0003). The normal villus surface area in cases of accelerated villus maturation means increased numbers of small villi which is commensurate with normal birth weight. The reduced vascular volume similar to PET-IUGR provides a possible explanation of previously unexplained intrapartum hypoxia.

Our aim was to determine the prevalence and sequelae of positive acquired thrombophilia serology in the asymptomatic low-risk primigravid population. We undertook a prospective blinded study of 1011 primigravid patients screening for lupus anticoagulant, anticardiolipin antibody, anti- β2 glycoprotein-1 and antinuclear antibody assessment at booking and 36 weeks gestation. Serial ultrasounds of the fetus with uterine and umbilical Dopplers and placental evaluation were performed at 24 and 36 weeks gestation. Antenatal course, labour and delivery outcome and placental histology were reviewed. The incidence of positive acquired thrombophilia serology was 27.4%. Overall, there was no difference in rates of fetal loss or maternal disease between women with positive acquired thrombophilia serology and the control population. Routine testing for acquired thrombophilic traits is therefore not warranted.

To investigate the role of abnormal placentation in birthweight discordance in dichorionic twins and evaluate antenatal sonography as a predictor of abnormal placental morphology. ESPRIT is a national prospective study of twin pregnancies. Dichorionic twin pregnancies within the study had placental histological examination performed in a single pathology laboratory. Placental villus maturation was compared in discordant and non-discordant twin pairs. Antenatal sonographic features of uteroplacental insufficiency were defined as abnormal umbilical artery blood flow or reduced amniotic fluid volume. Stereological assessment of placentas from twins with growth discordance and antenatal sonographic abnormalities was performed to quantify placental capillary and villus morphology. 154 dichorionic twin pairs had placental histological examination performed. 31(20.1%) had >20% birthweight discordance. Placentas of birthweight discordant twins were significantly more likely to exhibit histological abnormalities of villus maturation (37.1% vs 23.2%, p = 0.03). There was a higher rate of villus abnormalities in the subgroup of twins (n= 22) with antenatal ultrasound abnormalities.Stereological studies demonstrated significant differences in placental villus and capillary morphometry between the smaller twins with sonographic features of uteroplacental insufficiency and their larger co-twins. Placentas from the smaller twins were of lower volume (p= 0.015) with a decreased volume of terminal villi (p=0.04) and of capillaries (p=0.03). These placentas also demonstrated reduced surface area of both terminal villi (p=0.02) and capillaries (p=0.02). Birthweight discordance in a proportion of dichorionic twin pregnancies is attributable to abnormalities of placental villus maturation. Stereological assessment suggests that sonographic abnormalities in amniotic fluid volume and umbilical artery blood flow are predictive of underlying abnormalities in fetal vasculature and villli. This may cause reduced placental diffusion capacity, fetal hypoxia and growth restriction.

Methods. aEuro integral This study involves prospective recruitment of 1011 low-risk primigravids with placental ultrasound at 22--24 weeks and 36 weeks. Detailed postnatal review of all mothers and infants was undertaken. Retrospective analysis of ultrasound and clinical outcome data was performed.Results. aEuro integral Eight hundred ten women with complete outcome data were available. Anterior placentation was statistically associated with intrauterine growth restriction (IUGR) and preterm birth and fundal placentation was significantly associated with a higher incidence of pregnancy-induced hypertension and infants with a birthweight less than the 9th centile. Placental infarcts in the third trimester was significantly increased in cases complicated by pre-eclampsia (PET) and in cases with fetal acidosis. Placental calcification was associated a 40-fold increase in the incidence of IUGR. Placental lakes in the second trimester were more prevalent in patients with threatened miscarriage. Increased placental thickness was associated with a higher rate of fetal acidosis. The Grannum grade of the placenta was higher with threatened first or second trimester loss, PET and in infants born less than 9th centile for gestation.Conclusion. aEuro integral Placental site and architecture impact on the incidence of maternal and fetal disease.