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Background: The cause of meconium passage in utero is controversial, traditionally being considered evidence of fetal stress and hypoxia, and also associated with intra-amniotic inflammation/infect...

Introduction: The placenta is infrequently examined in developing countries. This study examined the role of placental pathology in perinatal deaths at Chulalongkorn University Hospital, Bangkok. M...

Background: Intrauterine fetal demise (IUFD) is an unpredictable and challenging obstetric complication. Its etiology is multifactorial with more than 60% attributed to the placental cause. The present study was done with a primary objective of understanding the placental lesions underlying IUFD. Methods: In this retrospective observational study, IUFD cases (>22 weeks) between January 2012 and September 2015 were collected from pathology database. The clinical details with ultrasound findings were collected from mother's charts. The lesions were classified into (A) maternal vascular malperfusion (MVM) including retroplacental hematomas, (B) fetal vascular malperfusion (FVM), (C) inflammatory lesions, and (D) idiopathic. The contributor to fetal death was classified as direct, major, minor, unlikely, or unknown. Placental findings of fetal hypoxia were recorded. Results: The study included 100 cases of IUFD. The mean maternal age was 26 years (18-36 years). Primipara were 46. There were 65 early preterm (PT) ( 37 weeks) IUFD. The mean gestation age was 30 weeks. The ratio of male:female fetuses was 1:1.7. Relevant obstetric complications included preeclampsia (n = 39), intrauterine growth restriction (IUGR) (n = 7), pre-gestational diabetes (n = 7), bad obstetric history (n = 6), oligohydramnios (n = 5). The mean placental weight was 256 g. Maternal vascular malperfusion had the highest incidence (30%), followed by combined maternal and FVM (10%). Exclusive inflammatory lesions and FVM were seen in 12 and 6%, respectively. No cause was identified in 18%. Direct contributor to IUFD was identified in 51 cases and major, minor, unlikely contribution in 21, 11 and nine cases, respectively. In nine cases, it was unknown. Lesions indicating fetal hypoxia were noted in 35 cases. In both early and late PT, MVM featured more commonly (23 and 5%). In term placentas, the most common cause was idiopathic. Conclusions: Lesions of MVM were the most common cause of IUFD and served as a direct contributor to fetal demise.

We assessed clinical outcomes and placental pathology among pregnancies complicated with gestational diabetes mellitus (GDM) according to their pregestational body mass index (BMI) and weight gain during pregnancy.Pregnancy outcome and placental pathological reports of all GDM deliveries, during 2009-2015, were reviewed. We compared women with pregestational BMI 30 and or gestational weight gain20 kg (high-BMI group), and women with pregestational BMI 30 and weight gain less than 20 kg (normal BMI group).Out of the 429 women with GDM, 221 (51.5%) were in the high-BMI group and 208 (48.3%) were in the normal BMI group. As compared to the normal BMI group, the high-BMI group displayed a higher rate of GDMA2 41.6 versus 30.2%, p = .01, higher birth weight, 3475 ± 508 g versus 3242 ± 503 g, p .001, more large for gestational age neonates, 33.1 versus 13.9%, p .001, and a trend for more cesarean deliveries (CD), 49.3 versus 40.8%, p = .07, respectively. By logistic regression analysis, past CD and high BMI were independently associated with CD, while GDM type and birth weight were nonsignificant. Pathological reports were available for 143 of these patients. Placental weight was increased among the high-BMI group, but did not retain significance after adjustment for birth weight, and GDM type. No differences were demonstrated in other placental histological findings.GDM pregnancies accompanied by increased weight gain or elevated pregestational BMI are associated with adverse obstetric outcomes, despite similar placental findings. Patient should be advised accordingly, as gestational weight gain may determine delivery mode.

Clinical, laboratory, and placental manifestations of perinatal listeriosis are highly variable. Herein, we retrospectively analyzed all patients treated for neonatal listeriosis at the Charité University Medical Center in Berlin, Germany, 1999-2013. A total of 16 cases were identified. In 14 patients listeriosis was confirmed in neonatal specimens, while in two only the placenta tested positive. Elevated C-reactive protein and/or interleukin-6 levels were only inconsistently found, while a marked white blood cell left shift was present in all infants, if available. All but one infant manifested symptoms on the first day of life. Most patients required respiratory support, while none developed meningoencephalitis as evidenced by clinical or cerebrospinal fluid findings. Two patients died, all other patients survived without sequelae. In conclusion, perinatal listeriosis is still associated with significant morbidity and mortality. Clinical and laboratory findings are highly heterogeneous, but extreme leukocyte left shift seems to be a common feature.

Our objective was to evaluate the placental histopathology (PH) in extremely low birth weight infants (ELBW, birth weight1000 g) and to determine if placental histopathological findings are associated with neonatal mortality in them. The PH of all ELBW infants (gestational age 23-30 weeks) born during a 3-year study period was prospectively evaluated and compared with term infants (gestational ageor = 37 weeks). Additionally PH of ELBW infants who expired within 28 days of life was compared with those who survived beyond 28 days. Student's t test, chi(2) test and Pearson's correlation coefficient tests were utilized for data analysis. The occurrences of placental infection (chorioamnionitis, HCA), umbilical cord inflammation (funisitis, vasculitis, and subacute necrotizing funisitis, analyzed collectively as HFV), and abruption were higher in ELBW (n = 105) compared to term infants (n = 61, p = 0.001, 0.0002, and 0.0002, respectively). Placental findings did not differ between the surviving (n = 71) and nonsurviving (n = 51) ELBW infants. Birth weight and gestational age were higher in the surviving group (p = 0.003 and 0.001, respectively). Placental abruption was found more commonly in the presence of HCA and HFV in ELBW infants as opposed to maternal hypertension in term infants. All ELBW placentas with HFV had concomitant findings of HCA whereas only 42% of ELBW placentas with HCA had findings of HFV compared to 24% in term infants (p = 0.09). There was a weak inverse correlation between HCA and birth weight in all (r = - 0.3, p = 0.01) but not in ELBW infants (r = 0.2, p = 0.07). We conclude that placental and umbilical cord inflammation and placental abruption are more commonly present in ELBW compared to term infants. However, these findings do not contribute to neonatal mortality in ELBW infants. Forty-two percent of placental (maternal) inflammation cases have concomitant cord (fetal) inflammation in ELBW infants. Finally HCA correlates inversely with birth weight in neonates.

A 27-year-old G1P0 woman at 16 weeks’ gestation was transferred to our hospital for a missed abortion combined with abnormal sonographic placental findings. Her medical history was unremarkable. Sh...

Objective: The small controlled trials reporting large reductions in the incidence of preeclampsia and intrauterine growth restriction (IUGR) in highrisk pregnant women treated with low-dose aspirin have recently been followed by large clinical trials suggesting less beneficial results. The effect of low-dose aspirin on placental lesions associated with preeclampsia and IUGR has not yet been studied.Methods: We participated in the large multicenter randomized collaborative low-dose aspirin study in pregnancy (CLASP) trial of low-dose aspirin for the prevention and treatment of preeclampsia and intrauterine growth restriction. As part of this study, we evaluated placentae submitted from 25 women treated with aspirin and 28 with placebo.Results: More of the pathological findings classically described in preeclampsia and IUGR were demonstrated in the placentae from the placebo group than from the aspirin group (54% vs. 16%, P = 0.02). The placental findings did not correlate with clinical pregnancy outcome o...

This article on the placenta includes considerations of chorioamnionitis, villitis, preeclampsia, and other low placental blood flow states and aspects of the circulating lupus anticoagulant syndrome. The author explains that, although gross and microscopic placental findings document placental features at one point in time, they also reflect ongoing pathophysiologic changes. Pathogenetic relationships between placental pathology, fetal hypoxia, intrauterine growth retardation, and cerebral palsy are discussed. The reader will learn that low placental blood flow states and chorioamnionitis are important means by which endothelins may eventually participate in the production of placental and fetal vasoconstriction and critical hypoperfusion. The author explains means by which reduced umbilical, placental, and fetal blood flow can result from chronic fetal exposure to meconium, meconium-induced vasoactivity, and ultimate vascular necrosis. Clinically important complications therein may include anoxic-ischemic neuronal necrosis in the brain, necrotizing enterocolitis, and ischemic lesions in the fetal heart, lungs, kidneys, and liver. The article includes a review of nucleated red blood cells that most often signify chronic fetal hypoxia rather than infrequent acute intrapartum asphyxia. The reader will also find information on chorangiosis (placental villous capillary hypervascularity), an important sign of placental malperfusion and very long-standing fetal hypoxia.

GM1 gangliosidosis (type 1) is a rare hereditary, autosomal recessive, lysosomal storage disease characterized by a marked deficiency of active acid beta-galactosidase resulting in accumulation of gangliosides and mucopolysaccharides in tissues. Disease status of newborns from affected kindreds may be diagnosed by placental examination. Typical findings include a characteristic vacuolar distension of the cytoplasm of syncytiotrophoblast and stromal Hofbauer cells. We report a case of unsuspected fetal storage disorder initially diagnosed by routine placental examination of a normal-appearing infant born to a previously unaffected family. Progressive, third-trimester oligohydramnios and fetal growth retardation had been documented by ultrasonography. Placental findings included vacuolization of syncytiotrophoblast, intermediate trophoblast, and stromal Hofbauer cells. Subsequent enzyme analysis confirmed the placental findings of storage disorder and diagnosed GM1 gangliosidosis.

The aim of the study was to document the role of laboratory investigations for unexpected stillbirths at term. It was a retrospective casenote review of 75 unexpected stillbirths at term from 1995 to 1999, at the National Maternity Hospital, Dublin, Republic of Ireland.Investigations performed included blood tests, chromosomal analysis, autopsy and placental histology. Perinatal autopsy was the most informative investigation with positive findings in 49% of cases. There were positive placental findings in 37% of cases. Six of the 26 cases showed abnormal karyotyping. Of the blood tests performed, the Kleihauer – Betke test was most informative, revealing a feto-maternal haemorrhage in 8% of cases and anticardiolipin antibodies were positive in 4% of cases. FBC, TORCH and glycosylated Hb were negative in all 75 patients. Despite thorough investigations 32 of cases (43%) remained unexplained.