Background: Single fetal death (sFD) in monochorionic twin pregnancies is associated with substantial morbidity and mortality in the survivor. The aim of our study was to evaluate the rate of cerebral lesions detected at fetal Magnetic Resonance Imaging (MRI) and to correlate the results with the neurologic outcome of the survivors of monochorionic twin pregnancies after sFD. Methods: Between 2005 and 2012, 11 monochorionic twin pregnancies with sFD and subsequent fetal MRI of the survivor were included. All neonates underwent neurologic assessment after birth and 56% of surviving infants underwent long-term neurologic assessment. MRI findings and neurologic outcome of the survivors were evaluated. Results: Gestational age at sFD was 20.9 (±2.9) weeks; 55% (6/11) of survivors of monochorionic twin pregnancies after sFD showed cerebral lesions at fetal MRI; 72% (8/11) of all survivors had normal neonatal neurologic outcome: all survivors with normal fetal MRI and 50% of survivors with cerebral lesions at fetal MRI. Long- term neurologic assessment was normal in all tested patients with normal fetal MRI and in one of three tested patients with cerebral lesions at fetal MRI. Conclusion: Survivors of monochorionic twin pregnancies after sFD show a high rate of cerebral lesions at fetal MRI. The importance of cerebral lesions at fetal MRI in survivors after sFD in monochorionic twin pregnancies is uncertain. All tested survivors with normal fetal MRI showed normal neurologic outcome but only one of three survivors with cerebral lesions at fetal MRI showed normal long-term neurologic outcome.
Finally, the possible postnatal injury to brain and gastro- intestinal tract cannot be excluded in this case. The pre- maturity and low birth weight are potential threats to the integrity of the brain which may worsen the long-term neurological outcomes of the survivors. However, it is dif- ficult to ascribe the causes of final outcomes to solely complication of antenatal related single intrauterine death and/or fetofetal transfusion syndrome since the survivors were also exposed to postnatal sources of brain insults. Normal antenatal fetal brain imaging cannot exclude the in-utero brain insults because brain injuries can take months to evolve and allow cavitation formation, and only become evident on the radiological examination after birth. The first baby’s brain lesion was likely related to a result of prematurity, while the second baby’s MCE was likely due to severe intrauterine hypoxic ischaemic injury leading to cerebral necrosis. Antenatal administration of magnesium sulphate before early preterm delivery can help to alleviate the prematurity related long-term neuro- logical impairment for these babies. However, this was not put into practise in our hospital at that time. Furthermore, the first baby suffered from jejunal atresia which might be related to discordant congenital anomaly. Congenital anomaly is commoner in multiple pregnancies than
The major finding of our study of twin pregnancies compli- cated by a single fetal death after 20 weeks was that deliv- ery occurred significantly earlier when the dead twin was presenting. Earlier delivery resulted in more neonatal mor- bidity for the surviving co-twin, with higher rates of admis- sion to intensive care for respiratory support to treat respi- ratory distress. After adjusting for differences in gestational age, birth order itself did not affect neonatal morbidity. The other major finding was that the rate of anomalies in the surviving co-twin was much higher if it was the present- ing twin who had died. In addition, maternal morbidity was largely unrelated to the order of fetal death, although emergency cesarean delivery was more common with IUFD Twin 1.
IMPORTANCE Programmed cell death (PCD) is a well-known phenomenon in higher eukaryotes. In these organisms, PCD is essential for embryonic development—for example, the disappearance of the interdigital web—and also functions in tissue ho- meostasis and elimination of pathogen-invaded cells. The existence of PCD mechanisms in unicellular organisms like bacteria, on the other hand, has only recently begun to be recognized. We here demonstrate the existence of a bacterial PCD pathway that induces characteristics that are strikingly reminiscent of eukaryotic apoptosis, such as fragmentation of DNA, exposure of phos- phatidylserine on the cell surface, and membrane blebbing. Our results can provide more insight into the mechanism and evolu- tion of PCD pathways in higher eukaryotes. More importantly, especially in the light of the looming antibiotic crisis, they may point to a bacterial Achilles’ heel and can inspire innovative ways of combating bacterial infections, directed at the targeted acti- vation of PCD pathways.
In our study, early manifestations of cerebral ischemia in monochorionic twin pregnancies were better diagnosed with MR imaging, especially with DWI. Early diagnosis of cerebral isch- emic lesions might influence the consultation, parents’ decisions, and management of the affected pregnancy. Because a large part of interventions in monochorionic pregnancies are performed at 22–24 weeks of gestation, any brain abnormality related to the procedure will be evident by sonography or T2 MR imaging only when the fetus is considered viable (after 24 weeks’ gestation). Therefore, early diagnosis of postprocedural severe brain abnor- malities is specifically important when fetal death occurs shortly before delivery (otherwise, patients should wait at least 2 weeks, relying on fetal sonography and T2 MR imaging) or when reach- ing a strict gestational age limit for termination of pregnancy, whenever patients choose to do so. DWI results can contribute to the decision in such a short period. However, making crucial de- cisions (ie, pregnancy termination) on the basis of DWI alone could be very difficult because experience in this field is at a very early stage. Our opinion is that termination of pregnancy should be discussed on the basis of DWI results only in cases of clear large cerebral ischemic lesions and not in cases of subtle findings such as germinal matrix or basal ganglia bleeding.
PCD has been recognized as an essential event in morpho- genesis as well as in the normal turnover of cells in adult tissues (Glücksmann, 1951; Saunders, 1966; Wyllie et al., 1980; Ellis et al., 1991). When various structures are formed during development, some cells are eliminated by means of PCD to achieve complicated morphogenesis. It has been suggested that developmental PCD enables (1) sculpting body parts, (2) deleting unnecessary cells, (3) controlling cell numbers in a given tissue, (4) eliminating abnormal, misplaced or harmful cells, and (5) producing specialized differentiated cells without organelles, such as lens epithelial cells and mammalian eryth- rocytes (Jacobson et al., 1997). However, there are many kinds of developmental cell death whose function is unknown. Al- though it has been widely accepted that PCD plays essential roles in palate development, some important questions remain to be answered such as: (1) at which stage(s) of palate development PCD occurs, (2) what is the actual biological role of PCD in palatogenesis, (3) what is the fate of MEE cells that disappear from the midline epithelial seam, and (4) whether or not PCD is really required for palatal fusion.
Methods: A prospective observational study was conducted in ESIC MC and PGIMSR, Rajajinagar, Bangalore, Karnataka, India. All cases of intrauterine fetal death confirmed either with ultrasound or on clinical examination by absence of fetal heart rate and fetal movements were studied. The age, parity, literacy, socio-economic status was recorded. Detailed history, clinical examination, associated conditions. Mode of delivery and details of the fetus and their placentas were noted. They were followed for 3 days for complications.
In recent times medical science has begun to unravel the genetic basis to numerous human disorders (McKusick, 1990). It has become apparent that many defects and disorders result from errors in the genetic makeup of an individual. These changes can be attributed to alterations in the sequence of deoxyribonucleic acid bases (DNA) that are found in the nucleus of every cell (Watson and Crick, 1953). This understanding has enabled the genetic status of an as yet unborn child to be assessed through prenatal diagnosis. Serious birth defects, many of them genetic, complicate and threaten the lives of 3-5% of new-born infants (McKusick VA. 1990; Shepard 1986) and about 0.7% of all live-born infants have a congenital abnormality associated with a chromosomal defect (Thompson et al., 1991). Such disorders account for 20% of deaths during the newborn period and an even higher percentage of serious morbidity in infancy and childhood (Contribution of birth defects to infant mortality; 1989). Other pregnancies are at risk of other serious inherited conditions, from deleterious single or numerous genes passed from one generation to the next. The fiscal and social cost of neonatal intensive care and rehabilitation programs for the severely handicapped is high, but higher still are the immeasurable emotional costs afflicting an affected family. With current social trends toward smaller families and delays in childbearing, coupled with the growing scientific knowledge regarding the basis of genetic disease, prenatal diagnosis has an important role in the management of many pregnancies. Prenatal diagnosis provides not only the option to parents of terminating a severely affected pregnancy, but in many situations the potential for the prevention of the clinical manifestations of a gene defect, such as with selected metabolic disorders by dietary restrictions soon after birth. Knowledge of fetal genetic errors is also paramount in the potential new field of genetic intervention, or gene therapy.
324 Read more
IUFD. Contraception advice and prenatal counselling before next pregnancy can be helpful for better obstetric outcome. Future research should focus on improved means of assessment of fetal wellbeing and defining pathophysiological pathways leading to IUFD associated with maternal disease and need to address gaps in knowledge by setting research priorities.
Fig. 5. IL-10 reduces cathepsin B expression in fetal type II cells exposed to hyperoxia. E19 type II cells exposed to 65%- and 85%-hyperoxia for the indicated periods of time. Cells in room air were used as controls. E19 cells were preincubated with 250 ng/mL rat recombinant IL-10 (rIL-10) before exposure to 65%- and 85%-hyperoxia. (A) Western blots showing that cathepsin B expression is reduced in rIL-10-treated cells compared to untreated cells. (B) Graphical de- piction showing relative intensities of cathepsin B from 3 independent experiments in rIL-10-treated and untreated cells. (C) Graphical depiction showing gene expression of cathepsin B from 3 different experiments in rIL-10-treated and untreated cells. E19, embryonic day 19.
Women with chorioamnionitis were identified by reviewing their hospitalization records for the ICD-9-CM code 658.4 (infection of amniotic cavity), their infant’s hospitalization records for the ICD-9-CM code 762.7 (fetus or newborn affected by complications of placenta, cord and membranes: chorioamnionitis), or documenta- tion of chorioamnionitis on the birth certificate. This case definition refers to clinical chorioamnionitis in the assess- ment of the clinician treating the mother and/or infant, as rates and results of pathological placental investigations could not be determined from these data sources . The definition of clinical chorioamnionitis is subject of ongoing debate and is variably diagnosed by presence of the following criteria: maternal intrapartum fever, mater- nal and/or fetal tachycardia, purulent amniotic or vaginal fluids, uterine tenderness and maternal leukocytosis . BPD was identified using ICD-9-CM code 770.7 (chronic respiratory disease arising in the perinatal period) in the infant’s hospitalization records, while RDS was identified using ICD-9-CM code 769 (respiratory distress syndrome). While the database does not give further diag- nostic detail, the definition of BPD followed the Eunice Kennedy Shriver National Institute of Child Health and Human Development consensus definition . The clinical definition of RDS was presumably based on the requirement for surfactant.
The aim of this study is to explore the outcome of Teucrium polium (TP) medicinal plant consumption on the early stage of fetal development. We used the chicken embryo at 3 days of incubation as a model to evaluate the effect of TP plant extract during embryogenesis. In addition, quantitative polymerase chain reaction (qPCR) was applied to explore the expression of six genes related to cell proliferation, apoptosis, sur- vival, angiogenesis, and migration. Our data revealed that TP exposure inhibits angiogenesis of the chicken embryo and its chorioallantoic membrane. In addition, we found that TP extract significantly harms the normal development of the embryos since around 95% of TP-exposed embryos died after 1–3 days of treatment. Macroscopic examination did not show any anomalies in these embryos. However, qPCR analysis of activation transcription factor-3, B-cell lymphoma-2, caspase-8, inhibin subunit beta A, vascular endothelial growth factor-C, and Cadherin-6 type-2 genes revealed that these genes are considerably deregulated in heart and brain tissues from TP-exposed embryos in comparison with their matched tissues from unexposed ones. Our study implies that TP plant can have very toxic effects on the early stage of the embryo. Therefore, it is important to alert expectant women to avoid the use of this medicinal plant during pregnancy.
Contrary to the observation of Dao et al. , our patient is primiparous and would appear to be at the beginning of the 2nd trimester; indeed, the fetal weight evaluated after laparotomy, would lead to a pregnancy of 19 to 20 weeks, which corresponds to the statements of the patient who evaluates her gestational age at 4 - 5 months.
ment strategies did not change dramatically at our center during the study period. The use of dopamine, which inhibits thyroid stimulating hormone production , did increase over time. However, increasing dopamine use would be expected with an increase in illness and would not explain an increase in SNAP. It also remains a possi- bility that low T 4 is an important part of the causal path- way in illness severity and that some primary change in thyroid function over time in our population contributed to the observed increase in illness severity. Even if a pri- mary decrease in T 4 was responsible for the observed increase in illness, the importance of a progressive decrease in T 4 is highlighted by the association of hypothyroxinemia with death , IVH , cystic periv- entricular leukomalacia , and cerebral palsy  in VLBW infants.
The deaths which are potentially preventable by AADP are those in categories 2 and 3. Over the period 1977 to 1989 there were 195 deaths in these two categories, an average of 15 per year. This equates to a rate of loss of 0.02% among RhD negative women with a RhD positive baby, assuming that they constituted 10% of all births during this period. This rate does not include fetal losses that occurred prior to 28 weeks’ gestation, unless the fetus was born alive. A review of fetal losses due to haemolytic disease at one tertiary referral centre in Glasgow over a 15 year period found that 21 out of 46 losses (46%) occurred before 28 weeks’ gestation. 14 Therefore, taking the rate of fetal loss before 28 weeks’ gestation to be
59 Read more
The Eunice Kennedy Shriver National Institute of Child Health and Human Development held a workshop March 23 to 24, 2015, entitled “Sudden Unexpected Death in Fetal Life Through Early Childhood: New Opportunities.” Its objective was to advance efforts to understand and ultimately prevent sudden deaths in early life, by considering their pathogenesis, at least in part, as a potential continuum with some common biological origins or pathways. Invited researchers shared work on biological factors relevant to sudden deaths from fetal life through early childhood, including intrinsic factors involved in unexpected death, underlying biological evidence of preceding conditions or circumstances that may contribute, or interactions between intrinsic vulnerabilities and adverse environmental factors in the pathogenesis of sudden death. A second objective was to highlight current issues surrounding the classification of SIDS in forensic practice, pediatric care, and research. Participants were also encouraged to consider new technologies and “omics” approaches to accelerate research. The Triple Risk Model for SIDS, proposing that SIDS occurs in infants with latent biological vulnerabilities, exposed to external threats during a critical period in development, served as a reference. 6
13 Read more
As regards to maternal factors associated with fetus death, several studies ad- dressed the relation between maternal age and IUFD, where childbearing wom- en younger than 20 and older than 40 years are more likely to have stillbirth than women in group age 24 - 35 years and the problem become more obvious in women aged ≥ 40 years  . In addition to that the relation between maternal age and both gestational age and birth weight are confirmed, where women older than 40 years have more chance to performed C/S and have macrocosmic neonate  . The results of the current study consistent with previous studies and showed that the mean age score was 30.6 ± 6.7.
developed countries and as high as 45 per 1000 pregnancies in developing countries. Fetal death, the largest subgroup of perinatal mortality worldwide consists of antepartum and intrapartum fetal deaths. The causes of fetal death include: fetal causes (25-40%), placental causes (25-35%), maternal causes (5-10%) and in 25-35% of cases the cause remains unknown. The maternal risk factors associated with intrauterine fetal death can be enlisted as antiphospholipid antibody syndrome, isoimmunisation, hypertensive disorders, cholestasis, vascular diseases, infections, cyanotic heart disease, severe anaemia. The fetal factors include ABSTRACT
Results: A total of 10,379 deliveries were attended A total of 242 uterine rupture cases were included in this study. The magnitude of uterine rupture was 2.44% (1 in 41 deliveries). Sixteen (6.6%) mothers died from uterine rupture. Fourteen (5.8%) had experienced Vesico Vaginal Fistula. The majority of the mothers, 72% (176), admitted for uterine rupture stayed in hospital for 6 – 10 days. Fetal outcome was grave, 98.3% (238) were stillborn. Place of labor [Adjusted odds ratio (AOR): 6.92, 95% confidence interval (CI): (1.16, 33.74)], occurrence of hypo volume shock [AOR: 3.48, 95% CI: (1.01, 11.96)] and postoperative severe anemia [AOR: 0.092, 95% CI: (0.01, 0.956)] were significantly associated with maternal death secondary to uterine rupture.
Present study is a step towards understanding and extrapolating the already known causes of intra uterine foetal death in the perspective of Jabalpur and its adjoining districts. Since a number of placental pathology adversely affect the perinatal outcome, an earnest effort can be made to diagnose them by prenatal ultrasound examination. Though it is less sensitive in detecting infections, it is highly specific in detecting retro-placental clot and placenta in lower segment. Since Jabalpur is endemic for many febrile illnesses, an early diagnosis and treatment can avoid many IUFDs. Similarly, vigilant follow up and careful management of subjects with pre- eclampsia and postmaturity can avoid many untoward accidents.