Fetal death indicated by transient hypofibrinogenemia.
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Adult↗
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Results for “Fetal Death--indications”
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A prospective evaluation of fetal movement screening to reduce the incidence of antepartum fetal death.
Fetal death is a tragedy for mother, family, and obstetrician. Recent reviews of fetal death indicate that nearly half occur in pregnancies that are not candidates for traditional antepartum testing. We conducted a prospective evaluation of the effectiveness of a fetal movement screening program in reducing the fetal mortality rate. During a 7-month control period, 2519 deliveries occurred, no formal fetal movement assessment was done, and the fetal mortality rate was 8.7 per 1000 births. A pilot study was conducted to validate a protocol in which the patient was instructed to record the elapsed time required to appreciate 10 fetal movements. The mean time interval was 20.9 +/- 18.1 minutes (mean +/- SD). Patients in whom 2 hours elapsed without 10 fetal movements (mean +/- 5 SD) were to report to the delivery unit for further evaluation. During the study period, 1864 patients were delivered of infants and the fetal mortality rate was 2.1 per 1000 (chi 2 = 6.8, p less than 0.01). During the study period the number of antepartum tests performed increased by 13%. Interventions for fetal compromise prompted by inadequate fetal activity tripled in the study period, resulting in a drop in fetal mortality among patients with decreased movement from 44 to 10 per 1000. We conclude that the count-to-10 fetal movement screening program is simple and effective in reducing the fetal mortality rate.
California↗
Effect of intrauterine death and fetectomy on ovine placental lactogen production.
Concentrations of ovine placental lactogen (oPL) were measured in the peripheral plasma of six ewes after the removal of fetuses (in four ewes) or after the intrauterine death of one of twin fetuses (in two ewes). Concentrations of oPL decreased after fetectomy or intrauterine fetal death, indicating that a living fetus is essential to the sustained secretion of oPL.
Animals↗
Catecholamines during therapeutic abortion induced with intra-amniotic prostaglandin F2alpha.
Serial plasma, amniotic fluid, and urine samples were analyzed for epinephrine (E) and norepinephrine (NE) in eight subjects during midtrimester abortion induced by intra-amniotic prostaglandin F2alpha (PGF2alpha). After PGF2alpha administration, plasma E increased and there was no change in plasma NE levels. Amniotic fluid levels of E and NE decreased initially. During the course of abortion the mean level of E in the amniotic fluid increased after fetal distress and decreased after fetal death, indicating that the midtrimester fetus of both E and NE increased following PGF2alpha. The observation that mean plasma levels and urinary excretion rate changes correlated better with the course of abortion and uterine contractility rather than with the time of PGF2alpha administration was consistent with the hypothesis that the catecholamine response may be due to the stress of labor rather than to the PGF2alpha per se.
Abortion, Therapeutic↗
AMNIOTIC FLUID ANALYSIS AS AN AID TO THE ANTE-PARTUM DIAGNOSIS OF HAEMOLYTIC DISEASE.
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Amnion↗
Does conception before marriage matter?
Data from the 1970 British Births survey were used to compare 1380 births conceived before marriage (women who were delivered less than 6 months after marriage) with 13,845 births to women who had been married for at least 6 months before delivery. Infants in the premarital conception group were at increased risk because of maternal youth, primiparity and maternal health behaviour such as smoking. Once these factors had been taken into account there was no residual risk of perinatal death or low birthweight. There was a slight excess of preterm deliveries.
Adolescent↗
Perinatal and infant mortality in urban slums under I.C.D.S. scheme.
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Child Health Services↗
Pathogenicity of minute virus of canines (MVC) for the canine fetus.
Minute Virus of Canines (MVC) was shown to cause transplacental infections with embryo resorptions, especially in dams given parenteral inoculations prior to gestational day 30. Responses to oral-nasal inocula were inconsistent. Direct exposures of embryos or fetuses to MVC via the amniotic sac, however, resulted in their deaths after an incubation period of approximately 2 weeks. Virus was prominent in fetal lung and small intestinal villi, but it could not be demonstrated in fetal or uterine tissues greater than 2 weeks after the estimated time of embryonic/fetal death. With 1 exception, dams inoculated during the last trimester of pregnancy gave birth to normal pups; some pups had developed active immune responses. The exceptional dam whelped dead or dying pups with anasarca or myocarditis. Antibody levels to MVC were generally higher in dams with infected fetuses than in bitches with normal pups at term. Failures to isolate virus, or demonstrate viral antigens in tissues by immunostaining, other than near the time of embryo/fetal death, indicate the need for more sensitive viral detection methods.
Animals↗
Genetic influences on craniofacial outcome in an avian model of prenatal alcohol exposure.
BACKGROUND: Understanding the basis for ethanol's teratogenic effects may inform the etiology of fetal alcohol syndrome. Here we investigate how genetic background and susceptibility to ethanol-induced neural crest apoptosis contribute to the distinctive craniofacial phenotype observed after prenatal alcohol exposure. METHODS: Nine different chick strains were exposed to ethanol at gastrulation. The sensitivity of these embryos to ethanol-induced neural crest apoptosis was reported elsewhere (Debelak and Smith, 2000). Here, these embryos were permitted to develop until embryonic day 10, when facial morphogenesis was largely complete, and cephalometric measurements were made on cleared skulls. Shifts in facial growth were correlated against the severity of ethanol-induced apoptosis in facial precursors. RESULTS: The facial shape produced by ethanol exposure was a function of the embryos' genetic strain. Three general responses were observed: apparent midfacial flattening (Babcock B300 x Hampshire Red, ISA-Babcock, HyLine W98, and HyLine W36 strains), overall facial expansion (Spafas and Babcock B300 strains), or overall facial hypoplasia (DeKalb strains). When dose and timing of exposure were held constant, the embryo's genetic background predicted the facial outcome. For ethanol-sensitive strains, apoptosis of facial precursor populations was required to produce the facial defects. That some strains had essentially normal faces despite extensive cell death indicated a capacity to recover from the earlier neural crest losses. CONCLUSIONS: We propose that ethanol's effects on craniofacial development are multifactoral, and these influences may include susceptibility to apoptosis, regenerative capacity, and compensatory outgrowth of the facial primordia. The embryo's genetic background may modulate these events. The high and low responder chick strains are useful tools to dissect these contributions.
Animals↗
Fetomaternal outcome in pregnancy with cardiac disease.
OBJECTIVE: To determine fetal and maternal outcomes in women presenting with heart disease during pregnancy and labor. DESIGN: Descriptive study. PLACE AND DURATION OF STUDY: Department of Gynae/Obstetrics, MCH, Center, Unit II, PIMS, Islamabad, during a period of 2 years from March 2001 to February 2003. PATIENTS AND METHODS: Forty-two pregnant women with heart disease delivered at MCH Center, Unit II, during the study period were included. Maternal outcome measures included obstetric and medical complications and maternal mortality while fetal outcome measures were prematurity, intrauterine growth restriction and perinatal mortality, intrauterine death and indicated terminations of pregnancy. RESULTS: The mean age was 27.50 -/+ 5.17 years (standard deviation). Of the 42 women, 33 (78.6%) were booked for antenatal care and 9 (21.4%) were non-booked. Congenital heart disease was present in 7 (16.7%) while 28 (65.3%) had rheumatic heart disease and mitral valve disease was the commonest. Among the remaining 7 women with acquired heart disease, 3 (7.1%) women had ischemic heart diseases (IHD), 1 (2.4%) had primary pulmonary hypertension, 2 (4.8%) patients had peripartum cardiomyopathy and 1 (2.4%) had aortic dissection. Based on New York Heart Association Functional classification (NYHA) 16 (38.1%) patients were asymptomatic (class I) and 3 (7.1%) in class IV. Thirty-two (76.2%) achieved spontaneous vertex delivery (SVD), LSCS was performed in 4 (9.5%) women, 2 (4.8%) women had spontaneous expulsions of dead fetus and 2 (4.8%) had suction and curettage for therapeutic termination of pregnancy on medical grounds. Obstetric complications occurred in 17 (40.4%) women, 5 (11.9%) had medical complications and 3 (7.1%) maternal mortalities occurred. Regarding fetal outcome, 6 (14.3%) infants had intrauterine growth restriction (IUGR), 2 (4.8%) perinatal deaths occurred due to prematurity while there was 1 (2.4%) intrauterine death. Indicated terminations of pregnancy were done for 4 gestations (7.1%). Low birth weight was noted in 12 (28.6%) infants. CONCLUSION: Heart disease with pregnancy is a very high risk condition and maternal mortality ratio (MMR) was 7142/100,000 births. The management of these cases should be multidisciplinary to optimize care for these patients and large families be strongly discouraged.
Adult↗
Reactive oxygen species participate in the control of mouse embryonic cell death.
Programmed cell death or apoptosis is an essential process during the morphogenesis of a large number of structures. Evidence obtained over the past few years indicates that, in some cases, the generation of reactive oxygen species (ROS) is an important event during the course of apoptosis. Using an in vitro culture system in which digit individualization of developing limbs normally occurs, we assayed the effect of different antioxidants on the cell death that takes place at interdigits. The addition of phenol, dimethyl sulfoxide, or 2',7'-dichlorodihydrofluorescein diacetate (DCDHF-DA) to murine developing limbs in culture prevented digit individualization as well as the typical interdigital cell death. Two ROS-sensitive dyes, 3-(4,5-dimethylthiazol)-2,5-diphenyl tetrazolium bromide and DCDHF-DA, stained interdigits and the so-called "necrotic zones," implying that they contain cells under oxidative stress. Very few interdigital cells were doubly stained with the ROS probes and two cell death indicators (i.e., acridine orange and propidium iodide), suggesting that they detect a different stage during the course of apoptosis. Furthermore, we found cells stained for ROS that did not express a specific macrophage marker and in a few cases were seen surrounded by a macrophage. Surprisingly, many regions of the midgestation mouse embryo that are undergoing cell death correlated with those that have a markedly higher level of ROS. Our data suggest that the generation of oxidative stress is a common requirement for cell death that occurs during mouse embryonic development.
Animals↗
Protective effect of epidermal growth factor on glutamate neurotoxicity in cultured cerebellar neurons.
The effects of epidermal growth factor (EGF) on glutamate-induced neuronal death were investigated in primary cultures of dissociated cerebellar neurons from fetal rats. Addition of an excess concentration of L-glutamate (5 mM) to the culture medium greatly decreased the number of surviving neurons 24 h later. When EGF was added to the culture medium 20 h prior to exposure to glutamate, glutamate-induced neuronal death was significantly reduced. The protective effects of EGF on glutamate neurotoxicity were concentration-dependent in the range of 0.01-10 ng/ml. When EGF was added 1 h prior to exposure to glutamate, it did not prevent glutamate-induced neuronal death, indicating that a longer exposure period is required for EGF to exert its protective effects. Furthermore, the protective effects of EGF on glutamate neurotoxicity disappeared in the presence of cycloheximide (0.1 microM), a protein synthesis inhibitor. These results suggest that EGF can protect brain neurons against glutamate toxicity through some protein synthesis.
Animals↗
Perinatal mortality and morbidity rates among singleton, twin, and triplet gestations.
Objective: To determine rates of perinatal mortality and morbidity from 24 to 43 weeks gestation among singletons, twins, and triplets.Methods: Successfully linked data from 1992 Californian maternal and infant discharge records as well as birth and death certificates from acute care civilian hospitals were examined for perinatal mortality and morbidity. Perinatal mortality was defined as the sum of all stillbirths and neonatal deaths. Deliveries from 24 to 43 weeks gestation among singleton, twin, and triplet pregnancies were collected as separate data sets. Perinatal mortality was identified using birth certificate death indicators excluding deaths caused by congenital anomalies. Neonatal deaths were identified from death indicators found in the death certificates. For the purpose of this study, perinatal morbidities were identified by ICD-9 codes and limited to respiratory distress syndrome (RDS), intraventricular hemorrhage (IVH), and necrotizing enterocolitis (NEC). Perinatal mortality and morbidity rates were expressed as a percent of live births stratified by gestational age. Perinatal mortality data were expressed in log scale and perinatal morbidity rates were statistically compared.Results: There were 571,390 total births in California of which 527,677 (92%) were singleton, 12,535 (2%) were twin, and 367 (0.06%) were triplet gestations. Across gestation, the rate of RDS between triplets and twins was comparable (6.6% vs 6.8%). However, the rates of IVH and NEC were significantly greater in triplets than in twins (20% vs 8%, P <.0001, and 25% vs 9%, P <.0001, respectively). The perinatal mortality rates are shown below.Conclusions: Perinatal mortality rates were comparable among singleton, twin, and triplet gestations delivered between 24 and 30 weeks gestation. Unlike singletons and twins, the triplet perinatal mortality rate did not fall between 31 and 36 weeks gestation and remained at 2.6%. Twin perinatal mortality rate was equivalent to singletons until 36 weeks gestation. IVH and NEC were significantly greater among triplets regardless of gestational age. These data suggest that antepartum fetal surveillance of triplet pregnancies should start as early as 30 weeks gestation while testing for twin pregnancies can begin at 36 weeks gestation.
Journal Article↗
Proliferation and death of cultured fetal neocortical neurons: effects of ethanol on the dynamics of cell growth.
Neuronal number in the mature CNS is determined by the balance of cell proliferation and death. The effects of ethanol on cell proliferation and death were examined in primary cultures of neocortical neurons derived from 16-day-old rat fetuses. The cells were treated with ethanol (0 or 400 mg/dl) and examined for (1) immunohistochemical identity, (2) cell cycle kinetics using a cumulative bromodeoxyuridine labeling technique, (3) viable cell number via a trypan blue assay, and (4) the incidence of cell death with terminal deoxy-nucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 3 immunhistochemistry. After two days in culture, most (>85%) cells expressed a neuron-specific antigen(s) whether or not ethanol was added to the culture medium. Ethanol affected the proliferation of the cultured cells, e.g., the length of the cell cycle was greater in the ethanol-treated cells than in controls. The number of trypan blue-negative (viable) cells was profoundly decreased by ethanol exposure. This decrease was accompanied by increases in the frequencies of TUNEL- and caspase 3-positive cells and of cells exhibiting nuclear condensations. Thus, ethanol decreases the number of viable cells in vitro by slowing cell proliferation and increasing the incidence of cell death. The expression of the death indices in untreated cultures is most consistent with a single (apoptotic) pathway of cell death, rather than simultaneous apoptotic and necrotic modes of death. Furthermore, it appears that ethanol initiates an apoptotic death among cultured cortical neurons.
Animals↗
Atm-null mice exhibit enhanced radiation-induced birth defects and a hybrid form of embryonic programmed cell death indicating a teratological suppressor function for ATM.
ATM (ataxia-telangiectasia mutated) is a genotoxic stress transducer. In this first report of Atm-dependent birth defects, Atm-null embryos were uniquely susceptible to low-dose (0.5 Gy) radiation, exhibiting severe runting, tail anomalies, and lethality, independent of cell cycle arrest or insulin-like growth factor 1. This treatment enhanced levels of p53 protein and central nervous system (CNS) apoptosis in wild-type mice, but not Atm-null mutants, at 6 h postirradiation. At 48 h, however, this pattern was reversed, with Atm-null mice exhibiting high levels of a hybrid form of programmed cell death within the CNS. Even heterozygous Atm-deficient embryos were radiosensitive to a higher radiation dose of 2 Gy. These results show that Atm is a novel teratologic suppressor gene protecting embryos from pathological cell death and teratogenesis initiated by even mild DNA damage.
Abnormalities, Radiation-Induced↗
Deaths from rhesus haemolytic disease in England and Wales in 1977: accuracy of records and assessment of anti-D prophylaxis.
All the death certificates for deaths in 1977 where haemolytic disease of the newborn (HDN) was the principal, an antecedent, or a contributory cause were obtained from the Office of Population Censuses and Surveys (OPCS). The hospital notes of all 54 of the live-born cases and all of the 101 stillbirths were also obtained. The cause of the death indicated by the notes was compared with the cause and coding on the death certificate. In about a quarter of the cases death was not due to haemolytic disease of any type. The commonest errors arose because the International Classification of Diseases (8th edition) stipulates that hydrops without mention of cause should be coded as HDN and because stillbirths to rhesus-negative mothers tend to be attributed to rhesus HDN automatically. Though deaths from HDN may be overestimated in this way, they are also underestimated because rhesus disease, although mentioned on the certificate, is not selected as the underlying cause, which it may be. These cases were found through multiple coding of all the contributory causes of death, which OPCS performs on a 25% sample of all death certificates for research purposes. These two sources of inaccuracy tend to cancel each other out, but statistics from death certificates give a misleading picture of the efficacy of anti-D prophylaxis because anti-D can never prevent cases which are not in fact due to rhesus HDN. Most of the mothers studied had become immunised before anti-D became available, but in those who could have been treated 75% had not received prophylaxis. As this was a sample of deaths, however, it would not be accurate to extrapolate this high figure to the population at risk. Nevertheless, the organisation of prophylaxis is clearly deficient and should be remedied before providing antenatal anti-D to supplement postnatal treatment.
Death Certificates↗
Verbal autopsy in establishing cause of perinatal death.
INTRODUCTION: Perinatal mortality is a sensitive indicator of health status of a community and is also highly amenable to intervention. The causes of perinatal deaths in developing countries are often difficult to establish. Verbal autopsy has been used in several countries for children and adults, but seldom for perinatal cause. OBJECTIVE: To establish the cause of perinatal deaths using verbal autopsy. DESIGN: Community-based cross-sectional, retrospective study to identify perinatal death over a one year period from July 1996-June 1997. Comparison was made with hospital records. An algorithm of signs and symptoms was used by trained personnel to identify the cause of perinatal death. The duration of collection of data was six months (August 1996-January 1997). SETTING: Hai district of Kilimanjaro region in Tanzania. SUBJECTS: All perinatal deaths within one year. RESULTS: The perinatal mortality was 58 per 1000 (121 deaths and 2088 live births). Verbal autopsy could establish the cause of death in 105 of the 121 deaths. Hospital records showed 79 deaths indicating that 42 deaths probably occurred at home. Among the 79 available hospital records, the cause of death could be established in only 30 (38%). The causes of postnatal death were compared between the verbal autopsy and hospital records. There was a good correlation between the same, however only 18 records were available from hospital among the total 31 postnatal deaths. The specificity of determining cause of death using verbal autopsy was 100% and sensitivity 61%. CONCLUSION: The commonest causes of perinatal deaths were related to obstetric care, therefore interventions to curb perinatal mortality should be directed to improvement of obstetric care. Verbal autopsy is a simpler and more sensitive tool in establishing the cause of perinatal death than hospital records in a rural district of Tanzania. Large-scale studies are needed to validate this.
Autopsy↗
Why perinatal mortality cannot be a proxy for maternal mortality.
In recent years, the perinatal mortality rate (PNMR) has been proposed as a proxy measure of maternal mortality, because perinatal deaths are more frequent and potentially more easily measured. This report assesses evidence for an association between these two statistics. This study, based upon data from Matlab, Bangladesh, shows that the maternal mortality ratio (MMR) and the PNMR do not vary together over time, and that the PNMR does not reliably indicate either the magnitude or the direction of change in the MMR from year to year. Statistical analysis shows that the correlation between the PNMR and the MMR is not significantly different from zero. An examination of the major causes of maternal and perinatal deaths indicates that the two measures cannot be expected to vary together. Almost half of perinatal deaths result from causes that do not pose a threat to the mother's life, and almost half of maternal deaths result from causes that do not lead to perinatal death. Monitoring of the PNMR can give an inaccurate picture of maternal mortality and should not be used as a proxy.
Bangladesh↗