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At least 19 recordsLinked to original sources

Statistical model for fetal death, fetal weight, and malformation in developmental toxicity studies.

The purpose of this paper is to present a statistical model for analyzing the joint effects of exposure on fetal death, fetal weight, and malformation in a developmental toxicity study. In addition to allowing for the usual litter effect, the model allows for correlations between different outcomes measured on the same fetus. Fitting the model requires first focusing on non-live outcomes by modeling the probability of fetal death or resorption as a function of dose. Then outcomes among live fetuses are modeled using a two-stage regression approach. The first stage models fetal weight as a function of dose and the second stage models fetal malformation as a function of dose, as well as residuals from the weight model. The regression coefficients from the malformation model have intuitive interpretations in terms of correlations between littermates and between different outcomes measured within the same fetus. Not only does the approach provide a useful way to investigate the relationship between adverse fetal outcomes, it also yields a natural framework for conducting quantitative risk assessment. A procedure is proposed for quantifying overall risk by incorporating the three outcomes in order to estimate safe dose levels and corresponding lower confidence limits. The method is illustrated using data from an experiment in mice conducted through the National Toxicology Program.

Abnormalities, Drug-Induced↗

Management of patients with intrauterine fetal death.

Fetal death incidence is 5-10 per 1,000 births. About 25% of the women who carry a dead fetus for more than 4 weeks will show significant alterations in their coagulation system. The treatment for a patient with endouterine fetal death depends on when the pregnancy is terminated, based on the ecographic fetus age. There were 15,070 births from January 1983 to December 1994 in Department B of the Institute of Obstetrics and Gynecology, University of Torino. We took into consideration the cases ofintrauterine fetal death between the 26th and 40th week before labour. This study is based on a cohort of 57 cases of intrauterine fetal demise from the 24th to the 40th week of pregnancy before spontaneous labour.

Abortion, Therapeutic↗

Amniotic fluid S100B protein in mid-gestation and intrauterine fetal death.

Fetal death in the mid-trimester of pregnancy is unexplained and no reliable markers are available to identify at-risk women. We aimed to assess use of alpha fetoprotein and S100B concentrations in amniotic fluid as markers. We did a case-control study in 758 healthy women undergoing amniocentesis at mid-gestation, of whom 12 had a spontaneous intrauterine fetal death before 28 weeks, and 746 matched controls. Concentrations were corrected for gestational age by conversion to multiples of median (MoM) of healthy controls of the same gestational age. Concentrations of S100B, but not alpha fetoprotein, were significantly higher (p<0.0001) in women who later had spontaneous fetal death (median 4.431 MoM [95%CI 3.605-6.197]) than in controls (1.000 MoM [1.062-1.121]). Sensitivity, specificity, and positive and negative predictive values of S100B as a diagnostic test were 100%, suggesting that measurement of this protein at amniocentesis could be useful to identify at-risk women.

Amniotic Fluid↗

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↗

The coding of underlying cause of death from fetal death certificates: issues and policy considerations.

Recently, plans to implement nationwide coding of underlying cause of fetal death have been promulgated. To examine the validity and potential utility of nationwide coding, this paper presents data from a five-state (Wisconsin, Arkansas, Maine, North Carolina, California) analysis of underlying causes of fetal death from vital records for 1985 through 1987. Nosological coding rules varied somewhat from state to state. Underlying causes were grouped into categories; distributions were similar for each state. Many deaths (20.3% to 32.9%) were coded as unspecified conditions. Congenital anomalies accounted for only 6.9% to 10.3% of fetal deaths, including implausible and nonspecific causes. In total, 29.5% to 42.8% of the reports were not valid or useful. To obtain better data, researchers must focus on improving fetal death reporting, which will entail the promotion of comprehensive autopsy, placental and laboratory evaluation, systematic vital records query procedures, and implementation of multiple-cause-of-fetal-death coding.

Arkansas↗

Maternal toxicity: a possible etiological factor in embryo-fetal deaths and fetal malformations of rodent-rabbit species.

Data from animal teratology studies were surveyed to determine whether embryo-fetal mortality and fetal malformations result from a primary action of the agent on the conceptus or if they are secondary to maternal toxicity--a consequence of administration with high dose levels of test chemicals. A fairly strong association between embryo-fetal mortality and maternal toxicity was revealed by analysis of data from hamsters, mice, rats, and rabbits in 234 studies of chemical and physical agents, of which 83 were conducted at both maternotoxic and nonmaternotoxic doses, 94 only at maternotoxic doses, and 49 at nonmaternotoxic doses. In the above studies, only nine chemicals (four each in hamsters and rabbits and one in rats) were reported to induce embryo-fetal deaths at apparently nonmaternotoxic doses. These findings tend to suggest a contributory role for maternal toxicity in the induction of embryo-fetal deaths. The previously reported hypothesis that certain fetal defects in mice may perhaps be caused by maternal toxicity was also found to be true in a review of data on hamsters, rats, and rabbits. Salient maternal toxicity-associated fetal malformations were exencephaly, encephalocele, micro- or anophalmia, and fused ribs in hamsters and defective (fused, missing, or extra) ribs, vertebrae, and sternebrae, ex-, an-, or microphthalmia, and cleft palate in rats and rabbits. These malformations occurred at low frequencies, generally with no readily apparent dose-response relationship. Presumptive evidence indicates that embryo-fetal deaths, and the above-mentioned fetal malformations in experimental animals, which in published literature are presently attributed to chemical induction for a large number of chemicals, may be a consequence of maternal toxicity per se.

Abnormalities, Drug-Induced↗

A comparative study of hospital fetal death records and Washington State fetal death certificates.

Hospital fetal death records were compared with Washington State fetal death certificates to ascertain the completeness of reporting. Washington State law requires reporting of all fetal deaths of 20 or more weeks gestation. For 16 hospitals reporting 603 fetal deaths, an additional 49 fetal deaths were identified in the mother's charts. The study documents underreporting, especially in the gestational ages closet to the 20-week age limitation where 71 per cent of the 48 unreported cases were 20 to 27 weeks gestation.

Death Certificates↗

A population study of the relationship between fetal death and altered fetal growth.

In order to describe the relationship between fetal death rate and impaired fetal growth, we examined over 850,000 births in Illinois between 1980-1984 (using the state computer data file) and assessed the mean/modal birth weights at each gestational age and the relationship between birth weight and fetal death rate at each gestational age. We were interested in the following questions: 1) Is the relationship between impaired fetal growth and fetal death rate the same at each gestational age? and 2) What birth weight would result in a quadrupling of the fetal death rate at each gestational age? Using exponential regression analysis, we determined for each gestational age the fetal death rate at the modal birth weight and similarly, the birth weight expected to result in a quadrupling of the fetal death rate. As gestational age advanced, the birth weight percentile resulting in the constant outcome also increased (second percentile at 25 weeks; 17th percentile at 42 weeks). We also compared these data with similar data from Denver. The findings indicate the following: 1) Fetal death rate increases exponentially as birth weight decreases at each gestational age; 2) the birth weight percentile that results in a constant outcome is not consistent at each gestational age; and 3) if assessment of risk is to be inferred based on the relationship between birth weight and gestational age, the tenth percentile (whether Denver, Illinois, or elsewhere) does not predict stillbirth accurately. The implications point to the use of outcome-oriented risk assessments to predict fetal death when examining the relationship between birth weight and gestational age.

Birth Weight↗

Fetal death following antepartum fetal heart rate testing: a review of 65 cases.

The nonstress test (NST) remains in widespread use for antepartum fetal surveillance. Our institutional experience with 14,028 patients and 38,645 tests over eight years reveals a fetal death rate of 2.6 per 1000 within seven days of a reactive NST. The autopsy findings of 53 fetal deaths are presented. The most common findings, in descending order of frequency, were meconium aspiration, perinatal infection, and abnormal umbilical cord position. These findings support changes we have made in our antepartum assessment protocols.

Female↗

Fetal death ratios in a prospective study compared to state fetal death certificate reporting.

A cohort of 6,254 pregnancies surviving at least 20 weeks of gestation was identified through pregnancy testing and follow-up at three Kaiser Permanente medical offices in northern California in 1981-82. Fetal death ratios per 1,000 live births were 12.1 for all fetal deaths versus 5.0 for the subset of fetal deaths reported to the California state registrar. Only fetal deaths resulting in overnight hospitalization of the mother were reported. Seventy-nine percent of fetal deaths over 28 completed weeks since the last menstrual period (LMP) were reported versus only 10 percent between 20 and 28 completed weeks since the LMP. Ninety-three percent of fetuses over 400 grams were reported. The unreported fetal deaths were mainly those perceived by attending physicians as spontaneous abortion, especially missed or incomplete spontaneous abortion. Physicians apparently preferred the label of spontaneous abortion over stillbirth or fetal death whenever fetal maturity could not be substantiated, regardless of prior estimates of the date of the LMP. Fetuses as large and developed as potentially viable infants were the most likely to be reported.

California↗

Consumption of PCB-contaminated sport fish and risk of spontaneous fetal death.

Spontaneous fetal death has been observed among various mammalian species after exposure to polychlorinated biphenyls (PCBs). Our exposure-based cohort study assessed the relationship between consumption of PCB-contaminated Lake Ontario sport fish and spontaneous fetal death using 1820 multigravid fertile women from the 1990-1991 New York State Angler Cohort Study. Fish consumption data were obtained from food frequency questionnaires and history of spontaneous fetal death from live birth certificates. Analyses were stratified by number of prior pregnancies and controlled for smoking and maternal age. No significant increases in risk for fetal death were observed across four measures of exposure: a lifetime estimate of PCB exposure based on species-specific PCB levels; the number of years of fish consumption; kilograms of sport fish consumed in 1990-1991; and a lifetime estimate of kilograms eaten. A slight risk reduction was seen for women with two prior pregnancies at the highest level of PCB exposure (odds ratio = 0.36; 95% CI, 0.14-0.92) and for women with three or more prior pregnancies with increasing years of fish consumption (odds ratio = 0.97; 95% CI, 0.94-0.99). These findings suggest that consumption of PCB-contaminated sport fish does not increase the risk of spontaneous fetal death.

Adolescent↗

The effect of race on the relationship between fetal death and altered fetal growth.

This population study examines racial differences in the relationship between birth weight and fetal death. An earlier report showed that a birth weight that results in a fourfold increased risk of stillbirth is not a constant birth weight percentile (2nd percentile at 25 weeks, 17th percentile at 42 weeks). This analysis was applied to 782,430 white and black births in Illinois from 1980 to 1984. Mean and 10th percentile growth for white and black infants is identical before 34 weeks' gestation and growth diverges by 250 gm at term, with white infants being larger. Race-specific birth weights resulting in quadrupling of the stillbirth rate were determined with an exponential regression analysis of the relationship between birth weight and fetal death rate for each gestational age. The data indicate (1) that the birth weights resulting in quadrupling the stillbirth rate are substantially above the Denver 10th percentile and the previously unpublished race-specific Illinois 10th percentiles and (2) that at term white infants demonstrate this constant risk at the 12th percentile, whereas black infants exhibit the risk at the 18th percentile. From these data we conclude that black fetuses are more sensitive than white fetuses to factors that adversely affect growth and that continued use of "race-neutral" data for clinical management in racially heterogenous populations will not accurately predict the risk of stillbirth.

Black or African American↗