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At least 19 recordsLinked to original sources
PubMed1999

Trauma in pregnant women: analysis of maternal and fetal mortality.

Twenty-seven traumatised pregnant women were analysed retrospectively over a period of 9 years. Mean age was 23.7 years (16-42 years). Gestational age ranged from 10 to 40 weeks (mean, 21.5 weeks), with most victims (46.1%) being in the second trimester. The predominant mechanism (65.3%) was blunt abdominal injury due to an automobile accident (the patient being run over or collision). At admission, 8 (30.7%) patients had haemodynamic alterations. 6 patients (23.0%) presented vaginal bleeding and 4 of these were haemodynamically normal. We analysed maternal mortality, fetal mortality and their causes. We also compared the median RTS and TRISS values for the groups with maternal-fetal survival and the group with maternal-fetal death. Fetal death occurred in all pregnant women admitted with vaginal bleeding. Maternal mortality due to haemorrhagic shock was 11.5%. Fetal mortality was 30.7%, with 37.5% of these deaths being caused by maternal death. The major cause of fetal mortality was a detached placenta (50.0%). The trauma indices, RTS and TRISS, were significantly lower (p = 0.0025 and p < 0.0001) in the group of maternal-fetal death but they were not of prognostic value in terms of fetal mortality.

Adolescent↗
PubMed2002

Infusion of pregnant rats with calcitonin gene-related peptide (CGRP)(8-37), a CGRP receptor antagonist, increases blood pressure and fetal mortality and decreases fetal growth.

Calcitonin gene-related peptide (CGRP) is the most potent endogenous vasodilatory peptide, and is involved in the regulation of blood flow to vital organs. We have previously shown that CGRP may be involved in vascular adaptations that occur during pregnancy, and that steroid hormones may be involved in these mechanisms. We hypothesized that endogenous CGRP is required for maintaining blood pressure and fetoplacental growth in pregnant rats, and that progesterone will enhance CGRP effects. The vasodilatory effects of CGRP are known to be inhibited by a competitive CGRP receptor antagonist, the C-terminal fragment CGRP(8-37). In the present study, we investigated whether continuous s.c. infusion of CGRP(8-37) to pregnant rats will reduce fetoplacental growth and increase systolic blood pressure. We also assessed whether progesterone will alter the effects of CGRP(8-37) on blood pressure during postpartum. Groups of five pregnant rats were s.c. infused with varying doses of CGRP(8-37) from Day 17 of pregnancy. Daily systolic blood pressures, pup weight, mortality at term delivery, and fetoplacental weights on Day 20 of gestation were measured. CGRP(8-37) at a dose of 0.083 mg day(-1) kg(-1) body weight (BW) showed no effects; however, doses of 0.33 and 1.33 mg day(-1) kg(-1) BW increased (P < 0.05) blood pressure during pregnancy, and these elevated blood pressures persisted during postpartum with the highest dose used. Progesterone (2 mg per injection, twice a day; s.c.) treatment significantly elevated blood pressure in rats infused with CGRP(8-37) during postpartum, suggesting that progesterone regulates CGRP-induced vascular effects. CGRP(8-37) infusion caused significant reductions in pup weight with an increase in mortality rate, and these effects were dose-dependent. Placental and fetal weights were also decreased prior to term on Day 20 of gestation, 72 h after CGRP(8-37) infusion, indicating effects on uteroplacental tissues. Therefore, we suggest that endogenous CGRP plays an important role in maintaining normal fetoplacental development, fetal survival, and vascular adaptations during pregnancy.

Animals↗
PubMed1997

Predictors of fetal mortality in pregnant trauma patients.

BACKGROUND: Fetal mortality after trauma is significant. This study was aimed at identifying factors responsible for this high fetal mortality. METHODS: All pregnant trauma patients admitted to the two major Toronto trauma institutions during the period of November of 1991 to February of 1996 with an Injury Severity Score (ISS) > or = 12 were assessed. Data on age, gestation, hypotension, ISS, hemoglobin, blood transfusion, length of stay, disseminated intravascular coagulation (DIC), and specific maternal injury were analyzed retrospectively to determine predictors of fetal mortality by comparison of patients with and without fetal survival. RESULTS: Twenty of a total of 68 pregnant trauma patients qualified for entry into the trauma registry by having an ISS > or = 12. Overall fetal mortality was 65% (13 of 20) for ISS > or = 12, and there was one maternal death (age, 29 years; ISS, 66). There were no statistically significant differences between the fetal death and fetal survival groups in age (29.2 +/- 6.2 vs. 30.4 +/- 3.9 years), gestation (25.3 +/- 10.5 vs. 24.1 +/- 9.2 weeks), lowest systolic blood pressure (98.3 +/- 33.8 vs. 112 +/- 18.0 mm Hg), head injury rate (3 of 13 vs. 1 of 7), extremity injury rate (8 of 13 vs. 2 of 7), abdominal injury rate (4 of 13 vs. 0 of 7), pelvic fracture rate (6 of 13 vs. 1 of 7), and chest injury rate (5 of 13 vs. 3 of 7). However, ISS (27.7 +/- 3.5 vs. 14.2 +/- 11.4), lowest hemoglobin level (78.8 +/- 17.0 vs. 101.9 +/- 17.1), blood transfusions (10.8 +/- 6.3 vs. 0.9 +/- 1.6 units), length of stay (20.9 +/- 16.7 vs. 8.2 +/- 4.9 days), and the incidence of DIC (8 of 13 vs. 0 of 7) were statistically significantly different between the two groups (p < 0.05). All eight patients with abruptio placentae had associated fetal mortality. CONCLUSIONS: Apart from ISS, blood loss, and abruptio placentae; the presence of DIC was the most significant predictor of fetal mortality. This finding may represent stimulation of DIC by placental products entering the maternal circulation after significant intrauterine injury.

Abruptio Placentae↗
PubMed1996

Medical and life-style risk factors affecting fetal mortality, 1989-90.

OBJECTIVES: This report presents fetal mortality data by medical and life-style risk factors of the mother and the fetus. METHODS: Deaths and fetal mortality rates are presented in this descriptive report. Data sources used are vital statistics data for fetal deaths and live births. RESULTS: The data that became available with the revision of the U.S. Standard Report of Fetal Death in 1989 expanded the medical and health data available on mothers and fetuses. Reporting of medical conditions is probably incomplete for fetal deaths as well as for live births. Therefore, caution should be exercised in using this data. Reported occurrences of medical and life-style risk factors of mother and fetus for fetal deaths and live births and fetal mortality rates are presented. Maternal medical conditions most often associated with having a fetal death were problems with amniotic fluid levels and blood disorders. Fetal mortality was 35 percent greater when tobacco was used during pregnancy and 77 percent higher when alcohol was consumed during pregnancy. The complication of labor most often associated with fetal mortality was abruptio placenta. Although a very small proportion of all deliveries have specific congenital anomalies reported, fetal mortality was close to 50 percent for anencephalus, about 25 percent for renal agenesis, and slightly more than 20 percent for hydrocephalus.

Adult↗
PubMedDate not supplied

Self-reported exposure to pesticides and radiation related to pregnancy outcome--results from National Natality and Fetal Mortality Surveys.

Although fetal development is known to be sensitive to environmental agents, relatively little epidemiologic research has addressed this concern. Effects on pregnancy outcome of self-reported parental exposure to pesticides and to radiation were examined using data from the National Natality and Fetal Mortality Surveys, large national probability samples of live births and stillbirths occurring in 1980. In case-control analyses, maternal exposure to pesticides at home or work was associated with increased risk of stillbirth (odds ratios (ORs) = 1.5-1.6). Paternal pesticide exposure was associated with stillbirth (ORs = 1.2-1.4) and delivery of small-for-gestational-age infants (ORs = 1.4-2.0). A small increased risk of stillbirth (OR = 1.3) was found in relation to either parent's reported exposure to radiation. In spite of limitations in the quality of exposure data and the possibility of biased recall related to pregnancy outcome, associations of reported pesticide exposure to either parent with risk of stillbirth and small-for-gestational-age infants warrant further evaluation.

Case-Control Studies↗
PubMed1983

Fetal mortality and cleft lip with or without cleft palate.

Analysis of fetal mortality in sibships of 406 probands with cleft lip with or without cleft palate (CL(P)) indicates that the incidence of fetal mortality is significantly greater in sibships of probands with bilateral CL(P) than in those of unilateral CL(P). The difference is even greater when fetal mortality in sibships of male probands with unilateral CL(P) is compared with that of female probands with bilateral CL(P). These findings support a multifactorial two-threshold concept in which a lower level of liability results in clefting while a higher level of liability causes fetal mortality.

Cleft Lip↗
PubMed1979

Fetal mortality and malformations associated with experimental infections of western equine encephalomyelitis vaccine virus in rhesus monkeys (Macaca mulatta).

Pregnant Rhesus monkeys were infected via installation of Western Equine Encephalomyelitis (WEE) vaccine virus into the amniotic sacs at 50 and 80 days gestation to determine if the resulting infections would produce fetal mortality or fetal malformations, particularly within the central nervous system. Of those receiving virus at 50 days gestation, 13 of 18 fetuses were aborted or dead in utero at time of Caesarean section; 2 of 18 were malformed (hydrocephalus and polyarthrosis); and 3 of 18 were anatomically normal. Of those receiving virus at 80 days gestation four of eight fetuses were aborted or dead in utero at time of Caesarean section, one of eight was malformed (hydrocephalus) and three of eight were anatomically normal. Three of three controls receiving neutralized virus at each gestational age were anatomically normal. Fetal WEE vaccine virus infection significantly increased fetal mortality and resulted in a significant incidence of fetal malformations.

Animals↗
PubMed1983

Fetal mortality in oral cleft families(IV): the "doubling effect".

Fetal mortality data from Lancaster, Penn., Chicago, Ill. and Minneapolis, Minn. are presented which support the authors' earlier findings in Indiana and Montreal that a positive relationship exists between the degree of liability to malformation and the incidence of fetal deaths in probands' sibships. Altogether, the study involved 189 CL sibships, 690 CLP sibships, and 3,416 pregnancies. On the basis of these data, which are derived from families of several different backgrounds of European ancestry, it is generalized that, as we proceed from CL sibships to CLP sibships, there is a doubling effect on fetal mortality. The consistency of this finding in several population samples is impressive. The implications of this observation are discussed with reference to genetic counseling.

Cleft Lip↗
PubMed1990

The temporal association of the implementation of a fetal diagnostic and surveillance program and decreased fetal mortality in a private hospital.

The purpose of this study was to determine whether there was a temporal association between the introduction of a Fetal Diagnostic and Treatment Center and changes in fetal mortality. Two consecutive 15-month pre-program periods (periods I and II) were compared with one 15-month post-program period (period III). The fetal death rates for the pre-program periods I (6.16) and II (6.02) were similar, and the combined rate was 6.09. After the introduction of the Fetal Diagnostic and Treatment Center, the fetal mortality rate decreased to 2.31 (period III). When periods I and II were compared with period III, the major decrease (73.8%) in fetal mortality occurred for fetuses of greater than 34 weeks' gestation. The perinatal mortality rate decreased from 8.76 in periods I and II to 4.42 in period III, reflecting the decrease in fetal deaths.

Cesarean Section↗
PubMed1987

The effect of a single dose of human chorionic gonadotropin at proestrus on embryonic mortality, fetal growth and gestation length in the rat.

The noxious effect of a single dose of 20 IU human chorionic gonadotropin (hCG) given at proestrus on embryonic and fetal survival as well as on fetal weight was studied. Fetal survival varied between 43.6 and 67.6%; the mortality rate was highest before implantation. The surviving fetuses of rats treated with hCG between days 17 and 20 of pregnancy weighed significantly less than controls. Embryonic mortality and fetal growth retardation could be prevented by giving anti-hCG monoclonals 28 or 45 h after hCG administration, but not when anti-hCG was given 69 or 93 h after hCG. 5 IU hCG did not induce embryonic or fetal mortality. On the other hand, 80 IU hCG increased the mortality to 100%; this was entirely due to preimplantation loss. It is speculated that due to a long metabolic half-life of hCG, the steroid metabolism is disturbed, causing implantation failure and/or delay of implantation. By day 21 of pregnancy, however, the fetuses of the hCG-treated rats had made up greatly for the growth retardation; they were born after a similar gestation length and with a similar birth weight as the pups of control rats.

Animals↗
PubMed1998

Eisenmenger's syndrome in pregnancy: maternal and fetal mortality in the 1990s.

To determine maternal and fetal mortality associated with Eisenmenger's syndrome in the UK, a postal questionnaire was sent to 225 NHS obstetric units with neonatal intensive care units, requesting information about maternal and fetal outcome in cases of Eisenmenger's Syndrome between 1991 and 1995. Fifteen cases were identified. The maternal mortality was 40% and fetal loss 8%. Only 15% of infants were born at term. Maternal mortality associated with Eisenmenger's syndrome remains as high as it has been for the past 50 years. Pooling of national data on rare medical conditions in pregnancy is required to aid management of individual cases.

Eisenmenger Complex↗
PubMed2006

Zinc supplementation to protein-deficient diet in CO-exposed mice decreased fetal mortality and malformation.

In developing countries, diet during pregnancy is frequently low in both protein and zinc contents and exposure to CO is common because of environmental pollution and smoking. This study was conducted to evaluate whether zinc supplementation ameliorates fetal mortality and malformations in protein-deficient, CO-exposed mice. Pregnant mice of the CD-1 strain were maintained on 17% (reference) or 9% protein diets mixed with deficient, normal, or supplemental zinc throughout gestation. The dams in each dietary group were exposed to air (control) or 500 ppm CO in air in environmental chambers from gestation days 7-18. As compared to the control group (normal protein, normal zinc), the incidence of fetal mortality was 66.8% and 57.2% higher, respectively, and malformation incidence was 74.4% and 72.4% higher (0 and 500 ppm CO, respectively) in mice fed both deficient protein-zinc diets. However, the highest malformation rate was observed in the group with normal protein, deficient zinc (96% mortality in both 500 and 0 ppm CO, as compared to the reference group, p < 0.0001). The fetal mortality rate was -3.5% (0 ppm CO) and 25.4% (500 ppm CO) lower in zinc-supplemented, protein-deficient groups compared to the control group. There was a significant negative association between fetal zinc concentrations and fetal malformations (p < or = 0.001). The result of this study might be relevant to populations that are exposed to CO and or consume marginal zinc and protein diets during gestation.

Animals↗
PubMed1984

Fetal mortality in oral cleft families (IX): factors relating to the occurrence of sporadic clefts.

Pedigree data on 854 probands with cleft lip and/or cleft palate from the State of Indiana are presented. These include 123 probands with cleft lip alone (CL), 453 with cleft lip and palate (CLP), and 278 with isolated cleft palate (CP). Probands and families were interviewed at the Indiana University Medical Center during the years 1962-1980. Among features of special interest are an excess of bilateral CLP (46% of all CLP cases) and a significantly greater number of older mothers and fathers (over 34 years old) than in the general population. An apparent increase in the proportion of sporadic cases with time may be due to bias in ascertainment. It is suggested that the increased proportions of more severe clefts and older parents are among several factors which contribute to the incidence of fetal mortality in a cleft population. The association of fetal mortality with liability to clefting introduces a more precise way to define a sporadic cleft. That is, a truly sporadic cleft is one conceived as a single occurrence event and has survived to become a liveborn cleft child whereas other apparently sporadic cleft individuals represent the surviving cleft in a sibship in which fetal mortality has eliminated all other cleft offspring already conceived. This observation has applications to the collection and interpretation of genetic pedigree data for clefts as well as many other genetic conditions.

Adult↗
PubMed1985

Fetal mortality in sibships with one or more affected members with oral clefts.

We investigated the fetal mortality in 903 sibships with at least one member having cleft lip with or without cleft palate [CL(P)] and 213 with at least one individual affected with cleft palate (CP) derived from three different data sources in México. The frequency of fetal wastage (abortion and/or stillbirth) was not increased in sibships where the propositi had cleft lip and palate (CLP) as compared with cleft lip (CL) nor in those where index cases had a bilateral lesion as compared to a unilateral one, nor when the index cases with CL(P) were female rather than males, nor when the index case was a female with bilateral lesion as compared to males with a unilateral one. Similarly fetal mortality was not increased in sibships in which the propositus had CP compared to those in which the index case was a female. These findings are contrary to some reports that claim to support a two-threshold model according to which individuals reaching the first one would be born with an oral cleft, and those reaching the second would be aborted. Our results, together with others, suggest the possibility that liability to oral clefts is independent of liability to fetal wastage.

Abortion, Spontaneous↗
PubMed2006

Does caffeine consumption during pregnancy increase the risk of fetal mortality? A literature review.

The aim of this study was to evaluate the available epidemiological evidence of the effect of caffeine consumption during pregnancy on fetal mortality. A systematic qualitative review of observational studies that referred to any source of exposure to caffeine from food in pregnancy and to fetal mortality as the outcome was conducted in the databases MEDLINE and LILACS. Studies published between January 1966 and September 2004 were searched. The following descriptors were used: "caffeine", "coffee", "tea", "cola", and "cacao" to define the exposure and "fetal death", "stillbirth", "fetal demise", and "fetal loss" to define the outcome. The search strategy retrieved 32 publications, but only six met the inclusion criteria and three were included. One more article was found using "see related articles" feature in PubMed. A total of four publications were included in the review. The small number of publications addressing this subject, methodological limitations, inaccurate exposure assessment in all the studies, overall risks only marginally significant in most cases, and the possibility of publication bias preclude stating with certainty that caffeine consumption is actually associated with fetal death.

Beverages↗
PubMed1988

[Fetal mortality in families with labio-palatal clefts].

Fetal mortality in 110 families of patients with cleft lip with or without cleft palate is analyzed and correlated with liability. Because there was no significant difference, authors discussed these findings with references to multifactorial two-threshold hypothesis.

Abnormalities, Multiple↗