Cause Of Fetal Loss Research Articles

Neosporosis and bovine abortion in Scotland

Serum samples were collected over a two-year period from aborting cows and their fetuses from throughout Scotland; 465 maternal sera were examined using an immunofluorescent antibody test for IgG antibody...

Zoonotic and viral infection in fetal loss after 12 weeks.

One hundred and thirty-six women from an urban, rural and farming community were recruited to a study of infectious causes of midtrimester miscarriage (n = 85), stillbirth (n = 32), or termination for developmental (n = 17) or chromosomal (n = 2) abnormalities. No woman had evidence of acute infection with toxoplasma, listeria, leptospira or Chlamydia psittaci (ovine enzootic abortion). One woman had midtrimester miscarriage associated with primary cytomegolovirus infection and five women had evidence of parvovirus B19 infection, although fetal infection was not proven. Zoonoses were not identified as a cause of fetal loss or malformation in this at-risk population, but parvovirus B19 was a significant cause of midtrimester fetal loss.

Motor vehicle accident during the second or third trimester of pregnancy.

To evaluate the need of immediate treatment, follow-up and consequences of different types of traffic accidents during pregnancy. A retrospective analysis covering five years involving thirty-five pregnant women involved in motor vehicle accidents at 22-39 weeks of gestation. Fifteen of the 35 women were involved in frontal impact collisions, and suffered mild subjective and objective symptoms; all their fetuses survived and were delivered at term. Fifteen other women were involved in broadside collisions; two of these were riding a bicycle. These 15 women had clear objective findings like uterine contractions or tenderness, and some of them needed tocolytic therapy and hospitalization up to eight days. This was significantly longer than in those involved in frontal impact collisions. However, the broadside accidents did not have any adverse effect on pregnancy outcomes either. Five women were involved in serious accidents at speeds of 80-110 km/h, and one mother and her fetus died immediately because of rupture of the uterus and the cervical joint and spinal canal. Four other fetuses were found dead on arrival at hospital or soon after. In all cases the cause of fetal loss was placental abruption. The presence of fetal blood cells in maternal blood was evaluated in 15 of 35 patients, but was positive in only one. Frontal collisions are associated with lower vehicular speed, less trauma and no acute or later effects on pregnancy, whereas broadside collisions and high speed (> 80 km/h) cause more symptoms. The latter type of accidents are associated with high risk of placental abruption and of fetal and maternal death. Fortunately the symptoms are evident immediately after the accident, and early hospital discharge is possible if no abnormalities are present during the first hours.

Thoughts on the Mechanism of Pregnancy Loss Associated with the Antiphospholipid Syndrome

Although far from conclusive, the available clinical and histopathological information are consistent with an hypoxic cause for aPL-related fetal loss. In turn, this is due to impairment of the maternal spiral arterial blood flow. To date, there is only one case report of detailed placental and uteroplacental vascular histopathological examination by a recognized expert in this field of pathology. This and the findings provided by the only study to take placental bed biopsies suggest that spiral arterial vasculopathy resulting in placental and fetal hypoxia is the immediate cause of fetal loss in women with aPL syndrome. Data from the large study by Out et al. are consistent with this. The absence of spiral arterial vasculopathy in several studies could be attributed to the fact that the vessels examined were those adherent to the separated placenta, too superficial to necessarily demonstrate the pathological changes. Our future efforts at defining the 'cause' of aPL-related fetal loss must include: (1) meticulous clinical details regarding the timing and nature of pregnancy loss, (2) thorough evaluation of the abortus, (3) examination of the placenta by a pathologist well versed in placental pathology, (4) examination of the placental bed biopsies whenever possible, (5) the cellular biology and biochemistry of maternal-fetal junction, with particular focus on how the cytotrophoblast invades the spiral arteries, and (6) the cellular biology and biochemistry of spiral arterial vasculopathy.

Rapid detection of trisomy 21 by quantitative PCR

Chromosomal aneuploidy is a major cause of fetal loss and genetic disease. We have devised a polymerase chain reaction (PCR)-based test that allows prenatal detection of trisomy 21 in as few as 15 fetal cells within 1 day. A pair of fluorescein-tagged primers directs amplification of a 216-bp fragment of the human S100B gene on chromosome 21. Primers that direct amplification of a 165-bp fragment of the IGF1 gene on chromosome 12 are included to generate an internal standard for quantitation. After 31 cycles of PCR, the amounts of S100B and IGF1 amplification products are determined on an Automated Laser Fluorescent DNA Sequencer. In trisomic cells, the relative amount of the S100B product is approximately 1.5-fold higher than that from normal cells. The test may be useful for non-invasive prenatal diagnosis performed on fetal cells isolated from maternal blood.

Pregnancy in Patients on Chronic Ambulatory Peritoneal Dialysis

Both conception and successful completion of pregnancy are rare occurrences in female patients on chronic renal replacement therapy. Only a handful of successful pregnancies and deliveries have been reported in patients receiving hemodialysis (HD). Even less common are reports of successful pregnancy and delivery in patients receiving chronic ambulatory peritoneal dialysis (CAPD). Among the more common causes of fetal loss are abruptio placentae and other causes of spontaneous miscarriage. We report here three cases of pregnancy in patients on CAPD; two of these pregnancies progressed successfully to spontaneous delivery, while the third terminated during an episode of acute peritonitis. Furthermore, we have reviewed the literature concerning the outcome of pregnancy in the dialysis population on CAPD.

Antiphospholipid antibody syndrome and recurrent fetal loss

The association between circulating antiphospholipid autoantibodies, anticardiolipin antibody and/or lupus anticoagulant with venous or arterial thrombosis, neural disorders, thrombocytopenia and fetal loss is well established (the antiphospholipid antibody syndrome). The mechanisms responsible for first trimester and later fetal losses may be different; the presence of placental infarction suggests mechanisms related to the syndrome. Since successful treatment of fetal loss is now possible, using antiplatelet therapy with low dose aspirin, with or without added immunosuppressive corticosteroids, identification of women with the syndrome is important. Screening is by the demonstration of anticardiolipin antibodies using radio-immunoassay (RIA) or enzyme-linked immunosorbent assay (ELISA) and detecting lupus anticoagulant by prolongation of phospholipid dependent coagulation tests, e.g. activated partial thromboplastin time (APTT), kaolin clotting time (KCT), or dilute Russell Viper Venom Time (dRVVT). Women may have no clinical or serological manifestations of autoimmune disorders apart from recurrent fetal loss; the screening tests may also be negative between pregnancies and early in pregnancy. Diagnosis of the antiphospholipid antibody syndrome identifies an important treatable cause of fetal loss and also indicates the potential for thrombotic and neurological problems that require ongoing active therapeutic and preventive measures.

Venom immunotherapy in the Hymenoptera-allergic pregnant patient

Natural or iatrogenic causes of anaphylaxis are significant risk factors in pregnancy. A 3% to 5% risk of sting anaphylaxis in any pregnant woman with insect-sting allergy untreated with venom immunotherapy (VIT) can be calculated. Insect-sting anaphylaxis has allegedly caused severe fetal abnormalities and is a potential cause of fetal loss and severe maternal morbidity and/or mortality. Hymenoptera anaphylaxis is a highly preventable cause of anaphylaxis, but VIT may itself carry a risk potential, with an appropriate 5% reaction during buildup and 1% reaction risk during maintenance VIT. To assess the safety of VIT in pregnancy, we have gathered data from 26 women with 43 pregnancies. All the women were receiving VIT. One woman was stung early in pregnancy with anaphylaxis resulting. Outcome of pregnancy was normal. Thirty-six of the pregnancies ended normally. There were two mild adverse reactions to VIT, neither of which required treatment. One child was born with multiple congenital abnormalities of unknown cause. Since congenital malformations may occur as frequently as one in 40 live births, these data do not suggest a significant increased risk from VIT during pregnancy.

Obstetric short communications

SummaryIntensive fetal surveillance using ultrasound to establish a biophysical profile score in multiple pregnancies can reduce perinatal mortality due to uteroplacental insufficiency. Prematurity remains a major cause of fetal loss.

Perinatal mortality in multiple pregnancy patients.

A study of perinatal mortality in multiple pregnancy over a period of 12 years, 1972 to 1984, showed prematurity and low birthweight as the major causes of fetal loss. The highest risk was found at 28 to 30 weeks gestation (306/1,000). There was a significantly greater risk to babies delivered by the breech (136/1,000), and likewise in the second twin when compared with the first, ratio 1:14. A significant drop in the perinatal mortality rate, from 98/1,000 to 39/1,000, was observed between 1972-1978 and 1979-1984. Ultrasound has facilitated the earlier diagnosis of twins and provides more accurate serial fetal assessment. Bedrest, more vigilant antenatal care, intrapartum surveillance and improved neonatal care, are required to maintain and further reduce the perinatal mortality rate. When regional analgesia was employed in labour, the number of babies lost was 41/1,000, vs 93/1,000 in patients not receiving regional analgesia. External cephalic version and vertex delivery of the second twin is preferable to internal version and breech extraction. It should also be contemplated, as an alternative to elective cesarean section for a transverse lie or breech presentation of the second fetus.

Tumor necrosis factor in malaria-induced abortion.

The cause of fetal loss in malaria is not known. We report that a small (1.5-5.0 micrograms) intravenous dose of recombinant human tumor necrosis factor (TNF) caused fetal death and abortion in 16 day pregnant mice that were carrying low densities of Plasmodium vinckei. In contrast, 50 micrograms human TNF did not cause fetal death or abortion in uninfected 16 day pregnant mice. Endogenous TNF, which was not detectable in plasma of low parasitemia animals, pregnant or not, was present (1.6 +/- 0.9 ng/ml) in samples from malarial pregnant mice when, on day 17, parasitemia was high and the first signs of impending abortion were evident. No TNF was detectable in the plasma of uninfected mice at day 17 of pregnancy. A small dose of TNF also caused fetal death in 16 day pregnant mice that had received an intravenous injection of Coxiella burneti extract 9-10 days earlier. Thus, TNF-induced abortion may occur in a range of infections in which systemic macrophage activation occurs and a trigger for TNF release is present.

Fetal Loss in the Dog and Cat

Occurrence and type (resorption, abortion, stillbirth, mummification) of pregnancy loss in the dog and cat depend on the cause of the loss and the stage of gestation at which it occurs. General categories of known causes of embryonic or fetal death in the dog and cat include chromosome and developmental abnormalities of the fetus, infectious agents, maternal endocrine abnormalities, trauma, exogenous drugs, uterine torsion, and dystocia. Diagnosis of fetal loss and of cause of fetal loss relies on the history, physical examination, abdominal radiography and ultrasonography, serology, hormone assay, and on culture, pathology, and karyotype of fetal/placental tissue. Aggressive diagnostics at the time of fetal loss are essential to preventive strategies at subsequent pregnancies.

Pregnancy in women with diabetes mellitus: Fifteen years' experience: 1970–1985

The perinatal mortality of 613 children who were born to women with diabetes mellitus who attended the Diabetic Clinic of The Royal Women's Hospital between 1970 and 1985 was 4.5%. In 399 children who were born to mothers with pre-existing diabetes (95% of whom were insulin-dependent) the over-all perinatal mortality was 7.5%. In successive five-year periods, perinatal mortality in this group declined from 12.2% to 3.9% (1981-1985). In 214 children who were born to mothers with gestational diabetes, the perinatal loss was 1.4%. Between 1970 and 1985, the fetal loss that was attributed to poor control of diabetes declined; however, the prevalence of congenital abnormalities remained unchanged and these were the major cause of fetal loss in 1981-1985. Other high-risk categories that were identified included obstetric complications, particularly that of pre-eclampsia. Neonatal complications had little effect on the eventual outcome, but respiratory distress, macrosomia, hypoglycaemia, jaundice, polycythaemia, hypocalcaemia and hypomagnesaemia were documented frequently and required specialized assessment. The causes of the improvement in the outcome of pregnancy in women with pre-existing diabetes appear to be multifactorial and due to team management in a specialized unit. A reduction in the increased prevalence of major congenital abnormalities is the major challenge for the future.

A possible association of long Y chromosomes and fetal loss.

Long Y chromosomes is a relatively unbiased large sample of newborn infants were measured. The proportion of prior abortions was increased twofold in mothers of long Y infants compared to the control in the Caucasian sample. Our results indicate that an increased length of Y chromosome may be an important cause of fetal loss.

Listeria monocytogenes as a cause of fetal loss

L. monocytogenes is a significant cause of perinatal loss in animals. Neonatal death and a wide spectrum of disease in all age groups can occur in man following infection with the organism. In the past decade listeriosis has been suspected of being an important cause of fetal loss, although the majority of recent reports have not substantiated this.We were unable to isolate L. monocytogenes from any of 76 patients with current fetal loss in a prospective study. Cultures were obtained from vaginal cervical swab, umbilical cord, meconium, and placenta.Six other patients who had meningitis with overt listeriosis were observed during the course of this study.