Single umbilical artery stenosis associated with intrauterine fetal death post-transfusion

Single umbilical artery is among the most common funicular vascular anomalies. In contrast, umbilical artery stenosis is rare, and has only been reported in three-vessel cords. We describe a case of single umbilical artery stenosis in a fetus with no associated malformations. Intrauterine fetal death occurred at 28 weeks' gestation following cordocentesis and intravascular transfusion for Rhesus alloimmunization. Single umbilical artery stenosis may place the fetus at increased risk, particularly in cases requiring interventions involving cord manipulation.     

Coagulopathy associated with dilatation and evacuation for intrauterine fetal death

Dilatation and evacuation was reported recently to be a safe and effective method for the treatment of intrauterine fetal death. The current authors have treated ten cases of intrauterine fetal death with dilatation and evacuation. Five patients (50%) developed coagulopathy, one of whom also developed endometritis. Patients who developed coagulopathy were significantly older than those who did not. Previous pregnancy also was associated with the development of coagulopathy. Five of six multigravidas developed coagulopathy, whereas none of the four primigravidas developed this complication. Other factors that may have contributed to the development of coagulopathy are discussed. The authors conclude that dilatation and evacuation for midtrimester intrauterine fetal death may not be as safe as has been reported.     

Clinically silent polymicrobial amnionitis and intrauterine fetal death associated with a Cu-7 intrauterine contraceptive device

This article presents a case of silent polymicrobial amnionitis with subsequent intrauterine fetal death in a 34-year old woman who conceived with a Cu-7 IUD in place. There were no apparent pregnancy complications or symptoms of uterine infection during early pregnancy. At 16 weeks gestation, the patient underwent amniocentesis for cytogenetic studies. 5 different microorganisms--Corynebacterium, Staphylococcus warneri, Staphylococcus epidermidis, Streptococcus mitis, and Ureaplasma urealyticum--were isolated from the amniotic fluid. 2 week later, intrauterine fetal death was detected. U. urealyticum was at this point isolated from the cervix and placental and fetal tissues. This organism, which has been associated with chorioamnionitis, spontaneous abortion, and neonatal death, is suspected to have contributed to the fetal death in this case. U. urealyticum can invade the amniotic sac with fetal membranes intact and persist for 8 weeks without overt effects. This case illustrates the risks associated with nonremoval of an IUD after contraceptive failure.     

Labor induction in intrauterine fetal death

The particulars of 78 patients with fetal demise of the last 14 years were evaluated retrospectively. The most important reason of fetal death was hypoxaemia or anoxaemia. 31 patients were delivered by cesarean section or had spontaneous uterine contractions. Induction of 47 abortions were started with oxytocin or prostaglandins. Within 12 hours 54% of the oxytocin and 67% of the prostaglandin group succeeded in spontaneous delivery. In both groups there were 5 management failure of therapy, so that alternative medication or a cesarean section lead to delivery.     

Cardiotocographic and sonographic findings in two cases of antenatally diagnosed intrauterine fetal brain death.

Intrauterine fetal brain death is a rare cause of a fixed fetal heart rate pattern. Seven cases have been previously reported in the literature, but only two of them were diagnosed prenatally and all the newborns died soon after delivery. Two additional cases of antepartum diagnosis of intrauterine fetal brain death, managed expectantly, are reported. We had the unique opportunity to document progressive sonographic cerebral changes during the follow-up period, following the neurological event, while the fetus continued life and growth in utero. The cardiographic and sonographic findings suggesting intrauterine fetal brain death were a prolonged fixed fetal heart rate, even following a vibroacoustic and contraction stress test; an atonic fetus without breathing and body movement; and the appearance of hydramnios and the development of ventriculomegaly.     

Restricted fetal growth in sudden intrauterine unexplained death

BACKGROUND: Unexplained antepartum stillbirth is a common cause of perinatal death, and identifying the fetus at risk is a challenge for obstetric practice. Intrauterine growth restriction (IUGR) is associated with a variety of adverse perinatal outcomes, but reports on its impact on unexplained stillbirths by population-based birthweight standards have been varying, including both unexplained and unexplored stillbirths. AIM: We have studied IUGR, assessed by individually adjusted fetal weight standards, in antepartum deaths that remained unexplained despite thorough postmortem investigations. METHODS: Antenatal health cards from a complete population-based 10-year material of 76 validated sudden intrauterine unexplained deaths were compared to those of 582 randomly selected liveborn controls. Birthweight <10th percentile of the individualized standard adjusted for gestational age, maternal height, weight, parity, ethnicity, and fetal gender was defined as growth restriction. RESULTS: 52% of unexplained stillbirths were growth restricted, with a mean gestational age at death of 35.1 weeks. Suboptimal growth was the most important fetal determinant for sudden intrauterine unexplained death (odds ratio 7.0, 95% confidence interval 3.3-15.1). Concurrent maternal overweight or obesity, high age, and low education further increase the risk. Overweight and obesity increase the risk irrespective of fetal growth, and while high maternal age increases the risk of the normal weight fetus, it is not associated to growth restriction as a precursor of sudden intrauterine unexplained death. CONCLUSIONS: IUGR is an important risk factor of sudden intrauterine unexplained death, and this should be excluded in pregnancies with any other risk factor for sudden intrauterine unexplained death.     

The severely anemic and hydropic isoimmune fetus: changes in fetal hematocrit associated with intrauterine death.

Hydrops caused by isoimmune hemolytic anemia is frequently associated with fetal death following intrauterine intravascular transfusion. To identify possible predictors of procedure-related fetal death, we examined changes in fetal blood volume and hematocrit resulting from the initial transfusion performed on 19 severely anemic, hydropic fetuses. Seven fetuses (36.8%) died at 24-72 hours after transfusion, but in no case was the procedure associated with fetal distress. There were no significant differences between fetuses who died and those who survived in terms of total volume of blood transfused, volume transfused as a percentage of total fetoplacental blood volume, hematocrit of transfused blood, post-transfusion hematocrit, umbilical vein pH, or gestational age at transfusion. Significant differences were noted between hydropic fetuses who died compared with those who survived in the mean pretransfusion hematocrit, 6.7% (+/- 2.0) versus 8.7% (+/- 1.6) (P = .03), and the relative increase in post- over pre-transfusion hematocrit, 5.5-fold (+/- 1.4) versus 3.5-fold (+/- 0.8) (P = .001). Stepwise logistic regression analysis confirmed that only the relative increase in hematocrit was predictive of fetal loss. Moreover, six of seven fetal deaths occurred when the relative increase in hematocrit was greater than fourfold, whereas ten of 12 surviving fetuses had relative increases of less than fourfold. We conclude that large, acute increases in fetal hematocrit following intrauterine transfusion are associated with substantial mortality in hydropic fetuses.     

A piece in the puzzle of intrauterine fetal death: Pathological findings in placentas from term and preterm intrauterine fetal death pregnancies

Objective.?To compare pathological findings of placentas from term and preterm pregnancies complicated by intrauterine fetal death (IUFD).

Study design.?A retrospective cohort study was conducted including deliveries complicated by IUFD. A comparison was made between placentas from term and preterm (<37 weeks' gestation) pregnancies complicated by IUFD. A second analysis was undertaken comparing IUFD placentas delivered before and after 34 weeks' gestation. Uteroplacental insufficiency was defined when one or more of the following pathological features were found: placental infarct, poor vascularity of the chorionic villi, intravascular thrombi and vascular occlusion.

Results.?During the study period, 849 placentas of IUFD were examined. Gross and microscopic pathological finding were noted. When comparing gross and microscopic findings in term and preterm (<37 weeks) IUFD placentas, higher rates of calcifications, tissue congestion and cellular metaplasia were found in term vs. preterm placentas. Significantly increased rates of poor tissue vascularity, placental vascular occlusion and uteroplacental insufficiency were demonstrated in preterm IUFD placentas. When comparing pathological findings in IUFD placentas delivered before and after 34 weeks' gestation, higher rates of abnormal cord insertion, calcifications, tissue congestion, infarcts and intravascular thrombi as well as poor tissue vascularity and placental vascular occlusion were demonstrated in IUFD placentas delivered before 34 weeks. Regardless of gestational age at the time of IUFD in more than 90% of placentas vascular wall thickening was found. A third of both term and preterm placentas demonstrated histological chorioamionitis.

Conclusions.?A vast majority of IUFD placentas reveal numerous pathological findings that reflect uteroplacental insufficiency and abnormal blood supply. Different characteristics were noted in term and preterm placentas of pregnancies complicated by IUFD. Better definition of causes and associated placental pathological findings of IUFD might aid clinicians in counseling such patients regarding the reason and risk of recurrence in subsequent pregnancies.     

Prothrombotic gene mutations in women with recurrent abortions and intrauterine fetal death

AIM: The factor V Leiden mutation (FVL) and the G20210 prothrombin gene mutation (FII G20210A) are well-established risk factors for venous thromboembolism. In the recent years many scientific reports have suggested that these defects are associated with an increased risk of intrauterine fetal death. The aim of our study was to investigate the prevalence of these molecular defects in subjects with history of unexplained pregnancy loss. METHODS: One-hundred and fifty women, 99 with history of unexplained recurrent pregnancy loss (between the 13th and the 20th week of gestation) and 51 with history of unexplained fetal death (pregnancy loss after the 20th week of gestation) were studied for hereditary thrombophilia. Physiologic coagulation inhibitors (antithrombin III, protein C, protein S) were in the normal range. RESULTS: The prevalence of FVL and FII G20210A mutations was compared in patients with recurrent pregnancy loss and in a control group of 115 healthy women, without history of pregnancy loss (6.1% and 8.1% for FVL and FII G20210A respectively vs 2.6% for both mutations in the control group, P=0.36 for FVL and P=0.13 for FII G20210A). FVL and FII G20210A mutations were significantly more prevalent in women with fetal death (19.6%, P=0.001 for both mutations). CONCLUSIONS: Our data suggest that the screening for the FVL and FII G20210A mutations is useful in the setting of unexplained early and late pregnancy loss. Further studies are necessary in order to clarify the real impact of prothrombotic molecular defects on the pregnancy outcome and then to evaluate the appropriate therapeutic approach.     

Parvovirus B19 infection: association with third-trimester intrauterine fetal death

Objective To identify the presence of parvovirus B19 infection as a possible cause of fetal loss in the third trimester.
Design Prospective study of women experiencing third-trimester intrauterine fetal death (IUFD).
Setting All cases of IUFD at Danderyd Hospital from 1992 to 1998.
Population Ninety-three women with IUFD in 33,759 deliveries (0.3%).
Methods Detection of B19 DNA by polymerase chain reaction (PCR) in placental and fetal tissue. Placental pathology and B19-specific immunohistochemistry. Maternal serology in consecutive samples.
Results Among 93 cases of IUFD, seven (7.5%) had detectable B19 DNA in freshly-frozen placental tissue. The detection of B19 DNA in these tissues was confirmed by detection of B19 DNA in six separately stored paraffin-embedded placental tissues. No other explanations for the fetal deaths were found. None of the women had experienced any clinical signs of infection prior to fetal demise. None of the seven fetuses were hydropic. Histopathologic examination of the placentas revealed only minor abnormalities. Serology on maternal samples at birth revealed delayed or absent B19 IgG responses in five of seven cases. Two women were B19 IgG seropositive at the time of delivery but had unusual infection patterns; persistent viraemia for at least five months before birth in one case and likely persistence or re-infection by B19 in the other.
Conclusion In our study, 7.5% of IUFDs in the third trimester may have been caused by parvovirus B19 infection, without signs of fetal hydrops. This finding indicates that B19 PCR should be included in the routine investigation of IUFD.     

Management of intrauterine fetal death with prostaglandin E2 vaginal suppositories

The recent Food and Drug Administration's approval of prostaglandin E₂ (PGE₂) vaginal suppositories provides the clinician with a technique for the immediate management of missed abortion and intrauterine fetal death (IUFD). During a 4-year period at our institution, 78 of 80 patients with gestations ranging from 13 to 42 weeks had pregnancy successfully terminated with PGE₂ suppositories with a dose schedule of 20 mg every 2 hours. The mean interval from induction to delivery of the fetus was 8.9 hours. Fifty percent of the patients spontaneously expelled the placenta; active intervention to remove the placenta within 2 hours of delivery of the fetus is recommended to avoid excessive vaginal bleeding. The most frequently encountered side effect was a temperature elevation, which was managed by less frequent administration of the prostaglandin. Gastrointestinal side effects were minimized by premedication with antidiarrheal and antiemetic agents, which also were administered during the induction period when indicated by the patient's symptoms. A concomitant oxytocin infusion was utilized in 38 patients. In gestations of less than 24 weeks the oxytocin was administered via intravenous drip at a rate of 10 U/hour. In the case of a patient with IUFD and a gestation of 24 weeks or more, oxytocin should be administered only with a constant-rate infusion pump starting at a dose schedule of 1 mU/minute with careful titration of the dose against the monitored uterine activity. The availability of the vaginal PGE₂ suppositories for missed abortion and IUFD makes it important for the clinician to fully acquaint himself with the drug, its administration, effects, and side effects.     

Genetic polymorphisms associated with thrombophilia and vascular disease in women with unexplained late intrauterine fetal death: a multicenter study

OBJECTIVE: We determined whether gene polymorphisms associated with thrombophilia and vascular disease as etiologic factors were involved in the pathogenesis of pregnancy-associated complications. METHODS: We conducted a multicenter case-control study in which we studied 94 women with late unexplained intrauterine fetal death (IUFD) and 94 healthy women with at least one uncomplicated full-term pregnancy and no history of IUFD. We obtained blood samples from all subjects and analyzed their DNA for 12 common polymorphisms of thrombophilic and vascular genes (factor V Leiden, factor V H1299R, prothrombin G20210A, factor XIII V34L, MTHFR C677T, MTHFR A1298C, beta-fibrinogen-455 G to A, PAI-1 4G/5G, GPIIIa L33P, HFE C282Y, apolipoprotein B R3500Q, and apolipoprotein E2/E3/E4). RESULTS: We found no significant association between any of the polymorphisms investigated and IUFD. Subgroup analyses involving various combinations of polymorphisms and in which gestational age and fetal weight were corrected for also showed no significant results. CONCLUSIONS: Our data represent the largest study to date with respect to thrombophilic and vascular gene polymorphisms in IUFD. In accordance with others, we challenge the importance of thrombophilic and vascular gene polymorphisms in the pathogenesis of this condition.