Intrauterine Fetal Growth Retardation Research Articles

Different Etio-Pathogenesis in Intrauterine Growth Retardation in Developing Country: Histomorphometric Evidence

The present study was conducted to compare histomorphometric parameters of umbilical cord and its vessels in intrauterine growth retarded fetuses and normally grown fetuses. The study was conducted on umbilical cords taken from thirty intrauterine growth retarded (IUGR) fetuses and thirty normally grown fetuses (NGA). Histomorphometric parameters were measured with the help of planimeter. In the present study it was found that in cross section the total umbilical cord area in IUGR group is 59.00+3.67 mm2 and in the control group is 75.91+4.77mm2 (p<0.05). Jelly area in IUGR group is 47.90+3.11 mm2 and in control group is 60.26+4.55 mm2 (p<0.05). Total vessel area in control group is 15.45+1.73 mm2 and in IUGR group is 10.95±1.20mm2 (p <0.05). Total umbilical cord area, umbilical cord jelly area and total vessel area are significantly lower in the IUGR group but no significant difference was observed in total luminal area, total area of blood vessels and wall thickness of umbilical blood vessels. So in the study it was found that histomorphometric parameters of umbilical cord of IUGR fetuses are significantly lower than that of normally grown fetuses of similar gestational age.

L-Arginine stimulates the mTOR signaling pathway and protein synthesis in porcine trophectoderm cells

Impairment of placental growth is a major factor contributing to intrauterine growth retardation (IUGR) in both human pregnancy and animal production. Results of recent studies indicate that administration of l-arginine (Arg) to gestating pigs or sheep with IUGR fetuses can enhance fetal growth. However, the underlying mechanisms are largely unknown. The present study tested the hypothesis that Arg stimulates the mammalian target of rapamycin (mTOR) signaling pathway and protein synthesis in porcine conceptus trophectoderm (pTr2) cells. The cells were cultured for 4 days in Arg-free Dulbecco's modified Eagle's Ham medium containing 10, 50, 100, 200, 350 or 500 μM Arg. Cell numbers, protein synthesis and degradation, as well as total and phosphorylated levels of mTOR, ribosomal protein S6 kinase 1 (p70S6K) and eukaryotic initiation factor 4E-binding protein-1 (4EBP1), were determined. The pTr2 cells exhibited time (0–6 days)- and Arg concentration (10–350 μM)-dependent increases in proliferation. Addition of 100 and 350 μM Arg to culture medium dose-dependently increased (a) protein synthesis and decreased protein degradation and (b) the abundance of total and phosphorylated mTOR, p70S6K and 4EBP1 proteins. Effects of 350 μM Arg on intracellular protein turnover were only modestly affected when nitric oxide synthesis was inhibited. Collectively, these results indicate a novel and important role for Arg in promoting growth of porcine placental cells largely via a nitric-oxide-independent pathway. Additionally, these findings help to explain beneficial effects of Arg supplementation on improving survival and growth of embryos/fetuses in mammals.

Fetal hydrops and anemia as signs of Down syndrome

Before the 20th week of gestation, the most common cause of nonimmune hydrops fetalis is chromosomal abnormalities. Herein, we report a case of fetal hydrops, anemia, and intrauterine growth retardation that presented at 27 weeks of gestation with a negative chromosomal abnormality screening. Cordocentesis and karyotype analysis revealed fetal pancytopenia and Down syndrome. Down syndrome rarely presents with fetal hydrops and anemia. Therefore, when hydrops and anemia are diagnosed, especially in the second trimester of gestation, the possibility of Down syndrome should be kept in mind. In addition, if the pregnancy results in a live birth, the baby should be examined for transient abnormal myelopoiesis.

The Over Roofing Rates of Caesarean Section

The Over Roofing Rates of Caesarean Section

ADAMTS13, FVIII, von Willebrand factor, ABO blood group assessment in preeclampsia

IntroductionPreeclampsia (PE) is a multifactorial disease characterized by high blood pressure and proteinuria after the 20th week of pregnancy. PE is associated with fibrin deposition in placental microcirculation and intrauterine fetal growth retardation. We evaluated FVIII activity, VWF and ADAMTS13 plasma levels, according to O and “non O” blood groups, in women with severe PE (sPE). MethodsThis case-control study included 140 women; 55 pregnant with sPE, 35 normotensive pregnant and 50 non-pregnant women. VWF and ADAMTS13 antigen levels were assessed by ELISA (American Diagnostica). FVIII activity was measured by automated coagulometric method (Dade Behring) and ABO blood groups phenotyping was performed by indirect technique. ResultsFVIII activity and VWF levels were significantly higher comparing either sPE to normotensive pregnant (P=0.01; P=0.05) and to non-pregnant women (P=0.00 in both cases) or normotensive pregnant and non-pregnant women (P=0.00 in both cases). A significant decrease in ADAMTS13 levels was observed comparing either sPE to normotensive pregnant (P=0.02) and non-pregnant women (P=0.00) or normotensive pregnant and non-pregnant women (P=0.00). FVIII activity and VWF levels were associated to O and “non O” blood groups only in non-pregnant women. ConclusionsThe increase of FVIII activity and VWF levels and the decrease of ADAMTS13 in sPE are not associated to O and “non O” blood groups. These alterations in hemostatic markers in sPE largely surpass those physiologically determined by ABO blood groups influence and may have masked the effect of O and “non O” groups in this disease. A concomitant analysis of VWF levels and ADAMTS13 activity and antigenic levels will be important to clarify the imbalance between these parameters found in sPE in the present study.

L27. Management of non severe gestational hypertension through the modulation of total vascular resistance

sometimes it is necessary. It is indicated to deliver when some specific maternal or fetal conditions develop. Maternal indications for delivery include: platelet count under 100,000, progressive liver function deterioration, progressive renal function deterioration, suspected abruptio placentae, refractory severe hypertension (>160/110), persistent severe headache or visual changes, persistent severe epigastric pain or emesis. Fetal indications for delivery are: severe fetal intrauterine growth retardation, low umbilical artery systolic/diastolic ratio by doppler ultrasound, non-reassuring fetal testing, oligohydramnios. If the gestation is greater than 34 weeks, delivery after stabilization is recommended.

Melatonin alleviates lipopolysaccharide‐induced placental cellular stress response in mice

Melatonin protects mice from lipopolysaccharide (LPS)-induced fetal death and intra-uterine growth retardation. Nevertheless, its molecular mechanism remains obscure. In the present study, we investigated the effects of melatonin on LPS-induced cellular stress in placenta. Pregnant mice were given with melatonin [5.0 mg/kg, intraperitoneal (i.p.)] 30 min before and 150 min after LPS (300 μg/kg, i.p.) on gestational day 15. Oxidative stress, endoplasmic reticulum (ER) stress, hypoxic stress, and heat stress in placenta were analyzed at 4 hr after LPS. As expected, maternal LPS administration resulted in placental glutathione (GSH) depletion and up-regulated the expression of placental antioxidative enzymes. In addition, LPS significantly increased the level of inducible nitric oxide synthase (iNOS) and enhanced the intensity of placental 3-nitrotyrosine residues. An ER stress, as determined by a decreased GRP78 expression, an obvious eIF2α and JNK phosphorylation, and an increased CHOP expression, were observed in placenta of pregnant mice injected with LPS. In addition, LPS significantly increased mRNA level of placental HIF-1α, VEGF, and ET-1, the markers of hypoxic stress. Heme oxygenase (HO)-1, a marker of heat stress, was also up-regulated in placenta of LPS-treated pregnant mice. Interestingly, LPS-induced placental oxidative stress, hypoxic stress, and ER stress were significantly alleviated when pregnant mice were given with melatonin, whereas melatonin had little effect on LPS-evoked placental HO-1 expression. In conclusion, maternally administered melatonin alleviates LPS-induced cellular stress in the placenta. Melatonin may be useful as pharmacological agents to protect the fetuses against LPS-induced intra-uterine fetal death and intra-uterine growth restriction.

Hyperlipidic hypercholesterolemic diet in prepubertal rabbits affects gene expression in the embryo, restricts fetal growth and increases offspring susceptibility to obesity

Maternal hypercholesterolemia has been shown to lead to fetal intra-uterine growth retardation (IUGR) in rabbits. The effects of a long term maternal hyperlipidemic and hypercholesterolemic diet on embryo, fetal and post-natal development, have not been addressed so far. Rabbit does were fed either a hypercholesterolemic (0.2%) hyperlipidic (8%) (HH) or a control (C) diet from 10 weeks of age. Sixteen does (N = 8 HH and N = 8 C) were euthanized at 18 weeks to assess the effect of the diet on dams before mating. Embryos from 18 females (N = 9 HH and N = 9 C) were collected from the oviducts at the 16–20 cell stage (embryonic genome activation stage) for gene expression analysis (micro array and quantitative RT-PCR). Thirty females (N = 16 HH and N = 14 C) were mated naturally and fetal growth was monitored by ultrasound. Six of them (N = 4 HH and N = 2 C) were euthanized at D28 of gestation to collect fetuses and placentas. Finally, the remaining 24 does delivered at term and litters were cross fostered and equilibrated in number to create 4 groups according to the biological dam and the foster dam (C-C, C-HH, HH-C, HH-HH). Growth was monitored until weaning. A subset of 26 offspring from the 4 groups was fed the control diet until 25 weeks of age and then fed the HH diet for three weeks. All does had similar growth rates and bodyweight. Transcriptomic analyses evidenced an overexpression of Adipophilin in HH embryos at the stage of embryonic genome activation. This was confirmed by quantitative RT-PCR. During pregnancy, IUGR was observed from D9 by ultrasound and subsequently, fetal weight at 28 days, birthweight and fat deposition in newborn offspring were significantly decreased in HH (P < 0.05). After weaning, there was no significant difference for weight between HH-HH and HH-C offspring and both groups became significantly heavier (P < 0.0001) than C-C and C-HH offspring. During the 3 weeks when offspring were fed the HH diet, the differences in feed intake were no longer significant between groups but the differences in body weight remained. At post-mortem, offspring from HH does had significantly more abdominal and inter-scapular fat than offspring from C does (P < 0.05). These data illustrate the importance of maternal nutrition before and during gestation in the establishment and control of the growth trajectory of the conceptus and in the onset of disease in adult life.

Pregnancy outcome in 396 pregnancies in patients with SLE in Saudi Arabia

The aim of this study was to examine the pregnancy outcomes in patients with systemic lupus erythematosus (SLE) and the effect of SLE flare and treatment on pregnancy outcomes. We performed a retrospective evaluation of all pregnancies occurring in patients with SLE during the 27-year period from 1980 to 2006. Of the 319 women with SLE planning pregnancy after SLE onset, 176 (55.2%) conceived resulting in 396 pregnancies. Live births were significantly lower in proportion (70.2% vs. 85.7%) and more likely to end in fetal deaths (29.7% vs. 14.2%) and preterm births (26.7% vs. 5.8 %) in pregnancies occurring after SLE onset than in pregnancies occurring before SLE onset (p < 0.0001). With respect to different disease manifestations, we found that fetal loss was significantly higher in patients with antiphospholipid (aPL) antibodies than without (p < 0.001). Preterm deliveries were significantly more frequent in patients with lupus nephritis, anti-Ro/SSA antibodies, hypertension, history of intravenous cyclophosphamide treatment and aPL than those without these features (p < 0.05). Neonates with intrauterine growth retardation (IUGR) neonates were more common in hypertensive and Raynaud's-positive pregnancies (p < 0.05). SLE flares occurred in 30.8% pregnancies. There was increased risk of fetal loss, preterm births and IUGR in pregnancies with SLE exacerbations than without (p < 0.05). Prednisolone was found to improve the rate of live births, although it was also a predictor of prematurity. The predictors of pregnancy loss were lupus nephritis (odds ratio (OR) 7.3), aPL (OR 3.9), and SLE flares in pregnancy (OR 1.9). There was higher risk of preterm deliveries in patients with lupus nephritis (OR 18.9), anti-Ro antibodies (OR 13.9), hypertension (OR 15.7) and SLE flares (OR 2.5). IUGR was found to be associated with hypertension (OR 37.7), Raynaud's (OR 12.3), and SLE flares (OR 4.2). In conclusion, pregnancies in SLE patients with active lupus nephritis, anti-Ro/SSA antibodies, aPL, hypertension, Raynaud's phenomenon, active disease at conception and SLE exacerbations are at a higher risk of adverse pregnancy outcomes. It is important to carefully plan pregnancy, and experienced rheumatologists and obstetricians should monitor SLE patients in pregnancy and postpartum.

The effects of vascular intrauterine growth retardation on cortical astrocytes

Objective. We sought to determine the pathogenesis of neurodevelopmental impairments in survivors of intrauterine growth retardation (IUGR).Methods. We used an experimental rabbit vascular IUGR model. We ligated 25% of uteroplacental vessels (partial ischemia) of one-half of the fetuses on day 25 at the end of the third trimester. We then determined hemispheral DNA and protein levels, and used glial fibrillary acidic protein (GFAP) staining to count the labeled astrocytes at the superficial cortical layers.Results. Ischemic fetuses were significantly smaller than control fetuses and presented a disproportionately small body and a relatively larger head compared with the normal body/head ratio, confirming the study model as that of asymmetric IUGR. Hemispheral DNA was unchanged in IUGR fetuses, but they had decreased brain weight, hemispheral protein content, and a reduced number of mature (GFAP-positive) cortical astrocytes compared with control fetuses.Conclusion. Vascular IUGR, as demonstrated in our asymmetric IUGR model, adversely affected brain growth, cell size, and cortical astrocytes maturation. In view of the neurotrophic and neuroprotective functions of astrocytes, a reduced number of mature astrocytes during this critical period of development may be implicated in the pathogenesis of the neurodevelopmental impairments observed in IUGR.

Ethanol-induced inhibition of fetal hypothalamic–pituitary–adrenal axis due to prenatal overexposure to maternal glucocorticoid in mice

Prenatal ethanol exposure has been well documented to be one of the etiological factors responsible for intrauterine growth retardation (IUGR). Previous studies have shown that chronic ethanol exposure during pregnancy elevated the basic level of corticosterone in fetus. However, the potential mechanisms behind them are still unclear. The aim of the present study was to investigate the effects of prenatal ethanol exposure on maternal and fetal hypothalamic–pituitary–adrenal (HPA) axis as well as placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), and to clarify the mechanism of ethanol-induced IUGR. Pregnant mice were intragastricly administrated with ethanol at a dose of 6.4 g kg −1 d −1 from day 11 to 17 of gestation and parameters representing fetal growth and development were recorded either. The level of corticosterone in maternal serum was determined by ELISA kit. The mRNA expressions of steroidogenic acute regulatory protein (StAR) and cytochrome P450 cholesterol side chain cleavage (P450scc) both in maternal and fetal adrenal, and placental 11β-HSD-2 were detected by real-time quantitative PCR, respectively. The results showed that fetal body weight significantly decreased, and the incidence of IUGR was obviously increased after prenatal ethanol exposure. Maternal serum corticosterone level was elevated, and the expressions of StAR and P450scc were increased in maternal adrenal while decreased in fetal adrenal. The expression of placental 11β-HSD-2 was significantly reduced. These results suggest that prenatal ethanol exposure induces an inhibition of fetal HPA axis activity and IUGR occurs. The mechanism may be associated with ethanol-induced maternal HPA axis activation and high glucocorticoid condition, which impair the placental barrier, and lead to an overexposure of elevated maternal glucocorticoid to fetus, and eventually result in the inhibition of the fetal HPA axis.

Präpartale Depression und Angst – Was ist relevant für den Geburtshelfer?

Fragestellung: Depressionen und Angststörungen stellen die häufigsten psychischen Erkrankungen dar und sind in unserer Gesellschaft weit verbreitet. Eine beachtliche Anzahl an Frauen leidet unter diesen psychischen Erkrankungen vor, während oder nach einer Schwangerschaft. Eine Schwangerschaft kann durch eine bereits vorbestehende oder neu auftretende Erkrankung erschwert werden. Im Gegensatz dazu haben sowohl die Angststörung als auch die Depression in ihrer klinischen Präsentation während der Schwangerschaft wenig Aufmerksamkeit erhalten. In diesem Artikel wird die aktuelle Literatur zu diesem Thema zusammengefasst mit dem Ziel, eine Übersicht über die Prävalenz und die klinische Präsentation depressiver Erkrankungen und Angststörungen im Prä- und Peripartalzeitraum zu geben. Klinische Implikationen werden diskutiert. Um in der Praxis ein besseres Verständnis dafür zu entwickeln, werden zuerst die Erkrankungen dargestellt, um dann auf die in der Literatur aufgeführten Schwangerschaftskomplikationen einzugehen. Im Vordergrund steht dabei die klinische Bedeutung dieser Erkrankungen. Des weiteren werden aktuelle Behandlungsoptionen und ein einfaches Screeninginstrument, an dem man sich im Alltag orientieren kann, vorgestellt. Methodik: Es wurde eine Datenrecherche in elektronischen Datenbasen (Medline, PubMed) in englischer Sprache anhand der Schlüsselwörter „Schwangerschaft“ und „Depression“ oder „Angststörung“ sowie „niedriges Geburtsgewicht“, „Wachstumsretardierung“, „Frühgeburt“ oder „Behandlung“ durchgeführt. Insgesamt 59 englischsprachige Artikel, publiziert innerhalb der Jahre 1986–2009 blieben nach Durchsicht übrig und wurden ausgewertet. Ergebnisse: Als Auswirkungen hoher Level an Depressivität und Angst auf die Schwangerschaft werden in aktuellen Studien besonders die intrauterine Wachstumsrestriktion sowie eine Frühgeburt herausgestellt. Eine Reihe von Autoren konnten hier Zusammenhänge demonstrieren. Über den Pathomechanismus herrscht Uneinigkeit. Am wahrscheinlichsten werden Regulationen über die Cortisolachse angenommen, was im Tierversuch demonstriert werden konnte. Die Diagnosestellung bedarf häufig der interdisziplinären Zusammenarbeit, um eine reaktive Symptomatik von tatsächlichen Psychopathologien zu unterscheiden. Behandlungsoptionen reichen von psychologischer Unterstützung bis hin zur Therapie mit Psychopharmaka. Schlussfolgerung: Angststörungen und depressive Erkrankungen zählen bei Frauen in den reproduktiven Jahren zu den häufigsten psychischen Störungen. Ihr Erscheinungsbild ist heterogen. Gerade das Erkennen dieser Erkrankungen in der Schwangerschaft und der Umgang mit ihnen ist erschwert. Unter der Annahme, dass sowohl die Erkrankung selbst durch Angst, Depression und Stress, jedoch auch eine psychotrope Medikation den Feten in seiner Entwicklung beeinflussen können, befindet sich der behandelnde Arzt in einem Dilemma. Sowohl die Behandlung als auch die Nichtbehandlung kann negative Konsequenzen nach sich ziehen. Eine frühzeitige Erkennung, Diagnosestellung und Zuführung zu Behandlungsangeboten stellt eine Möglichkeit dar, bereits präpartal entstehende Komplikationen zu mildern und postpartalen Störungen vorzubeugen.

The Effect of Intrauterine Growth Retardation on the Expression of Developmental Factors in Porcine Placenta Subsequent to the Initiation of Placentation

Intrauterine growth retardation (IUGR) hinders fetal growth and postnatal development in swine; however the etiology of IUGR is essentially unknown. Expression of fourteen candidate genes associated with placental development or IUGR was examined in gestational day 50 (gd50) control and IUGR fetus whole placental tissue or areolae by real-time PCR. Endothelial nitric oxide synthase (ENOS) mRNA expression was elevated in gd50 IUGR placenta and areola compared to gd50 control. Since ENOS could modulate vascular tone and angiogenesis via nitric oxide production, data suggest that the increase in IUGR may be an adaptive response to poor perfusion to maintain pregnancy.

Effects of Ginkgo biloba extract on the embryo‐fetal development in Wistar rats

Ginkgo biloba extract (GBE) is an herbal medicine used for treating neurodegenerative diseases, cerebrovascular insufficiency, peripheral arterial occlusive disease, and also vestibular disturbance. Some components of GBE have presented estrogenic effects and, in a previous study, high dosages of GBE caused intra-uterine growth retardation in fetuses of Wistar rats treated during the fetogenesis period. Pregnant Wistar rats were treated, through gavage, with different dosages of aqueous GBE (3.5, 7.0, and 14.0 mg/Kg/day), during the tubal transit and implantation period. Rats were killed on the 15th day of pregnancy and the following parameters were evaluated: clinical symptoms of maternal toxicity; maternal body weight; feed and water intake; maternal liver, kidney, and ovary weights; number of corpora lutea; implants per group ratio; pre- and post-implantation loss per group ratio; live fetuses mean; dead fetuses percentage; fetus and placenta weight per offspring ratio; and fetal external malformation. No significant alteration was found for both the maternal and embryonic parameters evaluated. The GBE treatment in pregnant Wistar rats, during the tubal transit and implantation period, caused no toxic effect on the maternal organism and did not induce embryonic death, growth retardation, and/or fetal malformations.

Sildenafil Citrate Treatment Enhances Amino Acid Availability in the Conceptus and Fetal Growth in an Ovine Model of Intrauterine Growth Restriction1–3

Adequate placental blood flow is essential for the optimal delivery of nutrients from mother to fetus for conceptus growth. Restricted fetal development results from pathophysiological and environmental factors that alter utero-placental blood flow, placental function, and, therefore, nutrient availability in the fetus. To test this hypothesis, 0, 75, or 150 mg/d sildenafil citrate (Viagra) was administered subcutaneously from d 28 to 115 of gestation to either nutrient-restricted [50% of NRC requirements) or adequately-fed ewes (100% of NRC requirements). On d 115, maternal, fetal, and placental tissues and fluids were collected. Concentrations of total amino acids and polyamines in uterine venous and arterial sera, amniotic and allantoic fluids, and fetal umbilical venous serum were lower (P < 0.05) in nutrient-restricted ewes than in adequately fed ewes, as were the ratios of total amino acids in fetal umbilical venous serum to uterine arterial serum. Sildenafil citrate dose-dependently increased (P < 0.05) total amino acids and polyamines in amniotic fluid, allantoic fluid, and fetal serum without affecting values in maternal serum. Fetal weight was lower (P < 0.05) in nutrient-restricted ewes on d 115. Sildenafil citrate treatment dose-dependently increased (P < 0.05) fetal weight in both nutrient-restricted and adequately fed ewes. This study supports the hypothesis that long-term sildenafil citrate treatment enhances fetal growth, at least in part, by increasing the availability of amino acids in the conceptus. These findings may lead to the clinical use of sildenafil citrate in human pregnancies suspected to be at risk for intrauterine fetal growth retardation.

The relationship between fetal growth restriction and small placenta in 6-mercaptopurine exposed rat

In order to investigate the effect of placental size on fetal intrauterine growth retardation (IURG), we examined the morphology and alterations in the expression of glucose transporter in the placentas of rats exposed to 6-mercaptopurine (6-MP). 6-MP was administered orally at 0 and 60 mg/kg/day on gestation day (GD) 9, 11, 13 or 15, and the placentas were sampled on GDs 17 and 21. The main findings in the treated groups were small placenta caused by mitotic inhibition and apoptosis, fetal resorption and IUGR with or without some malformations. The most sensitive period to 6-MP-induced fetal mortality was found to be in the GD9-treated group, and the small placenta and fetal abnormalities in the GD11-treated group, respectively. However, the litters in a quarter of the dams with the treatment on GD 11 had no fetotoxicity despite 25% decline in the placental weight. Histopathologically, the expression of glucose transporter GLUT3 was increased in the trophoblastic septa in all treated groups, particularly remarkable with proliferation of trophoblasts in the above litters, where the fetal–placental weight ratio was increased. Thus, we consider that the normal fetal growth and development can be maintained caused by adaptive change, even if the placental weight decreased by approximately 25% in 6-MP exposed rats.

Manganese and birth outcome

Manganese is an essential mineral nutrient needed for proper fetal development and other important aspects of metabolism. However, manganese excess can have a potent neurotoxicity effect, especially in infants. Little is known about the effects of manganese deficiency or excess on the developing human fetus. The findings of two recent studies indicate that lower maternal blood manganese is associated with fetal intrauterine growth retardation (IUGR) and lower birth weight. In light of the importance of IUGR and birth weight on neonatal morbidity and mortality, additional basic studies of maternal and fetal manganese physiology are needed, as well as more epidemiologic studies in different populations of the association of manganese exposure and birth outcome.

Respiratory insufficiency in a patient with preeclamsia and hypothyroidism developed after general anesthesia for emergency cesarean section: A case report.

Anesthesia and surgery in a patients with undiagnosed or untreated hypothyroidism can carries the risk of potential complications such as prolonged unconsciousness, respiratory insufficiency, hypotension, hyponatremia, congestive heart failure, and even coma. A 33-year-old gravida was admitted at 36 weeks gestation with hypertension, proteinuria, generalized edema, and intrauterine fetal growth retardation. She had thyroidectomy for thyroid mass six years ago. Because of doubt of uterine abruption, emergency cesarean section was performed without result of thyroid function test. Preeclamsia and mild hypothyroidism show similar symptoms and it can make difficult to diagnose hypothyroidism. We experienced delayed recovery and respiratory insufficiency in a patient with preeclamsia and undetected hypothyroidism during emergence from general anesthesia. She was fully recovered after ventilatory care in intensive care unit.

The effects of vascular intrauterine growth retardation on cortical astrocytes

We sought to determine the pathogenesis of neurodevelopmental impairments in survivors of intrauterine growth retardation (IUGR). We used an experimental rabbit vascular IUGR model. We ligated 25% of uteroplacental vessels (partial ischemia) of one-half of the fetuses on day 25 at the end of the third trimester. We then determined hemispheral DNA and protein levels, and used glial fibrillary acidic protein (GFAP) staining to count the labeled astrocytes at the superficial cortical layers. Ischemic fetuses were significantly smaller than control fetuses and presented a disproportionately small body and a relatively larger head compared with the normal body/head ratio, confirming the study model as that of asymmetric IUGR. Hemispheral DNA was unchanged in IUGR fetuses, but they had decreased brain weight, hemispheral protein content, and a reduced number of mature (GFAP-positive) cortical astrocytes compared with control fetuses. Vascular IUGR, as demonstrated in our asymmetric IUGR model, adversely affected brain growth, cell size, and cortical astrocytes maturation. In view of the neurotrophic and neuroprotective functions of astrocytes, a reduced number of mature astrocytes during this critical period of development may be implicated in the pathogenesis of the neurodevelopmental impairments observed in IUGR.

Small size‐specific umbilical vein diameter in severe growth restricted fetuses that die in utero

To study changes in umbilical vein (UV) blood flow velocity, diameter and blood flow volume in intrauterine growth retardation (IUGR) fetuses who die in utero (IUD-IUGR). Twelve singleton IUGR fetuses who died in utero below 600 g were included. All cases had abnormal uterine and umbilical arteries PI. UV diameter and velocity were measured at the time of diagnosis, and at the last exam, within 24 hours prior to intrauterine death. UV flow was calculated per unit weight (mL/min/kg) and abdominal circumference (AC) (mL/min/cm). UV diameter and velocity were normalized per unit AC. Findings were compared to 14 severe viable-IUGR and 22 normal gestational age-matched fetuses. UV flow (mL/min/kg) was significantly lower in IUD-IUGR compared to viable-IUGR (87 +/- 30 mL/min/kg) and control fetuses (131 +/- 33 mL/min/kg) both at the first (79 +/- 40 mL/min/kg) (P < 0.0001), and at the last exam (54 +/- 29 mL/min/kg) (P < 0.0001). No significant longitudinal flow changes were observed. UV velocity/AC was significantly reduced both in IUD-IUGR and viable-IUGR compared to normal fetuses. UV diameter/AC, was significantly reduced only in IUD-IUGR and not in viable-IUGR compared to normal fetuses. UV flow (mL/min/kg) was significantly lower in IUD-IUGR fetuses both versus viable-IUGR and normal fetuses. A low flow was due to a decreased UV flow velocity, but also due to a reduced vessel size. This significantly smaller UV size observed in IUGR fetuses with the worst outcome could be considered a severe prognostic sign because of the diagnosis of severe growth restriction.