Pregnancy-induced Hypertensive Disorders Research Articles

Ambient Air Pollution and Pregnancy-Induced Hypertensive Disorders

Pregnancy-induced hypertensive disorders can lead to maternal and perinatal morbidity and mortality, but the cause of these conditions is not well understood. We have systematically reviewed and performed a meta-analysis of epidemiological studies investigating the association between exposure to ambient air pollution and pregnancy-induced hypertensive disorders including gestational hypertension and preeclampsia. We searched electronic databases for English language studies reporting associations between ambient air pollution and pregnancy-induced hypertensive disorders published between December 2009 and December 2013. Combined risk estimates were calculated using random-effect models for each exposure that had been examined in ≥4 studies. Heterogeneity and publication bias were evaluated. A total of 17 articles evaluating the impact of nitrogen oxides (NO 2 , NO X ), particulate matter (PM 10 , PM 2.5 ), carbon monoxide (CO), ozone (O 3 ), proximity to major roads, and traffic density met our inclusion criteria. Most studies reported that air pollution increased risk for pregnancy-induced hypertensive disorders. There was significant heterogeneity in meta-analysis, which included 16 studies reporting on gestational hypertension and preeclampsia as separate or combined outcomes; there was less heterogeneity in findings of the 10 studies reporting solely on preeclampsia. Meta-analyses showed increased risks of hypertensive disorders in pregnancy for all pollutants except CO. Random-effect meta-analysis combined odds ratio associated with a 5-µg/m 3 increase in PM 2.5 was 1.57 (95% confidence interval, 1.26–1.96) for combined pregnancy-induced hypertensive disorders and 1.31 (95% confidence interval, 1.14–1.50) for preeclampsia. Our results suggest that exposure to air pollution increases the risk of pregnancy-induced hypertensive disorders.

Risk of pregnancy-induced hypertensive complications following assisted reproductive technology (ART) – a cohort study from the committee on nordic ART and safety

Women who conceive through ART are at increased risk of pregnancy-induced hypertensive disorders. In this large population based study, we studied whether in-vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) as well as fresh or frozen cycles differed with respect to risk of hypertensive complications in pregnancy.

Management of preeclampsia.

Most patients with a pregnancy-induced hypertensive disorder have no clinical symptoms. So it can only be reliably detected by repetitive searches (screening) for the early signs and symptoms in the 2nd half of pregnancy. Adequate and proper prenatal care is the most important part of management of preeclampsia. Maternal antenatal monitoring includes identifying women at increased risk, early detection of preeclampsia by recognizing clinical signs and symptoms, and to observe progression of the condition to the severe state. As the etiology of preeclampsia remains in question, the only effective treatment is to deliver the infant and placenta; ancillary therapy is predominantly symptomatic and not directed at underlying causes. Once the diagnosis of preeclampsia is made, subsequent therapy will depend on the results of initial maternal and fetal evaluation. The primary objective of management of preeclampsia must always be safety of the mother. Although delivery is always appropriate for the mother, it may not be optimal for the fetus that is extremely premature. The decision between delivery and expectant management depends on fetal gestational age, maternal and fetal status at time of initial evaluation, presence of labor or rupture of fetal membranes, and level of available neonatal and maternal services. It is important to emphasize that hypertension is merely one manifestation of this disease, albeit directly related to one of the most serious consequences for the mother, i.e cerebral involvement, which may manifest itself as convulsions, focal neurological events such as cortical blindness, and even cerebral hemorrhage. The benefits of acute pharmacologic control of severe hypertension prior to delivery are generally accepted. The more contentious issues are the role of pharmacologic therapy in allowing prolongation of pregnancy and the ability of such therapy to modify the course of the underlying systemic disorder and affect fetal and maternal outcome. Ali hypertensive drugs affect both the mother and the fetus; some may produce side effects in the mother and others may produce adverse effects on the fetus or the newborn. The indirect effects of antihypertensive drugs on the fetus may be by impairing uteroplacental perfusion or directly by influencing the fetal cardiovascular circulation. In general, women with mild disease developing at 37weeks' gestation or longer have a pregnancy outcome similar to that found in normotensive pregnancy. Thus, those patients should undergo induction of labor for delivery. Induction of labor and/or delivery is also recommended for those at or beyond 34 weeks' gestation in the presence of severe preeclampsia, labor or rupture of membranes, or non-reassuring tests of fetal well-being because the mother is at slightly increased risk for development of placental abruption and progression to eclampsia. In women who remain undelivered, close maternal and fetal evaluation is essential. The type of test and frequency of evaluation will depend on fetal gestational age as well as severity of maternal condition, and presence or absence of IUGR. These tests should be repeated promptly in case of worsening maternal condition (progression to severe disease) or fetal condition (reduced fetal movement or suspected IUGR). Expectant management of severe preeclampsia:The clinical course of severe preeclampsia may be characterized by progressive deterioration in both maternal and fetal conditions. Because these pregnancies have been associated with increased rates of maternal morbidity and mortality and with significant risks for the fetus, there is universal agreement that such patients be delivered if the disease develops after 34weeks' gestational, 243. Delivery is also clearly indicated when there is imminent eclampsia (persistent severe symptoms), multiorgan dysfunction, severe IUGR, suspected placental abruption, or non-reassuring fetal testing before 34 weeks' gestation. There is disagreement however, about treatment of patients with severe preeclampsia before 34 weeks' gestation where maternal condition is stable and fetal condition is reassuring. The Cochrane review on interventionist versus expectant care states that it is not possible to draw firm conclusions, as there are only two small trials (133 women) that have compared a policy of early elective delivery, with a policy of delayed delivery, and the confidence intervals for all outcomes are wide. However, the evidence is promising that short-term morbidity for the baby may be reduced by a policy of expectant care. Sibai and Barton recently reviewed the literature on maternal and perinatal of expected management of severe preeclampsia remote from term and reviewed the major studies in the literature. Based on this review, they concluded that the results of these studies suggest that expectant treatment in a select group of women with severe preeclampsia between 24 0/7 and 32 6/7weeks of gestation in a suitable hospital is safe and improves neonatal outcome. Most studies on expectant management report 7-10days of prolongation. For gestational age of 24 0/7weeks, expectant treatment was associated with high maternal morbidity with limited perinatal benefit.

Body weight, weight gain and hyperglycaemia are associated with hypertensive disorders of pregnancy in women with gestational diabetes

AimThe aim of this study was to measure the capacity of glucose- and weight-related parameters to predict pregnancy-induced hypertensive disorders in women with gestational diabetes. MethodsAn observational study was conducted involving 2037 women with gestational diabetes. The associations of glycaemic and weight-related parameters with pregnancy-induced hypertensive disorders were obtained by univariate and adjusted multivariate analyses. Also, model predictability and attributable predictor risk percentages were calculated, and collinearity and factor interactions examined. ResultsMultivariate analyses revealed that hypertensive disorders were mainly predicted by average third-trimester glycated haemoglobin (HbA1c) levels≥5.9%, by being overweight or obese before pregnancy and by excess gestational weight gain after adjusting for age, tobacco use, chronic hypertension, parity, urinary tract infections and gestational age at delivery. Prepregnancy body weight (overweight and obesity) had the strongest impact on pregnancy-related hypertensive disorders (attributable risk percentages were 51.5% and 88.8%, respectively). The effect of being overweight or obese on hypertensive disorders was enhanced by HbA1c levels and gestational weight gain, with elevated HbA1c levels multiplying the effect of being overweight before pregnancy. ConclusionThe average third-trimester HbA1c level is a novel risk factor for pregnancy-induced hypertensive disorders in women with gestational diabetes. HbA1c levels≥5.9%, prepregnancy overweight or obesity and excess gestational weight gain are all independent risk factors of pregnancy-related hypertensive disorders in such women. In treated gestational diabetes patients, the strongest influence on hypertensive disorders is prepregnancy obesity.

The Role of Metformin in Metabolic Disturbances during Pregnancy: Polycystic Ovary Syndrome and Gestational Diabetes Mellitus.

Maintenance of gestation implicates complex function of multiple endocrine mechanisms, and disruptions of the global metabolic environment prompt profound consequences on fetomaternal well-being during pregnancy and postpartum. Polycystic Ovary Syndrome (PCOS) and gestational diabetes mellitus (GDM) are very frequent conditions which increase risk for pregnancy complications, including early pregnancy loss, pregnancy-induced hypertensive disorders, and preterm labor, among many others. Insulin resistance (IR) plays a pivotal role in the pathogenesis of both PCOS and GDM, representing an important therapeutic target, with metformin being the most widely prescribed insulin-sensitizing antidiabetic drug. Although traditional views neglect use of oral antidiabetic agents during pregnancy, increasing evidence of safety during gestation has led to metformin now being recognized as a valuable tool in prevention of IR-related pregnancy complications and management of GDM. Metformin has been demonstrated to reduce rates of early pregnancy loss and onset of GDM in women with PCOS, and it appears to offer better metabolic control than insulin and other oral antidiabetic drugs during pregnancy. This review aims to summarize key aspects of current evidence concerning molecular and epidemiological knowledge on metformin use during pregnancy in the setting of PCOS and GDM.

MiR-34a expression, epigenetic regulation, and function in human placental diseases

Preeclampsia (PE) is the major pregnancy-induced hypertensive disorder responsible for maternal and fetal morbidity and mortality that can be associated with intrauterine growth restriction (IUGR). PE and IUGR are thought to be due to a placental defect, occurring early during pregnancy. Several placental microRNAs (miRNAs) have been shown to be deregulated in the context of placental diseases and could thus play a role in the pathophysiology of PE. Here, we show that pri-miR-34a is overexpressed in preeclamptic placentas and that its placental expression is much higher during the first trimester of pregnancy than at term, suggesting a possible developmental role. We explored pri-miR-34a regulation and showed that P53, a known activator of miR-34a, is reduced in all pathological placentas and that hypoxia can induce pri-miR-34a expression in JEG-3 cells. We also studied the methylation status of the miR-34a promoter and revealed hypomethylation in all preeclamptic placentas (associated or not with IUGR), whereas hypoxia induced a hypermethylation in JEG-3 cells at 72 h. Despite the overexpression of pri-miR-34a in preeclampsia, there was a striking decrease of the mature miR-34a in this condition, suggesting preeclampsia-driven alteration of pri-miR-34a maturation. SERPINA3, a protease inhibitor involved in placental diseases, is elevated in IUGR and PE. We show here that miR-34a overexpression in JEG-3 downregulates SERPINA3. The low level of mature miR-34a could thus be an important mechanism contributing to SERPINA3 upregulation in placental diseases. Overall, our results support a role for miR-34a in the pathophysiology of preeclampsia, through deregulation of the pri-miRNA expression and its altered maturation.

Maternal Near Miss Review: A Way Forward

Maternal Near Miss Review: A Way Forward

Two-hour insulinemia after oral glucose overload and women at risk of pregnancy-induced hypertensive disorders

Objective: Pregnant women with impaired insulin sensitivity are at risk for developing pregnancy-induced hypertensive disorders (PIHD). We analyzed glucose and insulin circulating levels throughout a 2-h oral 75 g glucose tolerance test in pregnant women, and related the 2-h insulinemias to PIHD prevalence. Methods: Pregnant women (gestational week 24–28) were submitted to a glucose overload, and glucose and insulin plasma concentrations were measured throughout the test. These peripheral metabolite levels, the homeostasis model assessment (HOMA) values and the glucose to insulin ratio (G:Ir) were analyzed. Anthropometric parameters and pregnancy outcome were recorded. Results: Women with normal fasting glycemia, insulinemia and HOMA values, G:Ir and 2 h-glycemia but whose 2 h-insulinemia was higher than 215.25 pM were at greater risk for developing late pregnancy hypertension and preeclampsia compared to women of similar characteristics but whose 2 h-insulinemias were lower than 215.25 pM. Conclusion: 2-h insulinemias higher than 215.25 pM after a 75 g glucose overload could be highly indicative of women at increased risk of developing PIHD.

Phenotyping and outcome on contemporary management in a German cohort of patients with peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is a life-threatening heart disease developing towards the end of pregnancy or in the months following delivery in previously healthy women in terms of cardiac disease. Enhanced oxidative stress and the subsequent cleavage of the nursing hormone Prolactin into an anti-angiogenic 16 kDa subfragment emerged as a potential causal factor of the disease. We established a prospective registry with confirmed PPCM present in 115 patients (mean baseline left ventricular ejection fraction, LVEF: 27 ± 9 %). Follow-up data (6 ± 3 months) showed LVEF improvement in 85 % and full recovery in 47 % while 15 % failed to recover with death in 2 % of patients. A positive family history of cardiomyopathy was present in 16.5 %. Pregnancy-associated hypertension was associated with a better outcome while a baseline LVEF ≤ 25 % was associated with a worse outcome. A high recovery rate (96 %) was observed in patients obtaining combination therapy with beta-blocker, angiotensin-converting enzyme (ACE) inhibitors/angiotensin-receptor-blockers (ARBs) and bromocriptine. Increased serum levels of Cathepsin D, the enzyme that generates 16 kDa Prolactin, miR-146a, a direct target of 16 kDa Prolactin, N-terminal-pro-brain-natriuretic peptide (NT-proBNP) and asymmetric dimethylarginine (ADMA) emerged as biomarkers for PPCM. In conclusion, low baseline LVEF is a predictor for poor outcome while pregnancy-induced hypertensive disorders are associated with a better outcome in this European PPCM cohort. The high recovery rate in this collective is associated with a treatment concept using beta-blockers, ACE inhibitors/ARBs and bromocriptine. Increased levels of Cathepsin D activity, miR-146a and ADMA in serum of PPCM patients support the pathophysiological role of 16 kDa Prolactin for PPCM and may be used as a specific diagnostic marker profile.Electronic supplementary materialThe online version of this article (doi:10.1007/s00395-013-0366-9) contains supplementary material, which is available to authorized users.

Altered Arterial Compliance in Hypertensive Pregnant Women Is Associated with Preeclampsia

Vascular alterations are present in pregnant women affected by preeclampsia. In this study, we assessed arterial compliance in women affected by hypertensive disorders of pregnancy. We hypothesized that arterial compliance is reduced in women affected by preeclampsia. Forty-three hypertensive pregnant women undergoing evaluation for preeclampsia were studied. Clinical data about each patient and pregnancy were collected. Large (C1) and small (C2) artery compliance were assessed by radial tonometry, while the patients underwent laboratory tests to diagnose preeclampsia. At the time of delivery, gestational age and newborn data were recorded. Eighteen women were diagnosed with preeclampsia. C2 levels were lower among preeclamptic versus hypertensive aproteinuric women (mean ± SD, 4.5 ± 1.3 vs 5.9 ± 2.3 mL/mm Hg · 100, P = 0.013, 95% confidence interval [CI] of difference 0.32-2.55), whereas C1 levels did not differ. In the preeclampsia group, C2 levels correlated with urine total protein concentrations measured the same day (Spearman ρ = -0.49, P = 0.047, upper 95% CI -0.01) and with gestational age at first occurrence of hypertension (Spearman ρ = 0.59, P = 0.010, lower 95% CI 0.17). Among singleton gestations, C2 also correlated with newborn birth weight measured at delivery (Spearman ρ = 0.43, P = 0.009, lower 95% CI 0.11). Women who were hypertensive but aproteinuric at the time of compliance assessment, but who subsequently developed preeclampsia (n = 6), had C2 levels similar to those with an early diagnosis of preeclampsia (mean difference 0.37 mL/mm Hg · 100, 95% CI -2.42 to 1.67) and lower C2 levels than women diagnosed with gestational hypertension (P = 0.019, 95% CI 0.33-4.42 mL/mm Hg · 100). The noninvasive assessment of arterial elasticity may contribute toward characterization of the nature of the pathophysiology in pregnancy-induced hypertensive disorders. The vascular alterations of the small arteries, as assessed by C2, may reflect the extent of vascular alterations present with preeclampsia.

Soluble VEGFR-1 in pathophysiology of pregnancies complicated by hypertensive disorders: the Indian scenario

An imbalance between angiogenic and anti-angiogenic factors has been hypothesized to have a major role in hypertensive disorders during pregnancy, which account for significant morbidity and mortality for the mother and neonate in India. There is a paucity of information on soluble vascular endothelial growth factor receptor-1 (sVEGFR-1, anti-angiogenic factor) concentrations in different subgroups of pregnancy-induced hypertensive (PIH) disorders particularly in gestational hypertension (GH) and eclampsia during pregnancy. This cross-sectional study was conducted in order to test the above hypothesis and to get more insight into the role of sVEGFR-1 in these disorders. The concentrations of sVEGFR-1 in serum were measured from women with 22-39 weeks of gestation in the control (n=180) and gestationally matched hypertensive (n=360) pregnant mothers by ELISA. These sVEGFR-1 concentrations were found to be significantly elevated in the study groups as the severity of disease increases from GH to eclampsia (24 076 pg ml(-1); 42000 pg ml(-1), P=0.0001) as compared with controls (3360 pg ml(-1)). According to Receiver operating characteristic curve analysis, at ≤ 34 weeks, the concentration cutoff, sensitivity, specificity for sVEGFR-1 in differentiating GH, pre-eclampsia and eclampsia were ≥ 7619.2 pg ml(-1), 75%, 75%; ≥ 16726.6 pg ml(-1), 89.1%, 89.1%; ≥ 26222.8 pg ml(-1), 91.6%, 91.6%, respectively. The gradual upregulation of sVEGFR-1 concentrations in these groups may be due to its intimate involvement in the etiopathogenesis of severity of various hypertensive disorders by antagonizing effects of VEGF during the placental development. These observations indicate the clinical utility of sVEGFR-1 in differentiating PIH disorders and also will be helpful for the evaluation of increased monitoring system for successful pregnancy.

Endothelin: Key Mediator of Hypertension in Preeclampsia

Preeclampsia is a pregnancy-induced hypertensive disorder characterized by proteinuria and widespread maternal endothelial dysfunction. It remains one of the most common disorders in pregnancy and remains one of the leading causes of maternal and fetal morbidity. Recent research has revealed that placental insufficiency, resulting in hypoxia and ischemia, is a central causative pathway in the development of the disorder. In response, the placenta secretes soluble substances into the maternal circulation which are responsible for the symptomatic phase of the disease. Among the most well characterized factors in the disease pathology are the anti-angiogenic protein soluble fms-like tyrosine kinase-1 (sFlt-1), inflammatory cytokines, and agonistic angiotensin II type-1 receptor autoantibodies. Each of these factors has been shown to induce hypertension experimentally through the production of endothelin-1 (ET-1), a powerful vasoconstrictor. Antagonism of the endothelin-A receptor has proved beneficial in numerous animal models of gestational hypertension, and it remains an intriguing target for pharmacological intervention in preeclampsia.

Pregnancy outcome after oocyte donation in patients with Turner's syndrome and partial X monosomy

Fertility expectations for patients with Turner's syndrome (TS) have clearly changed in the last three decades. However, medical risks during pregnancy are supposed to be highly increased. The aim of the study was to assess clinical outcome and obstetrical complications in a series of patients with TS in an oocyte donor programme. A retrospective study was carried out on 24 women with TS seeking a pregnancy in the Fertility Clinic of the Erasme Hospital from 1992 up until March 2011. Twenty-three patients with TS were included in an oocyte donation cycle. Forty-nine oocyte donation cycles were performed, which led to 45 fresh and 10 frozen-thawed embryo transfers. Altogether, 18 pregnancies were obtained, 10 deliveries (9 singletons and 1 pair of twins), 3 miscarriages and 5 biochemical pregnancies. The clinical pregnancy rate per transfer was 24.4% in fresh cycles and 20% in frozen replacement cycles. Complications of pregnancy occurred in 5 of 10 pregnancies (50%), which led to three premature deliveries because of pregnancy-induced hypertensive disorders. The mean birthweight (g) (±SD) for singletons and twins was 2728 ± 577 and 2335 ± 318, respectively. Four babies were below the 10th percentile. No cardiac complications were observed in any of the pregnant women. Pregnancy rates after oocyte donation in patients with TS are comparable with those previously published but a high risk of pregnancy hypertensive disorders and a high risk of low birthweight can be highlighted from our study. Strict inclusion criteria and single embryo transfer are necessary to minimize complications during pregnancy in this high-risk group.

Mechanisms and potential therapies for preeclampsia.

Preeclampsia is a pregnancy-induced hypertensive disorder found most commonly in nulliparous women. Recent research performed in animal models of the disease has revealed some of the underlying mechanisms of preeclampsia. Specifically, placental insufficiency and the resulting hypoxia/ischemia have been shown to be crucial to disease progression. In response to placental hypoxia/ischemia, several pathways are activated, which contribute to the clinical manifestations of the disease: increased circulating levels of the anti-angiogenic protein sFlt-1, activation of the maternal inflammatory response, suppressed nitric oxide production, enhanced endothelin-1 production, and induction of reactive oxygen formation. Despite advances in the understanding of the disorder, therapeutic approaches to the treatment of preeclampsia are severely limited. New lines of research, however, indicate some possible new therapeutic approaches for the management of preeclampsia and offer hope for an effective pharmacologic intervention.

Chorionic villus sampling and the risk of preeclamspia: a systematic review and meta-analysis

To perform systematic review and meta-analysis to evaluate the risk of preeclampsia after chorionic villus sampling (CVS). A systematic search of PubMED and Web of Science from inception through August 2010, and bibliographies of review articles and eligible studies were performed. Six studies reported the risk of preeclampsia after CVS. All of the identified studies were retrospective and included in analysis. Reporting quality of the identified studies according to quality assessment scale for methodology in retrospective clinical reporting was moderate. Pooling was performed in two strata for control: (1) patients without any invasive prenatal diagnostic procedure served as control group: no significant difference was found in the odds ratio (OR) of preeclampsia (OR 0.79, 95% CI 0.38-1.64), severe preeclampsia (OR 0.49, 95% CI 0.04-5.78), gestational hypertension (OR 0.76, 95% CI 0.46-1.26), all pregnancy-induced hypertensive disorders (OR 0.80, 95% CI 0.46-1.41) between CVS and control groups. (2) Patients with amniocentesis combined with patients without any invasive prenatal diagnostic procedure served as control group: no significant difference was found in the OR of preeclampsia (OR 0.76, 95% CI 0.37-1.53), severe preeclampsia (OR 0.83, 95% CI 0.14-4.85), all pregnancy-induced hypertensive disorders (OR 0.92, 95% CI 0.55-1.53) between CVS and combined control groups. None of the included studies were randomized prospective trials designed to investigate the effect of CVS on preeclampsia. Accordingly, this review is limited by the heterogeneity, small number and retrospective nature of the available studies. CVS does not seem to increase the risk of preeclampsia or other pregnancy-induced hypertensive disorders. However, randomized prospective trials that are designed to investigate the risk of preeclampsia after CVS are needed to make a definite conclusion.

Fetal MBL2 haplotypes combined with viral exposure are associated with adverse pregnancy outcomes

Objective. To investigate the roles of inherited polymorphisms in the MBL2 gene and exposure to viral infection in the development of a range of adverse pregnancy outcomes, including birthweight <10th percentile (small-for-gestational age, SGA), antepartum hemorrhage (APH), pregnancy-induced hypertensive disorders (PIHD), and preterm birth (PTB).Methods. This was a case–control study using DNA from newborn screening cards of 717 cases (babies with at least one of the adverse pregnancy outcomes listed above) and 609 controls, to screen for six polymorphisms within the MBL2 gene. These combine to create haplotypes with high (HYPA), intermediate (LYQA, LYPA), low (LXPA), and defective (HYPD, LYQC, LYPB) circulating MBL2 levels.Results. Significant associations were found between variant MBL2 haplotypes and SGA (LYPA <32 weeks OR 5.37, 95% CI 1.50–17.27), antepartum hemorrhage (LYPA <37 weeks OR 2.29, 95% CI 1.25–4.18), and PIHD (LYQC <32 weeks (OR 17.89, 95% CI 2.20–139.57). Evidence of exposure to infection increased the effect of these associations, (SGA OR 17.00, 95% CI 1.03–252.48; APH OR 5.67, 95% CI 1.73–18.84; PIHD OR 23.80, 95% CI 1.08–1414.76), while no evidence of exposure to infection demonstrated no associations. PTB was significantly associated with the defective HYPD haplotype with evidence of exposure to infection (OR 6.14, 95% CI 1.21–29.89).Conclusions. This research suggests that the combination of fetal MBL2 haplotypes and exposure to in utero viral infection increases the risk of adverse pregnancy outcomes, including PTB, antepartum hemorrhage, small-for-gestational age and PIHD.

Obstetric admissions to the intensive care unit in a tertiary referral hospital

Purpose The present study was conducted to evaluate the obstetric admissions to the intensive care unit (ICU) in the setting of a tertiary referral hospital in an attempt to identify the risk factors influencing maternal outcome. Materials and Methods All of the obstetric patients who seeked care for delivery at the emergency department and who were admitted to the ICU between January 2006 to July 2009 were retrospectively identified. The Simplified Acute Physiology Score (SAPS II) was calculated and the maternal mortality rate was estimated for each patient. The mean SAPS II scores and the mean estimated maternal mortality rates for the surviving patients and the nonsurviving patients were compared. Results Seventy-three obstetric patients were admitted to the ICU. There were 9 maternal deaths and 24 fetal deaths. For the surviving group of patients, the mean SAPS II score was 34 and estimated maternal mortality rate was 20%, whereas for the nonsurviving group of patients, the SAPS II score was 64 and estimated maternal mortality rate was 73%. The difference between the surviving group of patients and the nonsurviving group of patients was statistically significant regarding both the mean SAPS II scores and the mean estimated maternal mortality rates. Conclusions Pregnancy-induced hypertensive disorders and hemorrhage appear as the major risk factors influencing maternal outcome in obstetric patients. Considering that the use of the SAPS II scores have enabled the reliable estimation of the mortality rates in the present study, the attempts at defining the focus of care for the obstetric patients who bear the major risk factors and who are admitted to the ICU should be carried out under the guidance of the ICU scoring systems such as the SAPS II.

Snoring, Witnessed Sleep Apneas, and Pregnancy-induced Hypertension

Pérez-Chada, D.; Videla, A.J.; O'Flaherty, M.E.; Majul, C.; Catalini, A.M.; Caballer, C.A.; Franklin, K.A. Author Information

Fetal exposure to herpesviruses may be associated with pregnancy‐induced hypertensive disorders and preterm birth in a Caucasian population*

Objective To investigate the role of fetal viral infection in the development of a range of adverse pregnancy outcomes (APOs), including pregnancy‐induced hypertensive disorders (PIHD), antepartum haemorrhage (APH), birthweight <10th percentile (small for gestational age, SGA) and preterm birth (PTB). Design Population‐based case–control study. Setting Laboratory‐based study. Population The newborn screening cards of 717 adverse pregnancy cases and 609 controls. Methods Newborn screening cards were tested for RNA from enteroviruses and DNA from herpesviruses using polymerase chain reaction (PCR). The herpesviruses were detected using two PCRs, one detecting nucleic acids from herpes simplex virus (HSV)‐1, HSV‐2, Epstein–Barr virus (EBV), cytomegalovirus (CMV) and human herpesvirus (HHV)‐8, hereafter designated Herpes PCR group A viruses, and the other detecting nucleic acids from varicella‐zoster virus (VZV), HHV‐6 and HHV‐7, hereafter designated Herpes PCR group B viruses. Main outcome measure Odds ratios and 95% CIs for specific APOs. Results For both term and PTBs, the risk of developing PIHD was increased in the presence of DNA from Herpes PCR group B viruses (OR 3.57, 95% CI 1.10–11.70), CMV (OR 3.89, 95% CI 1.67–9.06), any herpesvirus (OR 5.70, 95% CI 1.85–17.57) and any virus (OR 5.17, 95% CI 1.68–15.94). The presence of CMV was associated with PTB (OR 1.61, 95% CI 1.14–2.27). No significant association was observed between SGA or APH and exposure to viral infection. Conclusions Fetal exposure to herpesvirus infection was associated with PIHD for both term and PTBs in this exploratory study. Exposure to CMV may also be associated with PTB. These findings need confirmation in future studies.

Snoring, Witnessed Sleep Apneas, and Pregnancy-Induced Hypertension

As many as 1 in 4 pregnant women snore habitually in the last week of pregnancy, and a study from Sweden has claimed an increased risk of both pregnancy-induced hypertension and fetal growth retardation in such women. The present study examined the association between self-reported snoring and witnessed sleep apneas on the one hand and pregnancy-induced hypertensive disease on the other in an Argentinian population of 447 women with singleton pregnancies who responded to a questionnaire administered on the day of delivery. Habitual snoring was reported by 7% of respondents, whereas more than one-fourth of those questioned (28%) acknowledged snoring at some time during pregnancy. Women who snored were more obese before pregnancy, gained more weight during gestation, and reported more frequently witnessed apnea than women who did not snore. In addition, snorers more often experienced daytime sleepiness. None of the women had used sedatives while pregnant. Pregnancy-induced hypertensive disease was documented in 42% of women who had snored at some time during pregnancy and in 27% of those who had never snored. The crude odds ratio (OR) for pregnancy-induced hypertensive disease in snorers was 2.01 (95% confidence interval [CI], 1.33–3.06), and increased with the frequency of snoring. The OR was 1.82 (95% CI, 1.16–2.84) when adjusting for prepregnancy body mass index, weight gain, smoking, alcohol use, and age. Witnessed sleep apneas also were associated with pregnancy-induced hypertension (OR, 8.00; 95% CI, 1.72–23.55). No relationship was found between snoring and delivery of a small-for-gestational-age infant. These findings lead the investigators to believe that snoring or sleep apnea could help to explain the development of pregnancy-induced hypertensive disorders in obese women.