ObjectiveThe objective of this study is to determine whether obstructive sleep apnea (OSA) is associated with reduced fetal growth, and whether nocturnal oxygen desaturation precipitates acute fetal heart rate changes.Study DesignWe performed a prospective observational study, screening 371 women in the second trimester for OSA symptoms. 41 subsequently underwent overnight sleep studies to diagnose OSA. Third trimester fetal growth was assessed using ultrasound. Fetal heart rate monitoring accompanied the sleep study. Cord blood was taken at delivery, to measure key regulators of fetal growth.ResultsOf 371 women screened, 108 (29%) were high risk for OSA. 26 high risk and 15 low risk women completed the longitudinal study; 14 had confirmed OSA (cases), and 27 were controls. The median (interquartile range) respiratory disturbance index (number of apnoeas, hypopnoeas or respiratory related arousals/hour of sleep) was 7.9 (6.1–13.8) for cases and 2.2 (1.3–3.5) for controls (p<0.001). Impaired fetal growth was observed in 43% (6/14) of cases, vs 11% (3/27) of controls (RR 2.67; 1.25–5.7; p = 0.04). Using logistic regression, only OSA (OR 6; 1.2–29.7, p = 0.03) and body mass index (OR 2.52; 1.09–5.80, p = 0.03) were significantly associated with impaired fetal growth. After adjusting for body mass index on multivariate analysis, the association between OSA and impaired fetal growth was not appreciably altered (OR 5.3; 0.93–30.34, p = 0.06), although just failed to achieve statistical significance. Prolonged fetal heart rate decelerations accompanied nocturnal oxygen desaturation in one fetus, subsequently found to be severely growth restricted. Fetal growth regulators showed changes in the expected direction- with IGF-1 lower, and IGFBP-1 and IGFBP-2 higher- in the cord blood of infants of cases vs controls, although were not significantly different.ConclusionOSA may be associated with reduced fetal growth in late pregnancy. Further evaluation is warranted to establish whether OSA may be an important contributor to adverse perinatal outcome, including stillbirth.

Sleep-disordered breathing (SDB) is reported commonly during pregnancy and is associated with an increased risk of adverse maternal and fetal outcomes, but the majority of these data are based upon self-report measures not validated for pregnancy. This study examined the predictive value of screening questionnaires for SDB administered at two time-points in pregnancy, and attempted to develop an 'optimized predictive model' for detecting SDB in pregnancy. A total of 380 women were recruited from an antenatal clinic in the second trimester of pregnancy. All participants completed the Berlin Questionnaire and the Multivariable Apnea Risk Index (MAP Index) at recruitment, with a subset of 43 women repeating the questionnaires at the time of polysomnog-raphy at 37 weeks' gestation. Fifteen of 43 (35%) women were confirmed to have a respiratory disturbance index (RDI) > 5 h À1. Prediction of an RDI > 5 h À1 was most accurate during the second trimester for both the Berlin Questionnaire (sensitivity 0.93, specificity 0.50, positive predictive value 0.50 and negative predictive value 0.93), and the MAP Index [area under the receiver operating characteristic (ROC) curve of 0.768]. A stepwise selection model identified snoring volume, a body mass index (BMI)≥32 kg m À2 and tiredness upon awakening as the strongest independent predictors of SDB during pregnancy; this model had an area under the ROC curve of 0.952. We conclude that existing clinical prediction models for SDB perform inadequately as a screening tool in pregnancy. The development of a highly predictive model from our data shows promise for a quick and easy screening tool to be validated for future use in pregnancy. IN TROD UCTI ON Self-reported symptoms of sleep-disordered breathing (SDB) such as snoring and witnessed obstructive apneas increase in frequency during pregnancy (Franklin et al., 2000; Pien et al., 2005); however, the accuracy of symptoms for detecting SDB in pregnancy is unclear. To date, there are no large studies that have confirmed a higher prevalence of SDB on polysomnography (PSG) among pregnant populations. The prevalence of SDB among pregnant women and the relationship of screening questionnaires to objectively confirmed SDB requires urgent clarification, given that preliminary studies suggest that SDB may increase the risk of adverse fetal and maternal outcomes, including hypertension, pre-eclampsia and impaired fetal growth (Bourjeily et al., 2010; Chen et al., 2011; Franklin et al., 2000). Clinical prediction models based on self-reported symptoms of SDB, along with demographic and anthropometric data, have been developed to identify and prioritize those at highest risk of having SDB. A number of prediction models for SDB have shown potential utility in clinical settings; however, they have been validated mainly in predominantly male and/or middle-aged populations (Chung et al., 2008; Netzer et al., 1999; Takegami et al., 2009), usually with suspected sleep difficulties (Maislin et al., 1995). Only two studies have commented on the pr...

This study compared self-reported sleep latency (SL) and total sleep time (TST) to objective measures on polysomnography (PSG) during pregnancy. Thirty-three women in the third trimester (T3) of pregnancy, 16 women in the first trimester (T1) of pregnancy, and 15 non-pregnant women underwent overnight PSG, and shortly after awakening reported their perceived SL and TST. Results showed that, on average, the T3 group slightly overestimated their TSTs, whereas the T1 and non-pregnant groups underestimated TSTs when compared with objective measurement. All groups overestimated SL, and perceived SL was closest to the first epoch of 10 min of uninterrupted sleep or the first epoch of slow-wave sleep, rather than the first epoch of sleep (the current definition used for diagnostic sleep studies). The wide variation in discrepancies between estimation and PSG measurement for both TST and SL shows that self-reports made by both pregnant and non-pregnant women tend to be unreliable, which has important implications both clinically and for the many studies based on self-reported sleep patterns in pregnancy.

Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper airway obstruction, resulting in hypoxemia, hypercapnia and sleep fragmentation. Pathophysiological sequelae include sympathetic activation, increased oxidative stress and a generalized inflammatory response, culminating in endothelial dysfunction. These are the proposed mechanisms that mediate the increased risk of hypertension and cardiovascular disease among patients with OSA outside of pregnancy. It is intriguing to consider the consequences of these events on pregnancy outcomes. There is a growing literature on the impact of maternal OSA on hypertensive disorders of pregnancy, gestational diabetes and impaired fetal growth. The data, while promising, require confirmation with larger numbers to verify the findings. OSA may be an important mediator of the poor perinatal outcomes associated with maternal obesity; moreover, one which may be amenable to treatment. This review discusses OSA and summarizes the current literature linking OSA with adverse perinatal outcomes.

Sleep-disordered breathing is more common in hypertensive disorders during pregnancy; however, most studies have not adequately accounted for the potential confounding impact of obesity. This study evaluated the frequency of sleep-disordered breathing in women with gestational hypertension and pre-eclampsia compared with body mass index- and gestation-matched normotensive pregnant women. Women diagnosed with gestational hypertension or pre-eclampsia underwent polysomnography shortly after diagnosis. Normotensive controls body mass index-matched within ±4 kg m underwent polysomnography within ±4 weeks of gestational age of their matched case. The mean body mass index and gestational age at polysomnography were successfully matched for 40 women with gestational hypertension/pre-eclampsia and 40 controls. The frequency of sleep-disordered breathing in the cases was 52.5% compared with 37.5% in the control group (P = 0.18), and the respiratory disturbance index overall did not differ (P = 0.20). However, more severe sleep-disordered breathing was more than twice as common in women with gestational hypertension or pre-eclampsia (35% versus 15%, P = 0.039). While more than half of women with a hypertensive disorder of pregnancy meet the clinical criteria for sleep-disordered breathing, it is also very common in normotensive women of similar body mass index. This underscores the importance of adjusting for obesity when exploring the relationship between sleep-disordered breathing and hypertension in pregnancy. More severe degrees of sleep-disordered breathing are significantly associated with gestational hypertension and pre-eclampsia, and sleep-disordered breathing may plausibly play a role in the pathophysiology of pregnancy hypertension in these women. This suggests that more severe sleep-disordered breathing is a potential therapeutic target for reducing the prevalence or severity of hypertensive disorders in pregnancy.