The impact of fetal umbilical artery Doppler pulsatility index on childhood respiratory function and atopy: a prospective case-control study.

Objective: To determine if an elevated fetal umbilical artery Doppler pulsatility index is associated with abnormal respiratory function and atopy in children aged 12 years.Methods: This prospective case-control study compared children that had an elevated fetal umbilical artery Doppler pulsatility index (>90th centile) to those with a normal pulsatility index (<90th centile). All subjects were delivered at full-term and with appropriate growth for gestational age. Outcome measures included; (i) presence of asthma and/or atopy; (ii) spirometry measurements and (iii) serum C-reactive protein and leptin. Multiple regression was used to account for parental smoking, childhood age, gender and socioeconomic status.Results: 174 children with an average age of 12.1 (±0.6 SD), 48% of who were male were included in the analysis. Of the 174, 99 (57%) were in the normal umbilical artery Doppler pulsatility index group and 75 (43%) elevated umbilical artery Doppler pulsatility index groups. The overall proportion of subjects with asthma was 28% (48/174) and atopy 56% (98/174). No association was found between elevated fetal umbilical artery Doppler pulsatility index and asthma (p = .47) or atopy (p = .75) at age 12 years. Similarly there was no association between FEV1(%) (p = .96), forced vital capacity (FVC)(%) (p = .98), elevated serum C-reactive protein (p = .69) or leptin (p = .20) and an elevated fetal umbilical artery Doppler pulsatility index.Conclusions: An elevated umbilical artery Doppler at 28-weeks gestation in the absence of prematurity or fetal growth restriction is not associated with altered respiratory function or the presence of atopy in children aged 12 years. These findings support the theory that such disease has a multifactorial pathophysiology.

Unrecognized maternal heart rate artefact in cases of perinatal mortality reported to the United States Food and Drug Administration from 2009 to 2019: a critical patient safety issue.

BACKGROUND: Maternal heart rate artefact is a signal processing error whereby the fetal heart rate is masked by the maternal pulse, potentially leading to danger by failure to recognize an abnormal fetal heart rate or a pre-existing fetal death. Maternal heart rate artefact may be exacerbated by autocorrelation algorithms in modern fetal monitors due to smooth transitions between maternal and fetal heart rates rather than breaks in the tracing. In response, manufacturers of cardiotocography monitors recommend verifying fetal life prior to monitoring and have developed safeguards including signal ambiguity detection technologies to simultaneously and continuously monitor the maternal and fetal heart rates. However, these safeguards are not emphasized in current cardiotocography clinical practice guidelines, potentially leading to a patient safety gap. METHODS: The United States Food and Drug Administration Manufacturer and User Facility Device Experience database was reviewed for records with event type "Death" for the time period March 31, 2009 to March 31, 2019, in combination with search terms selected to capture all cases reported involving cardiotocography devices. Records were reviewed to determine whether maternal heart rate artefact was probable and/or whether the report contained a recommendation from the device manufacturer regarding maternal heart rate artefact. RESULTS: Forty-seven cases of perinatal mortality were identified with probable maternal heart rate artefact including 14 with antepartum fetal death prior to initiation of cardiotocography, 14 with intrapartum fetal death or neonatal death after initiation of cardiotocography, and 19 where the temporal relationship between initiation of cardiotocography and death cannot be definitively established from the report. In 29 cases, there was a recommendation from the manufacturer regarding diagnosis and/or management of maternal heart rate artefact. CONCLUSIONS: This case series indicates a recurring problem with undetected maternal heart rate artefact leading to perinatal mortality and, in cases of pre-existing fetal death, healthcare provider confusion. In response, manufacturers frequently recommend safeguards which are found in their device's instructions for use but not in major intrapartum cardiotocography guidelines. Cardiotocography guidelines should be updated to include the latest safeguards against the risks of maternal heart rate artefact. An additional file summarizing key points for clinicians is included.

What is to blame for postnatal pelvic floor dysfunction in primiparous women-Pre-pregnancy or intrapartum risk factors?

BACKGROUND: The aetiology of pelvic floor dysfunction (PFD) is still poorly understood. However childbearing is recognized as a major risk factor. OBJECTIVES: To elucidate the natural history of PFD by investigating the impact of the mode of delivery on postnatal pelvic floor dysfunction in primiparas, when PFD existing before the first pregnancy is taken into consideration. STUDY DESIGN: 4P-study (Prevalence and Predictors of Pelvic floor dysfunction in Primips) is a prospective cohort study, nested within the Screening for Pregnancy Endpoints (SCOPE) study set in a tertiary referral teaching hospital with 9000 deliveries annually. Established and proposed risk factors for urinary, fecal, prolapse and sexual dysfunction and the severity of symptoms for each of these outcomes were assessed using the Australian Pelvic Floor Questionnaire in 1482 nulliparous women, who each completed the questionnaire in early pregnancy. Of these, 1060 (72%) repeated the questionnaire 12 months postpartum.Outcomes were analyzed using multivariate ordinal logistic regression. RESULTS: Significant (p<0.05) risk factors for postpartum PFD were pre-pregnancy presence of similar symptoms Odds Ratio (OR) (5.0-30.0), smoking (OR 2.2-4.6), recurrent UTI (OR 2.2-17.3), high hip circumference (OR1.4-1.6), vigorous exercising (OR 3.1-17.9), induction of labor (OR 1.5-2.3), forceps delivery (OR 1.8-8.8), and 3rd degree perineal tear (OR 2.4-2.7). Cesarean section was associated with a lower risk of stress urinary incontinence (OR 0.3-0.5). Other common pre-pregnancy significant (p<0.05) risk factors for various PFD types prior to the first pregnancy were: diagnosed depression - (OR 1.6-2.1), high BMI (OR 3.1), strenuous exercising (OR 1.3-2.2), recurrent UTI (OR 1.5-2.5) and lower educational achievement (OR 1.5-1.6). CONCLUSIONS: Pre-pregnancy PFD was mainly associated with modifiable risk factors such as smoking and exercising. The main risk factor for postpartum PFD was the presence of similar symptoms prior to pregnancy, followed by anthropometric and intrapartum factors. Hip circumference seems to be a better predictor of PFD compared to BMI. When pre-pregnancy PFD was included in the analysis, Cesarean section was protective only for stress urinary incontinence, while delivery by forceps increased the risk of prolapse.

Fetal umbilical artery Doppler pulsatility index and childhood neurocognitive outcome at 12†years.

OBJECTIVE: To determine whether an elevated fetal umbilical artery Doppler (UAD) pulsatility index (PI) at 28 weeks' gestation, in the absence of fetal growth restriction (FGR) and prematurity, is associated with adverse neurocognitive outcome in children aged 12 years. METHODS: Prospective cohort study, comparing children with a normal fetal UAD PI (<90th centile) (n=110) and those with an elevated PI (≥90th centile) (n=40). UAD was performed at 28, 32 and 34 weeks gestation. At 12 years of age, all children were assessed under standardised conditions at Queen's University, Belfast, UK to determine cognitive and behavioural outcomes using the British Ability Score-II and Achenbach Child Behavioural Checklist Parent Rated Version under standardised conditions. Regression analysis was performed, controlling for confounders such as gender, socioeconomic status and age at assessment. RESULTS: The mean age of follow-up was 12.4 years (±0.5 SD) with 44% of children male (n=63). When UAD was assessed at 28 weeks, the elevated fetal UAD group had lower scores in cognitive assessments of information processing and memory. Parameters included (1) recall of objects immediate verbal (p=0.002), (2) delayed verbal (p=0.008) and (3) recall of objects immediate spatial (p=0.0016). There were no significant differences between the Doppler groups at 32 or 34 weeks' gestation. CONCLUSIONS: An elevated UAD PI at 28 weeks' gestation in the absence of FGR or prematurity is associated with lower scores of declarative memory in children aged 12 years. A potential explanation for this is an element of placental insufficiency in the presence of the appropriately grown fetus, which affects the development of the fetal hippocampus and information processing and memory long-term. These findings, however, had no impact on overall academic ability, mental processing and reasoning or overall behavioural function.

Long-term flavor recognition in humans with prenatal garlic experience.

The human fetus learns about its chemosensory environment and this influences its behavior at birth and during the nursing period. This study examined whether prenatal experience could influence behavior much later in life. The dietary preference of two groups of children (8- to 9-years old) was examined. Mothers of one group had consumed garlic during pregnancy, mothers of the control group had not. Children received two tests, 1 month apart, of a meal containing two portions of potato gratin, one flavored with garlic. The total amount of potato, and the percentage of garlic flavored potato, eaten was calculated and examined separately by ANOVA for factors of prenatal exposure, the child's sex, and trial. Children prenatally exposed to garlic ate significantly more garlic flavored potato and a significantly greater overall amount of potato on trial 2, compared to controls. The results demonstrate prenatal experience may affect behavior well into childhood.

Fetal brain function in response to maternal alcohol consumption: early evidence of damage.

BACKGROUND: Studies of the adverse neurobehavioral effects of maternal alcohol consumption on the fetus have been largely confined to the postnatal period, after exposure to alcohol has finished. This study explored the brain function of the fetus, at the time of exposure to alcohol, to examine its effect on information processing and stability of performance. METHODS: Five groups of fetuses, defined by maternal alcohol consumption patterns, were examined: control (no alcohol); moderate (5 to 10 units/wk either drunk evenly across the week or as a binge, in 2 to 3 days); heavy (20+ units/wk drunk evenly or as a binge). Fetal habituation performance was examined on 3 occasions, separated by 7 days, beginning at 35 weeks of gestation. The number of trials required to habituate on each test session and the difference in performance across test sessions were recorded. RESULTS: Fetuses exposed to heavy binge drinking required significantly more trials to habituate and exhibited a greater variability in performance across all test sessions than the other groups. Maternal drinking, either heavily but evenly or moderately as a binge, resulted in poorer habituation, and moderate binge drinking resulted in greater variability compared with no, or even, drinking. CONCLUSIONS: Decreased information processing, reflected by poorer habituation, and increased variability in performance may reflect the initial manifestations of structural damage caused by alcohol to the brain. These results will lead to a greater understanding of the effects of alcohol on the fetus's brain, enable the antenatal identification of fetal alcohol spectrum disorders, and lead to the early implementation of better management strategies.

Alcohol delays the emergence of the fetal elicited startle response, but only transiently.

Prenatal exposure to alcohol may exert a significant detrimental effect on the functioning of the individual's brain, however few studies have examined this before birth. This longitudinal study examined the effect of maternal alcohol consumption on the elicited startle response of the fetus. Two groups of fetuses were examined: one whose mothers drank alcohol (approximately 10 units per week); the other whose mothers did not drink alcohol. Fetuses were examined at 29, 32 and 35 weeks gestation and their startle response observed using ultrasound in response to 2 presentations of a pink noise (70-250Hz) at 90dB(A) separated by 30s. Fetuses exposed to alcohol exhibited a weaker startle response at 29 weeks gestation than did fetuses not exposed to alcohol. There was no difference in the response at 32 and 35 weeks gestation. To ensure that the effects were not due to a more general effect of alcohol on fetal movement, a second experiment compared the spontaneous movements (observed on ultrasound for 45 min) of fetuses whose mothers drank alcohol and fetuses of mothers who didn't drink alcohol. There were no differences in movements exhibited by the fetuses. The results suggest that exposure to alcohol delays the emergence of the elicited startle response at 29 weeks gestation but this delay has disappeared by 32 weeks gestation. The possible role of altered neural development, acute exposure to alcohol and disruptions to the fetus's behavioural repertoire, in mediating these effects are discussed.

Sex differences in fetal habituation.

There is some evidence for sex differences in habituation in the human fetus, but it is unknown whether this is due to differences in central processing (habituation) or in more peripheral processes, sensory or motor, involved in the response. This study examined whether the sex of the fetus influenced auditory habituation at 33 weeks of gestation, and whether this was due to differences in habituation or in the sensory or motor components using a set of four experiments. The first experiment found that female fetuses required significantly fewer stimulus presentations to habituate than males. The second experiment revealed no difference in the spontaneous motor behaviour of male and female fetuses. The third experiment examined auditory intensity thresholds for the stimuli used to habituate the fetus. No differences in thresholds were found between males and females, although there was inter-individual variability in thresholds. A final experiment, using stimuli individualized for that particular fetus' auditory intensity threshold, found that female fetuses habituated faster than males. In combination, the studies reveal that habituation in the human fetus is affected by sex and this is due to a difference in central 'information processing' of the stimuli rather than peripheral aspects of the response. It is argued that male and female fetuses present different neurobehavioural developmental trajectories, with females more advanced at 33 weeks than males. This study suggests that research examining prenatal behaviour should consider the factor of fetal sex. This may be particularly pertinent where there is an intention to use the results diagnostically.

Detection of foetal growth restriction using third trimester ultrasound.

Foetal growth restriction is an important contributor to perinatal mortality, being responsible for up to 50% of stillbirths. Optimal prevention and accurate detection enabling timely intervention remain elusive, particularly in presumed low-risk pregnancy. Third trimester ultrasound seems a logical solution, but systematic review of evidence from randomised trials has shown that third trimester ultrasound does not have a significant impact on perinatal mortality but may increase interventions such as caesarean delivery. However, the evidence is difficult to interpret in the context of current obstetric practice as the evolution of ultrasound technology and rapid assimilation of newer techniques has resulted in questionable validity of the findings. If third trimester ultrasound were introduced routinely, there is a need to decide the optimal timing and number of examinations and what ultrasound parameters should be used to identify the foetus at risk.

Maternal alcohol consumption during pregnancy may delay the development of spontaneous fetal startle behaviour.

Maternal alcohol consumption during pregnancy may delay the development of spontaneous fetal startle behaviour. Previous study indicated that fetuses exposed to alcohol exhibited a significantly higher incidence of spontaneous startles compared to fetuses not exposed at 20 weeks gestation. This study examined startle behaviour longitudinally from 20 to 35 weeks gestation to determine whether the previous results were due to 'developmental delay' or a 'permanent effect'. The number of spontaneous startles exhibited by fetuses of mothers who drank during pregnancy and fetuses whose mothers did not drink was recorded at 20, 25, 30 and 35 weeks gestation during a 45-min observation. The results indicate that exposure to alcohol during pregnancy significantly increases the exhibition of spontaneous startles by the fetus but across gestation there is significant catch-up in startle behaviour. The results suggest exposure to alcohol delays the natural maturation of spontaneous startle behaviour of the fetus but also has a smaller 'permanent' effect. It is suggested that these effects are mediated by alcohol exerting an effect on the inhibitory pathways controlling startle behaviour.

Maternal alcohol consumption during pregnancy and fetal startle behaviour.

The startle behaviour of the fetus (both spontaneous and elicited) was examined in fetuses of mothers who drank alcohol and mothers who did not. Fetuses exposed to alcohol showed a higher frequency of spontaneous startles and were less likely to exhibit a normal startle in response to a vibroacoustic stimulus. These differences illustrate a teratogenic effect of alcohol on CNS functioning in utero, possibly associated with brainstem damage.