Autopsy-Based Growth Charts May under-Detect Fetal Growth Restriction at Autopsy.

Background: Accurate identification of fetal growth restriction in fetal autopsy is critical for assessing causes of death. We examined the impact of using a chart derived from ultrasound measurements of healthy fetuses (World Health Organization fetal growth chart) versus a chart commonly used by pathologists (Archie et al.) derived from fetal autopsy-based populations in diagnosing small-for-gestational-age (SGA) birth in perinatal deaths. Study Design: We examined perinatal deaths that underwent autopsy at BC Women's Hospital, 2015-2021. Weight centiles were assigned using the ultrasound-based fetal growth chart for birthweight and autopsy-based growth chart for autopsy weight. Results: Among 352 fetuses, 30% were SGA based on the ultrasound-based fetal growth chart versus 17% using the autopsy-based growth chart (p < 0.001). Weight centiles were lower when using the ultrasound-based versus autopsy-based growth chart (median difference of 9 centiles [IQR 2, 20]). Conclusions: Autopsy-based growth charts may under-classify SGA status compared to ultrasound-based fetal growth charts.

Improving the external validity of Antenatal Late Preterm Steroids trial findings.

BACKGROUND: The external validity of randomised trials can be compromised when trial participants differ from real-world populations. In the Antenatal Late Preterm Steroids (ALPS) trial of antenatal corticosteroids at late preterm ages, participants had systematically younger gestational ages than those outside the trial setting. As risk of respiratory morbidity (the primary trial outcome) is higher at younger gestations, absolute benefits of corticosteroids calculated in the trial population may overestimate real-world treatment benefits. OBJECTIVES: To estimate the real-world absolute risk reduction and number-needed-to-treat (NNT) for antenatal corticosteroids at late preterm ages, accounting for gestational age differences between the ALPS and real-world populations. METHODS: Individual participant data from the ALPS trial (which recruited 2831 women with imminent preterm birth at 34+0 to 36+5 weeks') was appended to population-based data for 15,741 women admitted for delivery between 34+0 and 36+5 weeks' from British Columbia, Canada, 2000-2013. We used logistic regression to calculate inverse odds of sampling weights for each trial participant and re-estimated treatment effects of corticosteroids on neonatal respiratory morbidity in ALPS participants, weighted to reflect the gestational age distribution of the population-based (real-world) sample. RESULTS: The real-world absolute risk reduction was estimated to be -2.2 (95% CI -4.6, 0.0) cases of respiratory morbidity per 100, compared with -2.8 (95% CI -5.3, -0.3) in original trial data. Corresponding NNTs were 46 in the real-world setting vs 35 in the trial. Our focus on absolute measures also highlighted that the benefits of antenatal corticosteroids may be meaningfully greater at 34 weeks vs. 36 weeks (e.g., risk reductions of -3.7 vs. -1.2 per 100 respectively). CONCLUSIONS: The absolute risk reductions and NNTs associated with antenatal corticosteroid administration at late preterm ages estimated in our study may be more appropriate for patient counselling as they better reflect the anticipated benefits of treatment when used in a real-world situation.

Technical Update No. 439: Antenatal Corticosteroids at Late Preterm Gestation.

OBJECTIVE: To update recommendations for administration of antenatal corticosteroids in the late preterm period. TARGET POPULATION: Pregnant individuals at risk of preterm birth from 340 to 366 weeks gestation. OPTIONS: Administration or non-administration of a single course of antenatal corticosteroids at 340 to 366 weeks gestation. OUTCOMES: Neonatal morbidity (respiratory distress, hypoglycemia), long-term neurodevelopment, and other long-term outcomes (growth, cardiac/metabolic, respiratory). BENEFITS, HARMS, AND COSTS: Administration of antenatal corticosteroids from 340 to 366 weeks gestation decreases the risk of neonatal respiratory distress but increases the risk of neonatal hypoglycemia. The long-term impacts of antenatal corticosteroid administration from 340 to 366 weeks gestation are uncertain. EVIDENCE: For evidence on the neonatal effects of antenatal corticosteroid administration at late preterm gestation, we summarized evidence from the 2020 Cochrane review of antenatal corticosteroids and combined this with evidence from published randomized trials identified by searching Ovid MEDLINE from January 1, 2020, to May 11, 2022. Given the absence of direct evidence on the impact of late preterm antenatal corticosteroid administration on neurodevelopmental outcomes, we summarized evidence on the impact of antenatal corticosteroids across gestational ages on neurodevelopmental outcomes using the following sources: (1) the 2020 Cochrane review; and (2) evidence obtained by searching Ovid MEDLINE, Embase, and Cochrane Central Register of Controlled Trials (CENTRAL) databases from inception to January 5, 2022. We did not apply date or language restrictions. Given the absence of direct evidence on the impact of late preterm antenatal corticosteroid administration on other long-term outcomes, we summarized evidence on the impact of antenatal corticosteroids across gestational ages on other long-term outcomes by combining findings from the 2020 Cochrane review with evidence obtained by searching Ovid MEDLINE for observational studies related to long-term cardiometabolic, respiratory, and growth effects of antenatal corticosteroids from inception to October 22, 2021. We reviewed reference lists of included studies and relevant systematic reviews for additional references. See Appendix A for search terms and summaries. VALIDATION METHODS: The authors rated the quality of evidence and strength of recommendations using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. See online Appendix B (Tables B1 for definitions and B2 for interpretations of strong and conditional [weak] recommendations). INTENDED AUDIENCE: Maternity care providers, including midwives, family physicians, and obstetricians. SUMMARY STATEMENTS: RECOMMENDATIONS.

Guideline No. 442: Fetal Growth Restriction: Screening, Diagnosis, and Management in Singleton Pregnancies.

OBJECTIVE: Fetal growth restriction is a common obstetrical complication that affects up to 10% of pregnancies in the general population and is most commonly due to underlying placental diseases. The purpose of this guideline is to provide summary statements and recommendations to support a clinical framework for effective screening, diagnosis, and management of pregnancies that are either at risk of or affected by fetal growth restriction. TARGET POPULATION: All pregnant patients with a singleton pregnancy. BENEFITS, HARMS, AND COSTS: Implementation of the recommendations in this guideline should increase clinician competency to detect fetal growth restriction and provide appropriate interventions. EVIDENCE: Published literature in English was retrieved through searches of PubMed or MEDLINE, CINAHL, and The Cochrane Library through to September 2022 using appropriate controlled vocabulary via MeSH terms (fetal growth retardation and small for gestational age) and key words (fetal growth, restriction, growth retardation, IUGR, FGR, low birth weight, small for gestational age, Doppler, placenta, pathology). Results were restricted to systematic reviews, randomized controlled trials/controlled clinical trials, and observational studies. Grey literature was identified through searching the websites of health technology assessment and health technology-related agencies, clinical practice guideline collections, clinical trial registries, and national and international medical specialty societies. VALIDATION METHODS: The authors rated the quality of evidence and strength of recommendations using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. See online Appendix A (Table A1 for definitions and Table A2 for interpretations of strong and conditional [weak] recommendations). INTENDED AUDIENCE: Obstetricians, family physicians, nurses, midwives, maternal-fetal medicine specialists, radiologists, and other health care providers who care for pregnant patients. TWEETABLE ABSTRACT: Updated guidelines on screening, diagnosis, and management of pregnancies at risk of or affected by FGR. SUMMARY STATEMENTS: RECOMMENDATIONS: Prediction of FGR Prevention of FGR Detection of FGR Investigations in Pregnancies with Suspected Fetal Growth Restriction Management of Early-Onset Fetal Growth Restriction Management of Late-Onset FGR Postpartum management and preconception counselling.

Directive clinique no 442 : Retard de croissance intra-utérin : Dépistage, diagnostic et prise en charge en contexte de grossesse monofœtale.

OBJECTIF: Le retard de croissance intra-utérin est une complication obstétricale fréquente qui touche jusqu'à 10 % des grossesses dans la population générale et qui est le plus souvent due à une pathologie placentaire sous-jacente. L'objectif de la présente directive clinique est de fournir des déclarations sommaires et des recommandations pour appuyer un protocole clinique de dépistage, diagnostic et prise en charge du retard de croissance intra-utérin pour les grossesses à risque ou atteintes. POPULATION CIBLE: Toutes les patientes enceintes menant une grossesse monofœtale. BéNéFICES, RISQUES ET COûTS: La mise en application des recommandations de la présente directive devrait améliorer la compétence des cliniciens quant à la détection du retard de croissance intra-utérin et à la réalisation des interventions indiquées. DONNéES PROBANTES: La littérature publiée a été colligée par des recherches effectuées jusqu'en septembre 2022 dans les bases de données PubMed, Medline, CINAHL et Cochrane Library en utilisant un vocabulaire contrôlé au moyen de termes MeSH pertinents (fetal growth retardation and small for gestational age) et de mots-clés (fetal growth, restriction, growth retardation, IUGR, FGR, low birth weight, small for gestational age, Doppler, placenta, pathology). Seuls les résultats de revues systématiques, d'essais cliniques randomisés ou comparatifs et d'études observationnelles ont été retenus. La littérature grise a été obtenue par des recherches menées dans des sites Web d'organismes s'intéressant à l'évaluation des technologies dans le domaine de la santé et d'organismes connexes, dans des collections de directives cliniques, des registres d'essais cliniques et des sites Web de sociétés de spécialité médicale nationales et internationales. MéTHODES DE VALIDATION: Les auteurs ont évalué la qualité des données probantes et la force des recommandations en utilisant le cadre méthodologique GRADE (Grading of Recommendations Assessment, Development and Evaluation). Voir l'annexe A en ligne (tableau A1 pour les définitions et tableau A2 pour l'interprétation des recommandations fortes et conditionnelles [faibles]). PROFESSIONNELS CONCERNéS: Obstétriciens, médecins de famille, infirmières, sages-femmes, spécialistes en médecine fœto-maternelle, radiologistes et autres professionnels de la santé qui prodiguent des soins aux patientes enceintes. RéSUMé POUR TWITTER: Mise à jour de la directive sur le dépistage, le diagnostic et la prise en charge du retard de croissance intra-utérin pour les grossesses à risque ou atteintes. DÉCLARATIONS SOMMAIRES: RECOMMANDATIONS: Prédiction du retard de croissance intra-utérin Prévention du retard de croissance intra-utérin Détection du retard de croissance intra-utérin Examens en cas de retard de croissance intra-utérin soupçonné Prise en charge du retard de croissance intra-utérin précoce Prise en charge du retard de croissance intra-utérin tardif Prise en charge du post-partum et consultations préconception.

Antenatal corticosteroid administration and attention-deficit/hyperactivity disorder in childhood: a regression discontinuity study.

BACKGROUND: Antenatal corticosteroids reduce respiratory morbidity in preterm infants, but their use during late preterm gestation (34-36 weeks) is limited because their safety for longer-term child neurodevelopment is unclear. We sought to determine if fetuses with higher probability of exposure to antenatal corticosteroids had increased rates of prescriptions for attention-deficit/hyperactivity disorder (ADHD) medication in childhood, using a quasiexperimental design that better controls for confounding than existing observational studies. METHODS: We identified 16 358 children whose birthing parents were admitted for delivery between 31 + 0 (31 weeks, 0 days) and 36 + 6 weeks' gestation in 2000-2013, using a perinatal data registry from British Columbia, Canada, and linked their records with population-based child ADHD medication data (2000-2018). We used a regression discontinuity design to capitalize on the fact that pregnancies presenting for delivery immediately before and immediately after the clinical cut-off for antenatal corticosteroid administration of 34 + 0 weeks' gestation have very different levels of exposure to corticosteroids, but are otherwise similar with respect to confounders. RESULTS: Over a median follow-up period of 9 years, 892 (5.5%) children had 1 or more dispensations of ADHD medication. Children whose birthing parents were admitted for delivery just before the corticosteroid clinical cut-off of 34 + 0 weeks' gestation did not appear to be more likely to be prescribed ADHD medication than those admitted just after the cut-off (rate ratio 1.1, 95% confidence interval [CI] 0.8 to 1.6; 1.3 excess cases per 100 children, 95% CI -2.5 to 5.7). INTERPRETATION: We found little evidence that children with higher probability of exposure to antenatal corticosteroids have higher rates of ADHD prescriptions in childhood, supporting the safety of antenatal corticosteroids for this neurodevelopmental outcome.

Which chart and which cut-point: deciding on the INTERGROWTH, World Health Organization, or Hadlock fetal growth chart.

OBJECTIVE: To determine how various centile cut points on the INTERGROWTH-21st (INTERGROWTH), World Health Organization (WHO), and Hadlock fetal growth charts predict perinatal morbidity/mortality, and how this relates to choosing a fetal growth chart for clinical use. METHODS: We linked antenatal ultrasound measurements for fetuses > 28 weeks' gestation from the British Columbia Women's hospital ultrasound unit with the provincial perinatal database. We estimated the risk of perinatal morbidity/mortality (decreased cord pH, neonatal seizures, hypoglycemia, and perinatal death) associated with select centiles on each fetal growth chart (the 3rd, 10th, the centile identifying 10% of the population, and the optimal cut-point by Youden's Index), and determined how well each centile predicted perinatal morbidity/mortality. RESULTS: Among 10,366 pregnancies, the 10th centile cut-point had a sensitivity of 11% (95% CI 8, 14), 13% (95% CI 10, 16), and 12% (95% CI 10, 16), to detect fetuses with perinatal morbidity/mortality on the INTERGROWTH, WHO, and Hadlock charts, respectively. All charts performed similarly in predicting perinatal morbidity/mortality (area under the curve [AUC] =0.54 for all three charts). The statistically optimal cut-points were the 39th, 31st, and 32nd centiles on the INTERGROWTH, WHO, and Hadlock charts respectively. CONCLUSION: The INTERGROWTH, WHO, and Hadlock fetal growth charts performed similarly in predicting perinatal morbidity/mortality, even when evaluating multiple cut points. Deciding which cut-point and chart to use may be guided by other considerations such as impact on workflow and how the chart was derived.

Should Fetal Growth Charts Be References or Standards?

BACKGROUND: Fetal growth standards (prescriptive charts derived from low-risk pregnancies) are theoretically better tools to monitor fetal growth than conventional references. We examined how modifying chart inclusion criteria influenced the resulting curves. METHODS: We summarized estimated fetal weight (EFW) distributions from a hospital's routine 32-week ultrasound in all nonanomalous singleton fetuses (reference) and in those without maternal-fetal conditions affecting fetal growth (standard). We calculated EFWs for the 3rd, 5th, 10th, and 50th percentiles, and the proportion of fetuses each chart classified as small for gestational age. RESULTS: Of 2309 fetuses in our reference, 690 (30%) met the standard's inclusion criteria. There were no meaningful differences between the EFW distributions of the reference and standard curves (50th percentile: 1989 g reference vs. 1968 g standard; 10th percentile: 1711 g reference vs. 1710 g standard), or the proportion of small for gestational age fetuses (both 9.9%). CONCLUSIONS: In our study, there was little practical difference between a fetal growth reference and standard for detecting small infants.

Short interpregnancy interval and pregnancy outcomes: How important is the timing of confounding variable ascertainment?

BACKGROUND: Estimation of causal effects of short interpregnancy interval on pregnancy outcomes may be confounded by time-varying factors. These confounders should be ascertained at or before delivery of the first ("index") pregnancy, but are often only measured at the subsequent pregnancy. OBJECTIVES: To quantify bias induced by adjusting for time-varying confounders ascertained at the subsequent (rather than the index) pregnancy in estimated effects of short interpregnancy interval on pregnancy outcomes. METHODS: We analysed linked records for births in British Columbia, Canada, 2004-2014, to women with ≥2 singleton pregnancies (n = 121 151). We used log binomial regression to compare short (<6, 6-11, 12-17 months) to 18-23-month reference intervals for 5 outcomes: perinatal mortality (stillbirth and neonatal death); small for gestational age (SGA) birth and preterm delivery (all, early, spontaneous). We calculated per cent differences between adjusted risk ratios (aRR) from two models with maternal age, low socio-economic status, body mass index, and smoking ascertained in the index pregnancy and the subsequent pregnancy. We considered relative per cent differences <5% minimal, 5%-9% modest, and ≥10% substantial. RESULTS: Adjustment for confounders measured at the subsequent pregnancy introduced modest bias towards the null for perinatal mortality aRRs for <6-month interpregnancy intervals [-9.7%, 95% confidence interval [CI] -15.3, -6.2). SGA aRRs were minimally biased towards the null (-1.1%, 95% CI -2.6, 0.8) for <6-month intervals. While early preterm delivery aRRs were substantially biased towards the null (-10.4%, 95% CI -14.0, -6.6) for <6-month interpregnancy intervals, bias was minimal for <6-month intervals for all preterm deliveries (-0.6%, 95% CI -2.0, 0.8) and spontaneous preterm deliveries (-1.3%, 95% CI -3.1, 0.1). For all outcomes, bias was attenuated and minimal for 6-11-month and 12-17-month interpregnancy intervals. CONCLUSION: These findings suggest that maternally linked pregnancy data may not be needed for appropriate confounder adjustment when studying the effects of short interpregnancy interval on pregnancy outcomes.

Etiologies and outcomes of prenatally diagnosed hyperechogenic kidneys.

OBJECTIVES: To determine etiologies and outcomes of fetal hyperechogenic kidneys (HEK). METHODS: We conducted a retrospective chart review of HEK in British Columbia (January 2013-December 2019) and literature review. RESULTS: We identified 20 cases of HEK without other anomalies (isolated) in our provincial cohort, one was lost to follow-up. Eight had testable genetic etiologies (autosomal dominant polycystic kidney disease [ADPKD], autosomal recessive polycystic kidney disease [ARPKD], Bardet-Biedl syndrome [BBS], and HNF1B-related disorder). The remaining seven did not have an identifiable genetic etiology. Of cases without a genetic etiology with postnatal follow-up (n = 6) there were no abnormalities of blood pressure, creatinine/estimated glomerular filtration rate or urinalysis identified with follow-up from 2-71 months. We report 11 cases with extrarenal anomalies (nonisolated), with outcomes and etiologies. We identified 224 reported cases of isolated HEK in the literature. A potentially testable genetic etiology was found in 128/224 (57.1%). The neonatal death rate in those with testable etiologies was 17/128 (13.3%) compared to 2/96 (2.1%) when testable etiologies were excluded. CONCLUSIONS: Genetic etiologies (ARPKD, ADPKD, BBS, HNF1B-related disorder, Beckwith-Wiedemann syndrome, tubular dysgenesis, familial nephroblastoma, and cytogenetic abnormalities) account for approximately half of prenatally isolated HEK; once excluded there are few neonatal deaths and short-term renal outcomes may be normal. There remains a paucity of knowledge about long-term renal outcomes.

Database Autopsy: An Efficient and Effective Confidential Enquiry into Maternal Deaths in Canada.

BACKGROUND: Maternal death surveillance in Canada relies on hospitalization data, which lacks information on the underlying cause of death. We developed a method for identifying underlying causes of maternal death, and quantified the frequency of maternal death by cause. METHODS: We used data from the Discharge Abstract Database for fiscal years 2013 to 2017 to identify women who died in Canadian hospitals (excluding Quebec) while pregnant or within 1 year of the end of pregnancy. A sequential narrative based on hospital admission(s) during and after pregnancy was constituted and reviewed to assign the underlying cause of death (based on the World Health Organization's framework). Maternal deaths (i.e., while pregnant or within 42 days after the end of pregnancy) and late maternal deaths (i.e., more than 42 days to a year after the end of pregnancy) were examined separately. RESULTS: We identified 85 maternal deaths. Direct obstetric causes included 8 deaths (9%) related to complications of spontaneous or induced abortion; 9 (11%), to hypertensive disorders of pregnancy; 15 (18%), to obstetric hemorrhage; 11 (13%), to pregnancy-related infection; 16 (19%), to other obstetric complications; and <5 (<6%), to complications of management. There were 21 (25%) maternal deaths with indirect obstetric causes, and <5 (<6%) with undetermined causes. Of 120 late maternal deaths, 16 (13%) had direct obstetric causes, among them, 9 deaths by suicide (56%). One hundred late maternal deaths (83%) had indirect obstetric causes; and <5 (<4%) had undetermined causes. CONCLUSIONS: The majority of maternal deaths in Canada have direct obstetric causes, whereas most late maternal deaths have indirect obstetric causes. Suicide is an important direct cause of late maternal death.

Antenatal corticosteroid administration and early school age child development: A regression discontinuity study in British Columbia, Canada.

BACKGROUND: There are growing concerns that antenatal corticosteroid administration may harm children's neurodevelopment. We investigated the safety of antenatal corticosteroid administration practices for children's overall developmental health (skills and behaviors) at early school age. METHODS AND FINDINGS: We linked population health and education databases from British Columbia (BC), Canada to identify a cohort of births admitted to hospital between 31 weeks, 0 days gestation (31+0 weeks), and 36+6 weeks, 2000 to 2013, with routine early school age child development testing. We used a regression discontinuity design to compare outcomes of infants admitted just before and just after the clinical threshold for corticosteroid administration of 34+0 weeks. We estimated the median difference in the overall Early Development Instrument (EDI) score and EDI subdomain scores, as well as risk differences (RDs) for special needs designation and developmental vulnerability (<10th percentile on 2 or more subdomains). The cohort included 5,562 births admitted between 31+0 and 36+6 weeks, with a median EDI score of 40/50. We found no evidence that antenatal corticosteroid administration practices were linked with altered child development at early school age: median EDI score difference of -0.5 [95% CI: -2.2 to 1.7] (p = 0.65), RD per 100 births for special needs designation -0.5 [-4.2 to 3.1] (p = 0.96) and for developmental vulnerability of 3.9 [95% CI:-2.2 to 10.0] (p = 0.24). A limitation of our study is that the regression discontinuity design estimates the effect of antenatal corticosteroid administration at the gestational age of the discontinuity, 34 + 0 weeks, so our results may become less generalisable as gestational age moves further away from this point. CONCLUSIONS: Our study did not find that that antenatal corticosteroid administration practices were associated with child development at early school age. Our findings may be useful for supporting clinical counseling about antenatal corticosteroids administration at late preterm gestation, when the balance of harms and benefits is less clear.

Infant and Maternal Outcomes for Women Who Experience Imprisonment in Ontario, Canada: A Retrospective Cohort Study.

OBJECTIVE: To describe the population-level risk of infant and maternal outcomes for women who experience imprisonment and compare outcomes with the general population. METHODS: We conducted a retrospective cohort study. We used linked correctional and health data for women released from provincial prisons in 2010. We defined three exposure groups for Ontario singleton deliveries from 2005-2015: deliveries to women who were in prison during pregnancy but not necessarily for delivery, prison pregnancies; deliveries to women who had been in prison but not while pregnant, prison controls; and general population deliveries. We compared groups using generalized estimating equations. Primary outcomes were preterm birth, low birth weight, and small for gestational age birth weight. Secondary outcomes included NICU admission, neonatal abstinence syndrome, placental abruption, and preterm prelabour rupture of membranes. RESULTS: In prison pregnancies (n = 544) and prison controls (n = 2156), respectively, preterm birth risk was 15.5% and 12.5%, low birth weight risk was 13.0% and 11.6%, and small for gestational age birth weight risk was 18.1% and 19.2%. Adjusted for maternal age and parity and compared with general population deliveries (N = 1 284 949), odds ratios were increased for prison pregnancies and prison controls, respectively, at 2.7 (95% CI 2.2-3.4) and 2.1 (95% CI 1.9-2.4) for preterm birth, 3.1 (95% CI 2.4-3.9) and 2.7 (95% CI 2.3-3.1) for low birth weight, and 1.6 (95% CI 1.3-2.1) and 1.8 (95% CI 1.6-2.0) for small for gestational age birth weight. CONCLUSION: There is an increased risk of adverse infant outcomes in women who experience imprisonment compared with the general population, whether they are in prison during pregnancy or not.

Short interpregnancy interval and poor fetal growth: Evaluating the role of pregnancy intention.

BACKGROUND: Previous studies have demonstrated that short interpregnancy interval (the interval between delivery and estimated last menstrual period of a subsequent pregnancy) is associated with small for gestational age birth. It is controversial if this association is causal, as few studies have accounted for likely confounding factors such as unintended pregnancy. We examined the association between interpregnancy interval and infant birthweight, adjusting for pregnancy intention and other socio-economic and obstetrical risk factors. METHODS: We used data from the Scandinavian Successive Small-for-Gestational-Age births study (1986-1988). Birthweight was expressed as a gestational age-standardised z-score. RESULTS: Among 1406 women, a trend towards lower birthweight z-score with short interpregnancy interval was not statistically significant (unadjusted difference in birthweight z-score of -0.25, 95% confidence interval (CI) -0.55, 0.05). After adjusting for pregnancy intention, detailed measures of socio-economic status, and other covariates, the estimated magnitude of effect between interpregnancy interval and birthweight z-score was further attenuated (adjusted difference in birthweight z-score of -0.13, 95% CI -0.46, 0.20). CONCLUSIONS: In this cohort study with detailed information on pregnancy intention and socio-economic status, short interpregnancy interval was not associated with lower birthweight. These findings suggest that previously observed associations between short interpregnancy interval and lower birthweight may reflect confounding by socio-economic and/or other unmeasured confounders.

A Common Language: What Exactly Does 34 Weeks Gestation Mean?

There are multiple conventions for gestational age notation, which lead to different interpretations of completed weeks. This variability is exemplified by the different gestational age ranges recommended for administration of antenatal corticosteroid prophylaxis. Antenatal corticosteroid prophylaxis is widely recommended for women at risk of preterm delivery up to 34 completed weeks gestation. According to the World Health Organization, 34 completed weeks refers to the time period from the first day of the last menstrual period (day zero) to 34 weeks and 6 days of gestation (i.e., to 34+6 34 weeks, or 244 days gestation). However, an alternative convention interprets 34 completed weeks as the period from the first day of the last menstrual period to 33+6 36 weeks' gestation (i.e., 237 days' gestation). These inconsistencies in gestational age notation may have led to different practice recommendations for antenatal corticosteroid prophylaxis worldwide. Agreeing on the World Health Organization notation and interpretation of completed weeks may help promote clear communication within our discipline and more precise and effective knowledge dissemination.

No. 364-Antenatal Corticosteroid Therapy for Improving Neonatal Outcomes.

OBJECTIVE: To assess the benefits and risks of antenatal corticosteroid therapy for women at risk of preterm birth or undergoing pre-labour Caesarean section at term and to make recommendations for improving neonatal and long-term outcomes. OPTIONS: To administer or withhold antenatal corticosteroid therapy for women at high risk of preterm birth or women undergoing pre-labour Caesarean section at term. OUTCOMES: Perinatal morbidity, including respiratory distress syndrome, intraventricular hemorrhage, bronchopulmonary dysplasia, infection, hypoglycemia, somatic and brain growth, and neurodevelopment; perinatal mortality; and maternal morbidity, including infection and adrenal suppression. INTENDED USERS: Maternity care providers including midwives, family physicians, and obstetricians. TARGET POPULATION: Pregnant women. EVIDENCE: Medline, PubMed, Embase, and the Cochrane Library were searched from inception to September 2017. Medical Subject Heading (MeSH) terms and key words related to pregnancy, prematurity, corticosteroids, and perinatal and neonatal mortality and morbidity were used. Statements from professional organizations including that of the National Institutes of Health, the American College of Obstetricians and Gynecologists, the Society for Maternal Fetal Medicine, the Royal College of Obstetricians and Gynaecologists, and the Canadian Pediatric Society were reviewed for additional references. Randomized controlled trials conducted in pregnant women evaluating antenatal corticosteroid therapy and previous systematic reviews on the topic were eligible. Evidence from systematic reviews of non-experimental (cohort) studies was also eligible. VALIDATION METHODS: This Committee Opinion has been reviewed and approved by the Maternal-Fetal Medicine Committee of the SOGC and approved by SOGC Council. BENEFITS, HARMS, AND/OR COSTS: A course of antenatal corticosteroid therapy administered within 7 days of delivery significantly reduces perinatal morbidity/mortality associated with preterm birth between 24 + 0 and 34 + 6 weeks gestation. When antenatal corticosteroid therapy is given more than 7 days prior to delivery or after 34 + 6 weeks gestation, the adverse effects may outweigh the benefits. Evidence on long-term effects is scarce, and potential neurodevelopment harms are unquantified in cases of late preterm, term, and repeated exposure to antenatal corticosteroid therapy. GUIDELINE UPDATE: Evidence will be reviewed 5 years after publication to evaluate the need for a complete or partial update of the guideline. If important evidence is published prior to the 5-year time point, an update will be issued to reflect new knowledge and recommendations. SPONSORS: The guideline was developed with resources provided by the Society of Obstetricians and Gynaecologists of Canada with support from the Canadian Institutes of Health Research (APR-126338). SUMMARY STATEMENTS: RECOMMENDATIONS: Gestational Age Considerations Agents, Dosage, Regimen, and Target Timing Subpopulations and Special Consideration.