No abstract

<b><i>Introduction:</i></b> Intrapartum cardiotocography (CTG) was used for several decades to detect a stressed fetus so that delivery can be expedited to prevent birth asphyxia. The main aim of the study was to calculate the risk of neonatal acidemia (pH ≤ 7.10) according to duration of the 2nd stage of labor and occurrence of the International Federation of Gynecology and Obstetrics (FIGO) 2015 CTG classification parameters. <b><i>Materials and Methods:</i></b> This was a retrospective case-control study on 552 pregnancies receiving continuous CTG monitoring in labor and immediate hemogasanalysis at birth. Cases with umbilical artery (UA) pH ≤ 7.10 and controls with UA pH ≥ 7.10 were matched for parity and gestational age at delivery, with ratio 1:5. Logistic regression analysis, adjusted for the expected risk in the general population, was used to calculate the baseline risk of UA pH ≤ 7.10 in the absence of any CTG pathological feature and those associated with pathological CTG patterns occurring in the 2nd stage according to FIGO 2015. <b><i>Results:</i></b> Seventy-three cases and 387 controls reached 2nd stage and were included in the analysis. For those reaching 2nd stage, the mean adjusted risk of acidemia associated with nonpathological CTG was 1.6%. Stratification of risk according to duration of the 2nd stage yielded risks of neonatal acidemia of 1.23, 2.08, 5.81, and 15.22% at 30, 60, 120, and 180 min, respectively. Bradycardia &#x3e;10 min was associated with risk of neonatal acidemia of 9.9 and 15.8% for 2nd-stage durations of 30 and 60 min, respectively. Risks associated with 1 prolonged deceleration &#x3e;5 min were 6.80, 11.08, 27.0, and 51.0% at 30, 60, 120, and 180 min, respectively. Repetitive late or prolonged decelerations &#x3e;30 min were associated with risk of neonatal acidemia of 2.43, 4.14, 11.17, and 26.45% at 30, 60, 120, and 180 min, respectively. <b><i>Conclusion:</i></b> The risk of neonatal acidemia is directly proportional to duration of the 2nd stage, irrespective of the presence of CTG abnormalities, increasing 12-fold (1.2–15.3%) from 30 to 180 min. Occurrence of FIGO 2015 pathological CTG patterns showed a decreasing impact from bradycardia &#x3e;10 min to decelerations &#x3e;5 min, recurrent later or prolonged decelerations &#x3e;30 min, and nonpathological CTG.

Right aortic arch presents a reported incidence of 0.1% of the general population; the aim of our study was to evaluate the risk of associated intracardiac (ICA), extracardiac (ECA), or chromosomal abnormalities in fetuses with right aortic arch (RAA) and concomitant right ductal arch (RDA). A systematic review of the literature selected 18 studies including 60 cases of RAA/RDA. A meta-analysis with a random effect model calculated for each outcome the pooled crude proportion of associated abnormal outcomes in cases of RAA/RDA and the pooled proportions and odds ratios in RAA with LDA or RDA. Quality assessment of the included studies was achieved using the NIH quality assessment tool for case series studies. RAA/RDA presents risk of associated conotruncal CHDs of about 30% and risk of 22q11 microdeletion in the region of 1%. Two-thirds of 22q11 microdeletions had concomitant thymic hypoplasia and no other chromosomal defects were described. Risks for ICA, ECA, 22q11 microdeletion, and aberrant left subclavian artery are not substantially different in RAA with right or left arterial duct. RAA increases the risk of associated cardiac defects regardless of laterality of the ductal arch. In isolated RDA/RAA cases, absolute risks of extracardiac associated problems or surgery are rather low, we would therefore recommend reassurance, particularly when the thymus and karyotype are normal.