Quantification of Posterior Risk Related to Intrapartum FIGO 2015 Criteria for Cardiotocography in the Second Stage of Labor

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 >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 >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 >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 >10 min to decelerations >5 min, recurrent later or prolonged decelerations >30 min, and nonpathological CTG.

Treatment of Fetal Arrhythmias

“…Unlike the postnatal setting, where analysis of the heart rhythm is done by electrocardiogram (ECG), the analysis of fetal heart rhythm is based on ultrasound [ 4 ]. Despite obvious limitations due to the difficult analysis of the fetal myocardial electric signal, a detailed analysis of fetal arrhythmia is possible using M-mode and Doppler echocardiography to assess mechanical processes [ 1 , 4 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ]. In the presence of a suspected or ascertained arrhythmia, the important features to be evaluated are: (1) FHR; (2) rhythm regularity; (3) the relation and time intervals of the atrial and ventricular contractions [ 13 ].…”

“…Pulsed Doppler echography is the method most used by fetal medicine specialists to assess the AV time intervals, on fetal echocardiography [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ]. For simultaneous recording of left ventricular inflow and outflow waveforms, a wide cursor (3–4 mm) is placed on the mitral and aortic valves, in the 5-chambers view of the heart.…”

“…In utero therapy options for fetal heart block include: beta-sympathomimetics; intravenous immunoglobulin and apheresis; and fluorinated glucocorticoids [ 2 , 67 , 68 ]. Hydroxychloroquine is used to prevent fetal heart block and neonatal lupus in women with anti-Ro/SSA or anti-La/SSB antibodies with a previous history of fetal heart block or neonatal lupus [ 12 , 14 ]. One study has shown a higher incidence of fetal AV block in winter months, implying that vitamin D maternal levels should be assessed, and deficiencies corrected [ 69 ].…”

“…This happens frequently in fetal growth restriction, oligohydramnios, or during labor and it is physiological up to a certain extent and duration. However, when the heart rate decreases below 80 bpm for more than 10 min in labor, the risk of neonatal acidemia increases rapidly and significantly [ 14 ]. Persistent bradycardia outside labor or in the absence of placental pathology is mainly due to atrioventricular block (AV block) [ 2 , 12 ].…”

“…Persistent bradycardia outside labor or in the absence of placental pathology is mainly due to atrioventricular block (AV block) [ 2 , 12 ]. Approximately fifty percent of fetal bradyarrhythmia cases are associated with structural heart defects, and the remaining cases that have normal cardiac structure are often caused by maternal anti-Ro/SSA antibodies [ 2 , 12 , 13 , 14 , 15 ]. The efficacy of treatment for fetuses with AV block is limited compared with that of treatment for fetal tachycardias, particularly when associated with structural defects [ 12 , 15 ].…”