Tachysystole and risk of cesarean section after labor induction using misoprostol: A cohort study.

OBJECTIVES: To investigate if tachysystole was associated with an increased risk of cesarean section or unfavorable maternal or neonatal outcomes following induction of labor by misoprostol vaginal inserts. STUDY DESIGN: We conducted a retrospective cohort study of 446 women over 37 weeks of gestation admitted for labor induction by misoprostol vaginal inserts between May 2016 and May 2017. Fetal heart rate and uterine activity tracings were assessed for tachysystole, defined as ≥ 6 contractions per 10 min, averaged over a 30-minute window. Univariate analysis was performed by using t-test and Chi-square, comparing demographics, pregnancy characteristics, intrapartum monitoring, mode of delivery, neonatal outcomes (Apgar score < 7 at 5 min, umbilical cord artery pH < 7.10, neonatal intensive care unit admission) and maternal outcomes, with regard to the presence of tachysystole. The association between tachysystole and cesarean section was evaluated after adjusting for potential confounders by a modified Poisson regression model, expressed as an adjusted risk ratio and 95 % confidence intervals. RESULTS: A total of 140 women (31.4 %) presented with tachysystole. The median duration of tachysystole was 2 h 12 min. The rate of cesarean section was 25.0 % (N = 35) among patients with tachysystole and 19.6 % (N = 60) for those without tachysystole. Presence of tachysystole during induction of labor with misoprostol vaginal inserts was not associated with cesarean section (adjusted risk ratio,1.0; 95 % confidence interval, 0.7-1.4). Neonatal and maternal outcomes were similar between mothers who did and did not experience tachysystole. CONCLUSIONS: This study illustrates that tachysystole is not associated with an increased risk of cesarean section after induction of labor by misoprostol vaginal inserts. The impact of excessive uterine activity on the fetal wellbeing defined by the frequency of uterine contraction alone is probably insufficient. Further research on the development of accurate measures of uterine contractility is necessary to better understand its effect on fetal well-being.

Fetal Tachycardia Is an Independent Risk Factor for Chromosomal Anomalies in First-Trimester Genetic Screening.

OBJECTIVES: The association of an abnormal fetal heart rate (FHR) and chromosomal anomalies in the first trimester of pregnancy remains unclear, probably because of the lack of control for known confounding factors. This study was designed to determine whether an increased FHR is an independent risk factor for chromosomal anomalies between 11 and 14 weeks' gestation. METHODS: This cohort study included women who underwent first-trimester genetic screening between 2011 and 2014 at a single institution. A multivariable logistic regression analysis was performed to determine whether an FHR of 170 beats per minute (bpm) or higher, derived from a receiver operating characteristic curve, is an independent risk factor for all chromosomal anomalies while controlling for known confounding factors. P < .05 was considered significant. RESULTS: An FHR of 170 bpm or higher was observed in 7% (228 of 3254), and chromosomal anomalies were present in 1.0% (31 of 3254) of the population. A higher proportion of fetuses with an FHR of 170 bpm or higher had chromosomal anomalies compared to those with an FHR lower than 170 bpm. An FHR of 170 bpm or higher was an independent risk factor for chromosomal anomalies after controlling for known confounding factors. Of note, in the group of fetuses with a nuchal translucency above the 95th percentile, the frequency of chromosomal anomalies was significantly higher among fetuses with an FHR of 170 bpm or higher compared to those with an FHR lower than 170 bpm. CONCLUSIONS: Fetal tachycardia is a risk factor for chromosomal anomalies during first-trimester genetic screening, independent of increased nuchal translucency, nuchal septations, and maternal age.

Transient Fetal Tachycardia After Intravenous Diphenhydramine Administration.

BACKGROUND: Fetal tachycardia is attributable to a variety of etiologies, including an untreated maternal medical condition or an indicator of potential fetal compromise. Maternal medication administration may also affect the fetal heart rate. CASE: A 28-year-old nulliparous patient at 41 weeks of gestation was treated for pruritus with intravenous diphenhydramine after epidural administration of fentanyl. Within 14 minutes, the fetal heart rate increased from a baseline of 155 beats per minute (bpm) to more than 200 bpm while maintaining moderate variability. This was accompanied by an increase in uterine contractions occurring every 1.5 minutes. The fetal tachycardia lasted 51 minutes; several hours later, a healthy neonate was delivered. CONCLUSION: Diphenhydramine may produce transient fetal tachycardia as well as increased maternal uterine activity.

Transplacental digoxin therapy for fetal tachyarrhythmia with multiple evaluation systems.

BACKGROUND: Sustained fetal tachyarrhythmia may result in congestive heart failure, hydrops fetalis, and fetal/neonatal death, which requires timely and appropriate therapy. AIM: To determine the value of transplacental digoxin therapy for fetal tachyarrhythmia with multiple evaluations. METHODS: Four cases of fetal tachyarrhythmia were diagnosed with fetal echocardiography and treated with transplacental digoxin therapy with an initial dosage of 0.25 mg qd. Fetal echocardiography and measurement of maternal serum digoxin concentrations were performed every 5-7 days. Echocardiographic information was further used for the calculation of three evaluation systems including, Tei index, cardiovascular profile score (CVPS), and umbilical artery resistance index (UARI). The dosage of digoxin was adjusted according to the serum concentration, as well as results from three evaluation systems. RESULTS: During the course of digoxin treatment, our patients show an increase of CVPS and decrease of Tei index and UARI, suggesting the recovery of heart function. Sinus rhythm was restored in 3-10 days in three cases and 42 days in one case. At the time of delivery, the placental transportation efficiency (neonate/mother ratio of serum digoxin concentration) was 76.45-84.31%. Following delivery, the general conditions of neonates were favorable. During the 4- to 14-month follow-up, reoccurrence of arrhythmia, neurological deficit, and retarded growth and development were not observed. CONCLUSIONS: Transplacental digoxin therapy with combined evaluation of Tei index, CVPS, and UARI systems is useful for treating fetal atrial flutter (AF) and supraventricular tachycardia (SVT).

[Fetal tachyarrhythmia--current state of knowledge]. / Tachyarytmie u plodów--aktualny stan wiedzy.

Fetal tachyarrhythmia occurs in approximately 10% of all fetal arrhythmias. The majority of fetal tachyarrhythmias occur due to atrioventricular reentrant type of supraventricular tachycardia. A fetal tachycardic heart is at risk of developing low cardiac output, hydrops and ultimately fetal death or significant neurological morbidity. Reliable diagnosis of fetal tachyarrhythmia is possible by echocardiography and is crucial for a managed therapeutic approach. The goals of therapy for fetal tachyarrhythmias are to restore sinus rhythm, resolve heart failure and postpone delivery before term. A review of fetal tachyarrhythmias has been reported in our work.

Neonatal cholestasis associated with fetal arrhythmia.

We evaluated the consequence of different types of fetal arrhythmia in the development of neonatal cholestasis. The charts of 38 children born at St. Justine Hospital between 1993 and 2001 with sustained and hemodynamically significant fetal arrhythmias were studied: 19 with supraventricular tachycardia, 14 with atrial flutter, and 5 with atrio-ventricular (AV) block. Six of these 38 children presented with cholestasis. The average duration of arrhythmia was 15.7 days in the noncholestatic group, compared with 40.3 days in the cholestatic group ( P <.05). The three infants with supraventricular tachycardia who developed cholestasis survived and resolved their cholestasis, whereas 2 of 3 infants with AV block died. No infant with atrial flutter developed cholestasis. We conclude that newborns who developed tachyarrhythmia during their fetal life can show transient neonatal cholestasis. In patients with AV block, severe and irreversible liver failure could be observed. In addition, extensive collapse of the stroma and the absence of hepatocytes (foie vide) also were observed in a patient with anti-Ro antibodies.

The type B brevetoxin (PbTx-3) adversely affects development, cardiovascular function, and survival in Medaka (Oryzias latipes) embryos.

Brevetoxins are produced by the red tide dinoflagellate Karenia brevis. The toxins are lipophilic polyether toxins that elicit a myriad of effects depending on the route of exposure and the target organism. Brevetoxins are therefore broadly toxic to marine and estuarine animals. By mimicking the maternal route of exposure to the oocytes in finfish, we characterized the adverse effects of the type B brevetoxin brevetoxin-3 (PbTx-3) on embryonic fish development and survival. The Japanese rice fish, medaka (Oryzias latipes), was used as the experimental model in which individual eggs were exposed via microinjection to various known concentrations of PbTx-3 dissolved in an oil vehicle. Embryos injected with doses exceeding 1.0 ng/egg displayed tachycardia, hyperkinetic twitches in the form of sustained convulsions, spinal curvature, clumping of the erythrocytes, and decreased hatching success. Furthermore, fish dosed with toxin were often unable to hatch in the classic tail-first fashion and emerged head first, which resulted in partial hatches and death. We determined that the LD(50) (dose that is lethal to 50% of the fish) for an injected dose of PbTx-3 is 4.0 ng/egg. The results of this study complement previous studies of the developmental toxicity of the type A brevetoxin brevetoxin-1 (PbTx-1), by illustrating in vivo the differing affinities of the two congeners for cardiac sodium channels. Consequently, we observed differing cardiovascular responses in the embryos, wherein embryos exposed to PbTx-3 exhibited persistent tachycardia, whereas embryos exposed to PbTx-1 displayed bradycardia, the onset of which was delayed.

Fetal sinus bradycardia and the long QT syndrome.

OBJECTIVE: Recent evidence in literature shows that the long QT syndrome accounts for a fraction of the sudden infant death syndrome. Newborn infants with prolongation of the Q-T interval often show sinus bradycardia, which led us to test whether children who were diagnosed with long QT syndrome also show sinus bradycardia in the cardiotocogram before birth. STUDY DESIGN: We identified 18 children who were born from singleton pregnancies at or near term in whom long QT syndrome (corrected QT interval, >0.440 second) was diagnosed after birth or in childhood. Cardiograms during pregnancy and delivery were available from 17 of the 18 children. RESULTS: The cardiotocogram showed persistent fetal sinus bradycardia (baseline heart rate permanently below 120 beats/min) in 12 of 17 fetuses (71%) with long QT syndrome. Two fetuses had additional intermittent tachyarrhythmias. CONCLUSION: Sinus bradycardia in the cardiotocogram during delivery or in pregnancy may indicate long QT syndrome in the fetus. Postnatal electrocardiography should be performed in these children to rule out or confirm a prolongation of the Q-T interval.

[Bundle of His tachycardia and chronic reciprocating rhythm: rare forms of prenatal tachycardia]. / Tachycardie hissienne et rythme réciproque chronique. Formes rares de tachycardie anténatale.

In cases of permanent tachycardia, ante-natal diagnosis of chronic reciprocating rhythms with long RP' intervals or His bundle tachycardias is difficult. The authors report two cases of permanent foetal tachycardia with 1/1 atrioventricular conduction. In one case, the tachycardia rate was 170/min with anasarca treated by amiodarone in view of a family history of His bundle tachycardia. In the other case, the tachycardia rate was 200/min but with no signs of cardiac failure and was, therefore, not treated. The ECG at birth confirmed the diagnosis of His bundle tachycardia in the first case and identified a chronic reciprocating rhythm in the other.

Does the onset of neonatal seizures correlate with the timing of fetal neurologic injury?

The onset of seizures after birth has been considered evidence of an intrapartum asphyxial event. The present study was undertaken to determine whether the timing of neonatal seizures after birth correlated with the timing of a fetal asphyxial event. Thus, singleton term infants diagnosed with hypoxic ischemic encephalopathy and permanent brain injury had a mean birth to seizure onset interval of 9.8 +/- 17.7 (range 1-90) hours. When these infants were categorized according to their fetal heart rate (FHR) patterns, the acute group (normal FHR followed by a sudden prolonged FHR deceleration that continued until delivery) tended to have earlier seizures than infants did within the tachycardia group (normal FHR followed by tachycardia, repetitive decelerations, and diminished variability) and the preadmission group (persistent nonreactive FHR pattern intrapartum). These seizure intervals were as follows: acute, 6.6 +/- 18.0 (range 1-90) hours; tachycardia, 11.1 +/- 17.1 (range 1-61) hours; and preadmission, 11.8 +/- 17.9 (range 1-79) hours (p < 0.05). But the range varied widely and no group was categorically distinct. In conclusion, the onset of neonatal seizures after birth does not, in and of itself, appear to be a reliable indicator of the timing of fetal neurologic injury.

[Modification of transplacental digoxin transfer in the isolated placental lobule]. / Einflussfaktoren des transplazentaren Digoxintransfers im isolierten Plazentalobulus.

Digoxin is widely used in the transplacental therapy of fetal tachyarrhythmia. Unfortunately, in cases with severe cardiac insufficiency and hydrops fetalis, transplacental passage of digoxin is often hampered and therapy therefore ineffective. The present study was designed to establish the isolated placental lobule to quantify transplacental digoxin passage under different experimental conditions. Ten human placentas were obtained immediately after delivery, and a lobule was dually perfused after cannulating a small artery and vein of the chorionic plate and piercing four catheters through the corresponding basal plate. Flow rates were 12 ml/min in the maternal circuit and 6 (I) respectively 3 ml/min (II) in the fetal circuit. The maternal circuit was spiked with digoxin to 6.18 +/- 0.40 ng/ml, and transplacental passage was calculated from repeated fetal and maternal perfusate samples (Fluorescence-Polarization-Immunoassay; TDx, Abbott Laboratories). Within three hours of recirculating perfusion with a fetal flow rate of 6 ml/min (I), digoxin concentrations in the maternal circuit (400 ml) declined to 3.56 +/- 0.09 ng/ml, whereas digoxin levels in the fetal compartment (200 ml) increased to 2.58 +/- 0.37 ng/ml. With a fetal perfusion rate of 3 ml/min (II), the efflux of digoxin out of the maternal circuit was lower (p < 0.05) and the influx in the total compartment was reduced (fetal digoxin concentrations reached only 26.9 +/- 10.6% vs. 39.1 +/- 5.5% of the initial maternal digoxin concentrations). These data suggest that severe fetal cardiac insufficiency with reduced placental perfusion may be in part responsible for the decrease of transplacental digoxin passage in fetuses with hydrops.

Intra-uterine tachycardia associated with multicystic encephalomalacia (MCE).

Multiple cystic brain lesions in neonates have been described as a result of a variety of causes. All events described thus far in association with multicystic encephalomalacia (MCE) seem to point to hypoxic-ischaemic injury as the common factor for this particular form of central nervous system damage. We describe a neonate in whom repeated, prolonged episodes of intrauterine tachycardia had been documented. Congestive heart failure and fetal hydrops were present at birth and MCE at the age of 13 wk. The obvious relationship between this child's intrauterine tachycardia and his MCE points to the fact that any fetus with prolonged tachycardia should be considered at risk of severe brain damage.

In utero diagnosis and management of fetal tachypnea. A case report.

Fetal tachypnea, defined as more than 60 fetal breaths per minute, has been reported to occur almost always in diabetic pregnancies. We treated a patient for fetal tachypnea and tachycardia, the initial presentation of which led to the diagnosis of diabetes mellitus.

Fetal supraventricular tachycardia: prenatal diagnosis and pharmacological reversal of associated hydrops fetalis.

Intrauterine fetal supraventricular tachycardia is a rare condition often associated with the syndrome of nonimmune hydrops fetalis. When the fetus is preterm it is vital to treat the arrhythmia with maternally administered drugs and different regimens have been reported in the literature. We report 1 case of this arrhythmia successfully treated in utero with maternally administered digoxin resulting in complete reversal of the hydrops fetalis and the birth of a healthy baby. A review of the relevant literature is brought forth.

Cardiac malformations presenting as congenital atrial flutter.

A case of congenital atrial flutter with tetralogy of Fallot is presented. Fetal tachycardia was detected three weeks prior to birth and digitalization converted the arrhythmia to a normal sinus rhythm at two days of age. The seven previously reported cases of congenital atrial flutter associated with congenitally malformed hearts are reviewed.