• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • br Case report A year


    Case report A 34-year-old Japanese woman, gravida 0, was admitted to the hospital for preterm labor at 24 weeks\' gestation. She was administered intravenous magnesium sulfate therapy for drug-induced liver injury caused by intravenous ritodrine hydrochloride. Five days later, the fetal heart rate dropped to 80–100bpm from its initial rate of 150bpm. She was then referred to our center for fetal bradycardia at 25 weeks\' gestation. Fetal echocardiography revealed a structurally normal heart with no extracardiac anomaly. There was no indication of fetal heart dysfunction or hydrops. The trigeminal rhythm of the blocked premature atrial contractions was shown to be fetal arrhythmia by Doppler echocardiography (Fig. 1). Intravenous magnesium sulfate administration was continued, since it is a commonly used tocolysis agent in Japan. Fetal magnetocardiography showed trigeminy and quadrigeminy of the blocked premature atrial contractions at 29 weeks\' BMI1 inhibitor (Fig. 2). The estimated PQ interval was 80ms. The magnesium sulfate dose was kept at 1.0g/h and the maternal serum ionized magnesium level was stabilized at 1.2–1.4mmol/L. Intravenous magnesium sulfate was discontinued after premature rupture of the membranes at 30 weeks\' gestation. Intrapartum cardiotocography findings indicated a baseline fetal heart rate of 120bpm with moderate variability. The patient went into labor and delivered a 1478g male infant. The newborn\'s 1- and 5-min Apgar scores were 7 and 8, respectively, and his umbilical artery pH was 7.37. The neonatal course was unremarkable and no ventilator support was required. No further arrhythmia was detected after birth. The maternal serum ionized magnesium level reduced to 0.65mmol/L at delivery, 10h after magnesium sulfate was discontinued. Maternal electrocardiography findings were unaltered regardless of the magnesium levels.
    Discussion Magnesium sulfate is well known to decrease the baseline fetal heart rate [2–4]. Hamersley et al. described a case of a dose-related decrease in the baseline fetal heart rate associated with magnesium sulfate administration [10]. As an endogenous calcium antagonist, magnesium slows the electrical activity of the sinoatrial node and prolongs atrioventricular conductance. Furthermore, it increases the refractory period of the atrioventricular node without major changes in ventricular physiology [11–13]. Studies on the effects of magnesium on fetal heart rate characteristics have reported a substantial decrease of 2–15bpm in the baseline fetal heart rate [2–4]. Under the normal conditions, magnesium has varying effects on fetal heart rate patterns with a lower baseline fetal heart rate within the normal range of 110–160bpm. In our case, magnesium might have created a “de novo” blocked premature atrial contraction. However, there are no reports of magnesium-induced “de novo” premature contractions in either children or adults. Therefore, we speculate that the fetus initially had bigeminy or trigeminy of premature atrial contractions with a coupled QRS complex and that magnesium changed the timing of the premature atrial contraction to occur during the refractory period of the ventricle to induce fetal bradyarrhythmia. Consequently, the baseline fetal heart rate dropped to <100bpm after magnesium sulfate administration. Although the origin of the fetal premature atrial contraction was unclear, this condition spontaneously resolved, as is often the case, and did not appear to have any detrimental effects either during pregnancy or during the neonatal period [10,14]. On the other hand, the maternal electrocardiography findings were unaltered regardless of the magnesium levels. Magnesium readily crosses the placenta, and fetal blood magnesium levels correlate well with maternal levels [4]; therefore, we suggest that the fetal cardiac conductance system is more susceptible to magnesium sulfate than the maternal system.