Maternal and fetal effects of low-dosage bupivacaine paracervical block

Publisher Website
Google Scholar
Abstract
Vasoconstriction of the uterine arteries, hypertonus of the uterus, and the direct toxic effects of a local anesthetic on the fetus, or a combination of the above, have been presented as etiological factors of fetal bradycardia following paracervical block. To reduce fetal side-effects a superficial and low-dosage technique of PCB have been advocated. The effects of 25 mg of bupivacaine PCB using the above technique on fetal heart rate pattern (FHR), fetal acid-base balance, uterine activity, placental blood flow and maternal and fetal plasma levels of bipivacaine were studied in 38 patients. The analgesic effect of a single 25 mg of bupivacaine PCB was good in 76%, moderate in 12% and poor in 12% of the cases. No changes in maternal heart rate or in blood pressure were noted. Fetal bradycardia defined as a decrease of mean fetal heart rate of at least 20 bpm or an absolute rate < 100 bpm and a duration > 2 min occurred in 12% of the cases. The mean amplitude of the baseline fetal heart rate variability decreased significantly after PCB and a silent pattern (an amplitude < 5 bpm) was observed in 20% of the cases. The most frequent (27%) pathological finding in the study was the disappearance of FHR accelerations after PCB. Similarly early and late decelerations of FHR occurred more often after PCB than during the control period before the block. The fetal pH from scalp blood samples did not, on average, decrease after PCB, but did so in cases with fetal bradycardia. Intervillous blood flow as measured by the 133Xe washout method did not change when measured before and after PCB. In addition in 3 cases with fetal bradycardia the changes in the intervillous blood flow were minimal. No significant changes in the mean uterine tone, amplitude and frequency of contractions were observed after PCB. An obvious uterine hypertonus was observed after PCB was observed in 3 cases of fetal bradycardia, but not in 2 other cases of bradycardia or in the 8 cases of silent FHR pattern. Mean maternal bupivacaine concentration 20 min after PCB was 0.14 .+-. 0.06 .mu.g/ml and 0.07 .+-. 0.04 .mu.g/ml at birth. Simultaneous fetal and umbilical venous and arterial concentrations were correspondingly 0.04 .+-. 0.02 .mu.g/ml, 0.03 .+-. 0.01 .mu.g/ml and 0.03 .+-. 0.01 .mu.g/ml, and they were significantly lower than respective maternal concentrations. It seems possible to decrease fetal and maternal levels of bupivacaine by using a low dosage and superficial injection technique without loosing anything of the analgesic effect. Several significant changes in fetal heart rate pattern can occur. About 1/3 of the block were associated with noticeable FHR changes in the present series. The etiopathology of FHR changes in connection with PCB is obviously multifactorial. According to observations the most important factor in these mechanisms seems to be the rapid transplacental passage of the local anesthetic into fetal circulation. A decrease in placental blood flow after PCB was not found even in cases with fetal bradycardia. Then the initial bradycardia obviously represents a direct toxic effect of bupivacaine on the regulatory centers of the fetal heart rate. Disappearance of FHR accelerations and the decrease of FHR variability observed represent a pharacological effect of bupivacaine at fetal level. In some cases uterine hypertonus following PCB may be an additional etiological factor of fetal bradycardia. It seems possible that even after carefully applied PCB a rapid absorption of the local anesthetic agent may sometimes occur leading to an abrupt rise in the fetal blood concentrations and to fetal heart rate changes.

This publication has 10 references indexed in Scilit: