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We would like to thank Dr Cooper for his interest in our article and appreciate his points about fetal acidosis.1
Our study was designed to determine the effective bolus dose of norepinephrine to prevent postspinal hypotension in elective cesarean delivery using the biased coin up-and-down design. Although the safety of any new proposed treatment is always a concern, our study was not powered to assess the safety of norepinephrine boluses by way of fetal blood gases or any other means. The arterial and venous gases presented in our article were reported as secondary outcomes. We acknowledge that the incidence of pH <7.2 seems high in comparison to the study on norepinephrine infusion2; however, a direct comparison between the studies is not possible. Although we are unable to explain the reason for this high incidence, the consensus at our institution is that a pH <7.1 is a cause for concern, which did not occur in any of the cases. This is in keeping with the clinical practice guidelines of the Society of Obstetricians and Gynaecologists of Canada.3 Additionally, base excess is likely a better indication of acidosis, such that the threshold for moderate or severe fetal complications is −12 mEq/L.4 Reassuringly, the umbilical artery base excess was not less than −12 mEq/L in any case.
The question of a uteroplacental versus a fetoplacental mechanism for the acidosis seen presents an interesting discussion. We analyzed our data and did indeed find a significant negative linear relationship between umbilical arterial pH and arteriovenous PCO2 difference as shown in the Figure. This finding may point to a fetoplacental mechanism5; however, as stated, our study was not powered to be able to assess this. Further study in this area would certainly provide some much-needed insight into the safety profile of norepinephrine.
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