To the Editor:
I read with interest the article by Lee et al.1 and the accompanying editorial by Farber and Bateman2 regarding the effects of maternal supine position during planned cesarean delivery with spinal anesthesia on neonatal acid-base status as well as on maternal blood pressure and cardiac output. I congratulate Lee et al.1 for their hard work in producing this demanding study to test the noninferiority of supine position during contemporary clinical use of a crystalloid coload and phenylephrine infusion. I have several points, however, that I wish to address regarding this study by Lee et al.
First, although the primary outcome of the study was mean umbilical artery base excess and the secondary outcomes were mean umbilical artery pH and umbilical vein base excess and pH, the authors did not describe their umbilical cord blood sampling procedure. It was not mentioned whether a segment of the umbilical cord was double-clamped. If only a single clamp was applied, the umbilical cord blood would remain in continuity with the placenta. The ongoing placental metabolism and gas exchange could result in changes in umbilical base excess and pH. Base excess significantly decreases (becomes more negative) after 20 min onward if the umbilical cord was not double-clamped and after 40 min onward if the umbilical cord was double-clamped. The pH steadily decreases after 60 s of delivery onward if the umbilical cord was not double-clamped; a difference of approximately 0.20 pH units may be reached by 60 min after delivery.3 In their protocol registered on www.ClinicalTrials.gov (NCT02243423), Lee et al. state that the time frame for their sample is within 2 h. Absence of data regarding the umbilical cord blood sampling procedure may make the results unreliable.
Second, it was mentioned in the Results section1 that the baseline cardiac output was 8.4 l/min in the tilted position versus 8.1 l/min in the supine position, resulting in a difference of 0.3 l/min and giving a P value of 0.002 using the paired t test. From figure 4,1 it seems that 8.4 l/min and 8.1 l/min are the mean cardiac output over the first 15 min after spinal anesthesia in the tilted and in the supine position respectively and not the baseline cardiac outputs as stated. From the same figure, it seems that baseline cardiac outputs are around 9.25 l/min. In addition, the correct test to be done is the unpaired t test. The explanation is that the paired t tests consider the differences between each paired observation when computing the P values while the unpaired t tests consider the differences in group means.4
Third, some variables that may influence the neonatal or maternal outcomes were not included in the study. Such confounding variables include induction-to-delivery interval and uterine incision-to-delivery interval for neonatal outcomes and include block height for maternal outcomes.
Fourth, a strange pharmacologic response occurred during treatment of the patient who had an acute drop in blood pressure to 44/22 mmHg with a heart rate of 130/min at 6 min after spinal anesthesia. The minute after receiving a single dose of ephedrine 10 mg intravenously, the patient’s blood pressure rebounded to 198/104 mmHg with a heart rate of 61/min. Ephedrine causes increase in the heart rate unlike what happened in the current incident. Is this due to a drug error wherein phenylephrine was given instead of ephedrine or due to a writing error?
Finally, the added examples to the American Society of Anesthesiologists (ASA) Physical Status Classification System approved by the ASA House of Delegates on October 15, 2014 considered pregnancy to be ASA II. The current study by Lee et al. stratified some pregnant patients as ASA I, which does not comply with the latest updates of the ASA Physical Status Classification System.5
Competing Interests
The author declares no competing interests.