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Sir,

We thank A. Butwick and R. Dyer1 for their interest in our paper ‘ST depression at caesarean section and the relation to oxytocin dose. A randomised controlled trial’,2 and we wish to respond to their comments.

Practice regarding the administration of oxytocin for caesarean section varies widely. In Sweden an intravenous (i.v.) bolus is common. During the preparatory work of this study in 2004, a questionnaire was sent to the majority of the obstetric units in Sweden, and we found that 70% administered an i.v. bolus of 10 iu oxytocin, 21% administered an i.v. bolus of 5 iu oxytocin, and that infusions were rare. Thus, the use of 10 iu of oxytocin in the study reflected the routine in Sweden at that time.

Additional oxytocin, as well as other uterotonics, were spaced out from the initial oxytocin bolus (11 minutes in mean), and in the event of the occurrence of ST depression it had resolved within that time. Therefore, we do not think that the requirement of additional oxytocin limited the comparison of ST changes between groups.

Oxytocin was diluted with normal saline to a total volume of 10 ml and then given as an i.v. bolus dose in 1 minute. ST changes occurred within 120 seconds of the bolus, and as electrocardiograms (ECGs) were recorded by continuous ambulatory ECG monitoring, these observations are accurate and could not have occurred earlier. In the study by Svanstrom et al.,3 oxytocin was undiluted, and was given as a quick bolus over a few seconds, which could explain the difference in time of occurrence.

We agree to the fact that atropine use was relatively high in this study, and it cannot be excluded that the effects of atropine may have had an influence on outcome variables. However, there was no difference in the number or quantity of doses between groups. The timing of atropine administration was 11 ± 4 versus 16 ± 7 minutes (mean ± SD) prior to delivery in the 5- and 10-iu groups, respectively (P = 0.1).

We did not find a reason to stop the study after the interim analysis, despite the high prevalence of ST depressions, as the calculation was uncertain, there were only a few cases with an elevation of troponin I, and, as pointed out previously, the use of 10 iu oxytocin was common practice in Sweden at that time. The procedure used for the sample size calculation could possibly have biased the results in favour of a type-I error, which was addressed as a limitation to the study.

The aim of our study was to investigate whether there was a difference in the rate of ECG changes indicating myocardial ischemia between two different doses of oxytocin, and not to investigate the optimal dose of oxytocin for maintenance of uterine tone. Valuable studies on these issues have shown that oxytocin bolus doses can be reduced or omitted in the non-labouring women, although the requirement of additional uterotonics is not uncommon in these low-dose regimens.4–6

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