1 Department of Anaesthesia and Intensive Care and 2 Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Hong Kong, China
*Corresponding author: Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong, China. E-mail: KimKhaw@cuhk.edu.hk Presented as a poster at The South African Society of Anaesthesiologists Congress, Sun City, South Africa, 1420 March 2003.
Accepted for publication: November 14, 2003
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Abstract |
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Methods. We allocated randomly 204 women having elective Caesarean section under spinal anaesthesia to breathe 21, 40 or 60% oxygen. We recorded the UD interval, umbilical arterial (UA) and venous (UV) blood gases and oxygen content and Apgar scores. Subgroup analysis was performed according to whether the UD interval was prolonged (>180 s) or not.
Results. The UD interval was <180 s in 159 patients and >180 s in 45 patients. There were no differences in UV or UA blood gases, oxygen content or Apgar scores between cases with and without a prolonged UD interval. In cases without a prolonged UD interval, administering 60% oxygen increased UV PO2 (mean 4.3 (SD 1.1) vs 3.7 (1.0) kPa, P=0.003) and oxygen content (14.4 (3.3) vs 12.9 (2.7) ml dl1, P=0.007) compared with air. In cases with a prolonged UD interval, administering 60% oxygen increased UV PO2 (4.6 (0.6) vs 3.9 (0.8) kPa, P=0.019) compared with air but there was no difference in UV oxygen content. There was no increase in the UV PO2 or oxygen content when 40% oxygen was administered compared with air.
Conclusions. Supplementary oxygen did not increase fetal oxygenation in cases where the UD interval was prolonged. Our data do not support the routine administration of supplementary oxygen during elective Caesarean section for this purpose.
Br J Anaesth 2004; 92: 51822
Keywords: anaesthesia, obstetric; anaesthetic techniques, subarachnoid; complications, acidosis; oxygen, supplementary; statistics, Apgar scores; surgery, Caesarean section; surgery, uterine incision to delivery
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Introduction |
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Materials and methods |
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Patients were allocated randomly, by drawing of shuffled opaque sealed envelopes, to breathe 21% (Group 21), 40% (Group 40) or 60% (Group 60) oxygen from the time of skin incision. Air or oxygen was supplied from a flowmeter to a masked high-flow Venturi-type facemask (Intersurgical, Wokingham, UK) to provide the assigned FIO2. Before each case, to maintain blinding of the investigators, an assistant connected the tubing from the flowmeters via an opaque relay box and confirmed the FIO2 using an oxygen analyser.
The times from starting oxygen supplementation to delivery, skin incision-to-delivery (ID) interval and UD interval were recorded using a stopwatch. A paediatrician who was unaware of group allocation attended each delivery and assessed Apgar scores.
Umbilical arterial (UA) and venous (UV) blood samples were collected into heparinized syringes from a segment of umbilical cord that was double-clamped before the infants first breath, and were analysed immediately. Blood gas analysis was performed using a Corning 278 pH/blood gas analyser (Medfield, MA, USA). Oxyhaemoglobin saturation and oxygen content were measured using an IL 682 Co-oximeter (Instrumentation Laboratory, Lexington, MA, USA) with correction for 70% fetal haemoglobin. The investigator performing all the blood analyses was blinded to patient allocation and did not participate in patient care. Results were recorded for analysis after completion of the study.
Identical management according to a set of predetermined protocols was provided by an anaesthetist who was blinded to the FIO2. Our contingency for patients who developed a pulse oximetry reading of <95% was to withdraw the patient from the study, and to administer the appropriate FIO2 to restore the oximetry reading to 95%. Such cases were noted, but were excluded from analysis. Hypotension, defined as a decrease in systolic arterial pressure by >20% from baseline or to <100 mm Hg,6 was treated with i.v. boluses of ephedrine 9 mg as required. Nausea and vomiting were treated with metoclopramide 10 mg i.v. once hypotension had been excluded.
Statistical analysis
Using previously recorded data, we estimated the mean and standard deviation of UV oxygen content to be 13.1 and 2.2 ml dl1 respectively. Prospective power analysis was performed to determine the number of cases with prolonged UD interval that would be required. This showed that a sample size of 13 patients in each group would yield 80% power to detect a 2.6 ml dl1 (20%) increase in oxygen content with a type I error probability of 0.05. This effect size of 2.6 ml dl1 was proposed on the basis of Ramanathans report of an increase in oxygen content by 2.74 ml dl1 when FIO2 was increased from 0.21 to 0.47.7 For the purposes of the study, the UD interval was defined a priori as being prolonged when it was >180 s, which is the magnitude shown previously by Datta and Bader et al. 3 4 as being associated with fetal acidosis. Thus, patients were recruited into the study continuously until the study termination criterion of having at least 13 patients with a prolonged UD interval in each group was reached. For analysis, patients were subdivided according to whether or not the UD interval was prolonged.
Intergroup comparisons were made using analysis of variance (ANOVA) and the KruskalWallis test with post hoc comparisons using the Tamhane and Bonferroni procedures. The 2 test for trend was used to assess any doseresponse relationship, and the association between the parameters (UV PO2 and UV oxyhaemoglobin saturation) were compared using multiple regression analysis and Pearson correlation. Results are presented as mean and standard deviation or median and range where appropriate. A value of P<0.05 was considered significant.
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Results |
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The indications for surgery are summarized in Table 1. Maternal characteristics, operative time intervals, incidence of hypotension and ephedrine consumption were similar among groups (Table 2). Maternal arterial oxyhaemoglobin saturation was maintained in all cases, with no case requiring a change in the assigned FIO2. Neonatal oxygen data and outcome are summarized in Tables 3 and 4.
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Patients with prolonged UD interval
The UV PO2 was significantly different among groups and was greater in Group 60 than in Group 21 (4.6 (0.6) vs 3.9 (0.8) kPa; mean difference 0.7 kPa, 95% CI of difference 0.131.30 kPa, P=0.019). The UV oxygen content and other blood gas measurements were similar among groups. No Apgar score was <7 at 1 or 5 min.
Combined patients
There was no difference in blood gas measurements, oxygen content or Apgar scores between cases with and without prolonged UD interval. The incidence of fetal acidosis, defined as UA pH <7.2, was similar between cases with and without a prolonged UD interval (4/45 (8.9%) vs 11/159 (6.9%), P=0.90). The overall incidence of fetal acidosis was evenly distributed among groups (Group 21, 7.2%; Group 40, 9.6%; Group 60, 6.9%; P=0.92) and there was no relationship between the severity of acidosis and the magnitude of the UD interval (r=0.098, P=0.165). Using multiple regression analysis to adjust for the FIO2, there was no association between prolonged UD interval and UV PO2 (P=0.103), UA pH (P=0.17) or Apgar scores (P=1.0). A correlation was found between UV PO2 and UV oxygen content (r=0.7, P=0.0004). A plot of UV PO2 against UV oxyhaemoglobin saturation (Fig. 1) confirmed the presence of a sigmoid relationship, with the curve described by the equation:
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Discussion |
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Our results contradict the findings of some previous studies. Datta and colleagues4 reported that a UD interval >180 s was associated with worsening neonatal acidbase status and low Apgar scores in patients who had spinal anaesthesia. Bader and colleagues3 reported that a prolonged UD interval was correlated with a greater incidence of low Apgar scores and worsening neonatal acidbase values in patients who had spinal and epidural anaesthesia. It was suggested that the fetal hypoxia and acidosis were the result of compromised placental circulation caused by prolonged UD intervals.4 5 Because of this, it has been suggested that administration of supplementary oxygen might improve fetal oxygenation when the UD interval is prolonged.5 Our results, however, suggest that this is unlikely.
The reasons why our results differ from the previous reports are unclear. It is possible that some aspects of anaesthetic technique or operative practice have improved since the previous publications. For example, hypotension is treated more rapidly, and advances in imaging techniques have resulted in better awareness of the position and orientation of the feto-placental unit to facilitate a smooth delivery. The range of UD intervals in our study was 31310 s and may have differed from the range of prolonged UD intervals which were not reported in the previous studies. Unlike our study, in the reports by Datta and Bader, patients who developed hypotension were specifically excluded. However, because hypotension occurs in most cases of spinal anaesthesia in obstetrics,8 it can be argued that the previous papers were not truly representative of the usual clinical situation. In previous work, we analysed the factors associated with fetal acidosis during spinal anaesthesia for Caesarean section.9 We found that although a prolonged UD interval was a significant predictor of fetal acidosis, its magnitude of association was small compared with other factors, such as hypotension and the use of ephedrine.
Because of the unpredictable nature of UD intervals, our study faced several design obstacles. In particular, it would be necessary to recruit a very large number of patients to include the required numbers with a prolonged UD interval in each group. Our approach in this studyto identify patients with prolonged UD intervals retrospectively after each casewas more efficient, although it is theoretically possible that such patients may differ from other patients in some other unknown confounding variable. We were, however, unable to detect such a variable in our multiple regression analysis.
In our previous study, we found that administering 60% oxygen during elective Caesarean section under spinal anaesthesia increased the UV PO2 by 20% compared with air.2 However, in that study we did not measure oxygen content. Similarly, most other studies have relied solely on the PO2 or derived values of oxygen content as comparators. In contrast, in the present study we used co-oximetry as a more direct measure of oxygen content. Previously, Ramanathan et al.7 estimated UV oxyhaemoglobin saturation from measured UV PO2 and suggested that there was an almost linear increase of oxygen content with increasing FIO2. They estimated that oxygen content increased by 2.74 ml dl1 when FIO2 was increased from 0.21 to 0.47. In comparison, our results using co-oximetry showed that increasing FIO2 from 0.21 to 0.60 resulted in a smaller increase in oxygen content, of 1.36 ml dl1. The plot of UV PO2 against UV oxyhaemoglobin saturation from our study (Fig. 1) confirmed a sigmoid relationship, with a value for P50 of 3.0 kPa, which is similar to the published reference mean (SD) value of 2.87 (0.21) kPa.10 Although the nature of the curve is influenced by our assumption that the proportion of fetal haemoglobin was 70%, it is based on directly measured variables and takes into account the dynamic effects of factors such as acids, carbon dioxide, adenosine triphosphate and 2,3-diphosphoglycerate. Thus, our plot represents an in vivo estimate of the relationship between oxyhaemoglobin saturation and PO2. This may explain the difference in our results compared with those of Ramanathan et al., as their calculated values may not have taken into account all of these factors.
Finally, in our study we found there was no increase in the UV PO2 or oxygen content when 40% oxygen was administered compared with air. This is consistent with studies by Kelly and colleagues,11 who administered 35% oxygen, and Cogliano and colleagues,12 who administered 40% oxygen, and also found no increase in UV PO2. This may be a reflection of the functional shunting of the placental circulation, which means that a much greater maternal FIO2 is required to increase UV blood oxygenation.13
In summary, our findings did not show any benefit of routine administration of supplementary oxygen during elective Caesarean section for cases in which the UD intervals were prolonged.
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Acknowledgements |
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References |
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2 Khaw KS, Wang CC, Ngan Kee WD, Pang CP, Rogers MS. Effects of high inspired oxygen fraction during elective Caesarean section under spinal anaesthesia on maternal and fetal oxygenation and lipid peroxidation. Br J Anaesth 2002; 88: 1823
3 Bader AM, Datta S, Arthur GR, Benvenuti E, Courtney M, Hauch M. Maternal and fetal catecholamines and uterine incision-to-delivery interval during elective cesarean. Obstet Gynecol 1990; 75: 6003[Abstract]
4 Datta S, Ostheimer GW, Weiss JB, Brown WU Jr, Alper MH. Neonatal effect of prolonged anesthetic induction for cesarean section. Obstet Gynecol 1981; 58: 3315[Abstract]
5 Jordan MJ. Women undergoing caesarean section under regional anesthesia should routinely receive supplementary oxygen. Int J Obstet Anesth 2002; 11: 2825.[CrossRef][ISI]
6 Rout CC, Akoojee SS, Rocke DA, Gouws E. Rapid administration of crystalloid preload does not decrease the incidence of hypotension after spinal anaesthesia for elective Caesarean section. Br J Anaesth 1992; 68: 3947[Abstract]
7 Ramanathan S, Gandhi S, Arismendy J, Chalon J, Turndorf H. Oxygen transfer from mother to fetus during cesarean section under epidural anesthesia. Anesth Analg 1982; 61: 57681[Abstract]
8 Ngan Kee WD, Khaw KS, Lee BB, Lau TK, Gin T. A doseresponse study of prophylactic intravenous ephedrine for the prevention of hypotension during spinal anesthesia for cesarean delivery. Anesth Analg 2000; 90: 13905
9 Ngan Kee WD, Lee A. Multivariate analysis of factors associated with umbilical arterial pH and standard base excess after Caesarean section under spinal anaesthesia. Anaesthesia 2003; 58: 12530[CrossRef][ISI][Medline]
10 Lentner C. Heart and circulation: blood gases. In: Lentner C, ed. Geigy Scientific Tables. West Caldwell, New Jersey: Ciba-Geigy, 2003; 198200
11 Kelly MC, Fitzpatrick KT, Hill DA. Respiratory effects of spinal anaesthesia for caesarean section. Anaesthesia 1996; 51: 11202[ISI][Medline]
12 Cogliano MS, Graham AC, Clark VA. Supplementary oxygen administration for elective Caesarean section under spinal anaesthesia. Anaesthesia 2002; 57: 669[ISI][Medline]
13 Bassell GM, Marx GF. Optimization of fetal oxygenation. Int J Obstet Anesth 1995; 11: 23843[CrossRef]