- Email: [email protected]
Women undergoing caesarean section under regional anaesthesia should routinely receive supplementary oxygen
Controversies difficulties are encountered at delivery, it is too late to give oxygen. REFERENCES 1. Backe S K, Lyons G. Oxygen and elective Caesarean section. Br J Anaesth 2002; 88: 4–5. 2. Khaw K S, Wang C C, Ngan Kee W D, Pang C P, Rogers M S. 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: 18–23. 3. Cogliano M S, Graham A C, Clark V A. Supplementary oxygen administration for elective Caesarean section under spinal anaesthesia. Anaesthesia 2002; 57: 44–81. 4. Ramanathan S, Gandhi S, Arismendy J, Chalon J, Turndorf H. Oxygen transfer from mother to fetus during Cesarean
5. 6.
7. 8. 9.
285
section under epidural anesthesia. Anesth Analg 1982; 61: 576–581. Marx G F, Mateo C V. Effects of different oxygen concentrations during general anaesthesia for elective Caesarean section. Can Anaesth Soc J 1971; 18: 587–593. Saugstad O D, Rootwelt T, Aslen O. Resuscitation of asphyxiated newborn infants with room air or oxygen: an international controlled trial: the Resair 2 study. Pediatrics 1998; 102: 130–137. Corke R C, Datta G, Ostheimer J, Weiss J B, Alper M H. Spinal anaesthesia for caesarean section. Anaesthesia 1982; 37: 658–662. Kelly M C, Fitzpatrick K T J, Hill D A. Respiratory effects of spinal anaesthesia for Caesarean section. Anaesthesia 1996; 51: 1120–1122. Perreault C, Blaise G A, Meloche R. Maternal inspired oxygen concentration and fetal oxygenation during Caesarean section. Can J Anaesth 1992; 39: 155–157.
doi: ijoa.2002.0991, available online http://www.idealibrary.com on
Opposer: David Hill Ulster Hospital, Belfast, UK It is common practice to give supplementary oxygen to mothers undergoing caesarean section under regional anaesthesia. This intuitive act is based on the perception that the mother and especially the fetus will benefit. The perceived maternal benefits include compensation for the respiratory effects of a high regional block and a reserve of oxygen should an untoward event occur.1 The perceived fetal benefits include the ability to withstand the uterine incision to delivery interval, the loss of blood volume back into the placenta during delivery and the period of suctioning and hypoxia immediately after delivery.2 The principle of supplying the mother an overdose of what the fetus is lacking, however, appears too simple and a close appraisal of the evidence questions this practice. Maternal–fetal gas exchange It is generally agreed that fetal oxygenation takes place by diffusion, although it appears that more shunting occurs in the placenta than in the normal lung.2 Physiological changes during pregnancy ensure that oxygenation of the fetus occurs. Maternal factors 1. Respiratory: maternal hyperventilation and reduction in FRC cause a small rise in maternal PaO2 and a larger fall in maternal PaCO2 . 2. Haematological: the maternal O2 -dissociation curve is shifted to the right increasing the release of oxygen from haemoglobin. This is caused by an increase in 2,3 DPG.
Fetal factors 1. Fetal haemoglobin rises to 16–17 g/100 mL. 2. The fetal O2 -dissociation curve is shifted to the left by a low 2,3 DPG level. This facilitates oxygen binding. 3. Perfusion of fetal organs is high relative to their oxygen demand. 4. Transfer of fetal acid waste products to the mother facilitates fetal oxygen transfer (the double Bohr effect) and likewise the transfer of CO2 from the fetus (the double Haldane effect). It is also worth noting that maternal hyperoxia shifts the CO2 dissociation curve downward and decreases the ability of haemoglobin to transport CO2 (the Haldane effect). As fetal PaO2 is only 25–30% of maternal, increasing maternal PaO2 will raise umbilical PO2 . However, functional shunting on both sides of the placenta, and a high oxygen demand by the placenta, mean that fetal PO2 does not rise pro-rata with maternal PO2 . Maternal hyperoxia It has been shown in many studies that by increasing maternal inspired oxygen (causing maternal hyperoxia), delivery of oxygen to the fetus is improved.3 The relationship between maternal and umbilical PaO2 has been demonstrated during general, epidural and spinal anaesthesia for caesarean section. However, whether maternal hyperoxia is beneficial to the fetus remains uncertain. Studies during labour
David Hill Consultant Anaesthetist, Ulster Hospital, Belfast, UK. E-mail address: [email protected] (D. Hill).
As far back as 1963, Saling,4 using fetal scalp blood samples, found that whilst maternal hyperoxia caused an initial
286
International Journal of Obstetric Anesthesia
rise in fetal scalp PO2 , this was followed by a fall in pH and a simultaneous rise in PCO2 . Saling suggested firstly that maternal hyperoxia caused hypoventilation and CO2 retention and secondly placental vasoconstriction occurred, which impaired feto-maternal gas exchange. Khazin and colleagues,5 also using fetal scalp blood, found that if the fetal PO2 was low (<10 mmHg) maternal hyperoxia increased fetal PO2 and reduced fetal PCO2 . However, if the initial fetal PO2 was normal (>20 mmHg) maternal hyperoxia resulted in little change in fetal scalp gases. Using Doppler ultrasound, Jouppila and collegues6 examined the influence of maternal hyperoxia on the placental circulation in 22 women with fetal impairment secondary to hypertension, diabetes, isoimmunisation or preterm labour. They found a clear decrease in placental blood flow on the maternal side. This was thought to be due to placental vasoconstriction. Studies during caesarean delivery Three studies using general anaesthesia found that fetal PO2 either declined,7 attained a plateau8 or correlated poorly with maternal PO2 .9 Only one general anaesthesia study has claimed fetal benefit. Marx and Mateo8 reported faster times to first respiration and higher Apgar scores with maternal hyperoxia, although their control group did include hypoxic women! Studies of maternal hyperoxia during regional anaesthesia for caesarean section are interesting. Ramanathan and colleagues10 studied 4 groups of 10 women comparing normoxia with 3 levels of hyperoxia. They found a correlation between maternal and umbilical PO2 , but Apgar scores and umbilical pH did not differ between the groups. Based on a small difference of base excess between the normoxic and hyperoxic groups they concluded that maternal hyperoxia improves fetal oxygen stores and acid-base status during caesarean section under epidural anaesthesia. If we examine mean umbilical vein base excess values in their study for normoxic women (−4.5 ± 0.5 mEq/L) we realise that these are perfectly acceptable when normal vaginal delivery reports base excesses between –6 and −10 mEq/L. Furthermore, the authors failed to emphasise the significant increase in umbilical PCO2 that occurred in the hyperoxic groups, which counters the already clinically irrelevant benefit from maternal hyeroxia. More recent studies where spinal anaesthesia was employed questioned any benefit from maternal hyperoxia. Kelly and colleagues1 investigated the effect of spinal anaesthesia for caesarean section on maternal spirometry and the influence of breathing 35% oxygen. Whilst a restrictive ventilatory defect was associated with spinal blockade, maternal PO2 was well maintained even on room air (mean PO2 15.5 kPa). Administration of maternal oxygen (35%) failed to change umbilical blood gases
Table 1. Maternal and fetal blood gases following maternal inhalation of room air (group N) or 35% oxygen (group O). Values are mean (SD)
M1 PaO2 (kPa) M1 PaCO2 (kPa) M2 PaO2 (kPa) M2 PaCO2 (kPa) MBP (mmHg) UvPO2 (kPa) (Uv-Ua)PO2 (kPa) UvpH
Group N
Group O
P
16.6 (3.51) 3.6 (0.22) 15.5 (2.39) 3.4 (0.46) 79 (14.6) 3.59 (0.62) 1.67 (0.62) 7.365 (0.0465)
17.2 (2.80) 3.6 (0.61) 23.6 (4.44) 3.6 (0.41) 81 (11.9) 3.92 (0.83) 1.76 (0.55) 7.336 (0.0857)
0.65 0.95 <0.001 0.2 0.77 0.19 0.62 0.18
M1, maternal values before spinal anaesthesia and M2 after spinal anaesthesia; MBP, mean blood pressure. From Kelly et al.1 with permission.
(Table 1). This has been further substantiated by Cogliano and colleagues.11 They reported that in women undergoing spinal anaesthesia for caesarean section, maternal hyperoxia demonstrated no significant changes in umbilical blood gases (Fig. 1). A third recent study examining the effect of maternal hyperoxia on neonatal outcome during spinal anaesthesia for caesarean section has added to the debate.12 The concern raised in this study is the formation of free radicals with hyperoxia and the potential for harm. Oxygen free radical activity Knaw and colleagues12 investigated the effect of high inspired oxygen fraction (FiO2 0.6) on maternal and fetal oxygenation and oxygen free radical activity in women having caesarean section under spinal anaesthesia. They found that maternal hyperoxia modestly increased umbilical oxygenation but caused a concomitant increase in the activity of oxygen free radicals in both mother and fetus (Fig. 2). Direct detection of free radicals is difficult because of their brief lifespan, therefore the products of attack by free radicals, the lipid hydroperoxides were measured. Interestingly lipid peroxides were much greater in umbilical vein than the umbilical artery blood, suggesting the main site of free radical activity is the placenta. The clinical relevance of this finding is as yet uncertain. We already know that free radicals exacerbate tissue damage in ischaemia reperfusion injury.13 It has been suggested that since free radicals cause depletion of intrinsic antioxidant systems, this could impair the neonate’s ability to withstand any insult. Malondialdehyde, a product of lipid peroxidation, is toxic because it forms disulphide brides across nucleotide or amino acid chains.14 It is already known that hyperoxia mediates tissue injury in bronchopulmonary displasia, retinopathy of prematurity, persistent ductus arteriosus, necrotising enterocolitis and intracranial haemorrhage.15−17 Even the administration of supplemental oxygen in routine neonatal resuscitation is being questioned. Two recent
Controversies
287
Fig. 1 Partial pressure of oxygen in the umbilical artery and vein when mothers inhale room air (air), 40% oxygen (oxygen) or 2 L/min of oxygen via nasal cannulae (NC). From Cogliano et al., with permission.
studies have found worse neonatal outcome associated with hyperoxia and the generation of free radicals.18,19 Other practical issues In clinical practice many mothers complain about the discomfort of oxygen masks, which give them feelings of
claustrophobia and interfere with the bonding experience if left in place following delivery.11,20 Also of practical importance is the potential for error in breathing systems when the fresh gas supply pipe is disconnected to facilitate supplemental oxygen to the mother. Should the need for general anaesthesia arise without remembering to reconnect the fresh gas supply, hypoxia and maternal awareness could ensue.
Summary and conclusion From the available literature we have seen that maternal hyperoxia may disadvantage the fetus by: • Causing maternal hypoventilation and impaired fetal CO2 excretion. • Causing placental vasoconstriction. • Not giving any clear benefit to the fetus during labour. • Not giving any clear benefit to the fetus during caesarean section. • Producing free radical activity particularly from the placenta. • Potentially causing persistent ductus arteriosus.
Fig. 2 Maternal plasma concentrations of malondialdehyde (MDA, a product of lipid peroxidation) at 10-min intervals. Data are mean concentration (95% confidence intervals) for each interval after starting oxygen supplementation. +P < 0.05, *P < 0.01. From Khan et al., with permission.
With all these concerns it is difficult to justify routine supplementary oxygen for caesarean section under regional anaesthesia, particularly when an elective caesarean section is a low risk to both mother and fetus. Even for the compromised fetus the evidence for hyperoxia is not outstanding. However, if the aim is to restore normoxia in a compromised fetus, this is reasonable, but the benefits of hyperoxia have to be questioned.
288
International Journal of Obstetric Anesthesia
Therefore, I oppose the motion that women having caesarean section under regional anaesthesia should routinely receive supplemental oxygen.
11. 12.
REFERENCES 1. Kelly M C, Fitzpatrick K T, Hill D A. Respiratory effects of spinal anaesthesia for Caesarean section. Anaesthesia 1996; 51: 1120–1122. 2. Bassell G M, Marx G F. Optimization of fetal oxygenation. International Journal of Obstetric Anesthesia 1995; 4: 238–243. 3. Bartnicki J, Saling E. The influence of maternal oxygen administration on the fetus. Int Fed Gynecol Obstet 1994; 45: 87–95. 4. Saling E. The effect of maternal oxygenation on the blood gases and the acid-base balance of the fetus. Geburtsh Frauenheilk 1963; 23: 528–532. 5. Khazin A F, Hon E H, Hehre F W. Effects of maternal hyperoxia on the fetus. Am J Obstet Gynecol 1971; 109: 628–637. 6. Jouppila P, Kirkinen P, Koivula, Jouppila R. The influence of maternal oxygen inhalation on human placental and umbilical venous blood flow. Eur J Obstet Gynecol Reprod Biol 1983; 16: 151–156. 7. Rorke M J, Davey D J, Du Toit H J. Fetal oxygenation during caesarean section. Anaesthesia 1968; 23: 585–596. 8. Marx G F, Mateo C V. Effects of different oxygen concentrations during general anaesthesia for elective caesarean section. Can Anaesth Soc J 1971; 18: 587–593. 9. Baraka A. Correlation between maternal and fetal PO2 and PCO2 during caesarean section. Br J Anaesth 1970; 42: 434–438. 10. Ramanathan S, Ghandi S, Arismendi J, Chalon J, Turndof H.
13. 14. 15. 16. 17. 18. 19. 20.
Oxygen transfer from mother to fetus during Cesarean section under epidural anesthesia. Anesth Analg 1982; 61: 576–581. Cogliano M S, Graham A C, Clark V A. Supplementary oxygen administration for elective Caesarean section under spinal anaesthesia. Anaesthesia 2002; 57: 66–69. Khaw K S, Wang C C, Ngan Kee W D, Pang C P, Rogers M S. The effects of high inspired oxygen fraction during elective Caesarean section under spinal anaesthesia on maternal and fetal oxygenation and lipid-peroxidation. Br J Anaesth 2001; 88: 18–23. Wu S, Tamaki N, Nagashima T, Yamaguchi M. Reactive oxygen species in reoxygenation injury of rat brain capillary endothelial cells. Neurosurgery 1998; 43: 577–583. Ward R J, Peters T J. Free radicals. In: Marshall W J, Bangert S K, (eds). Clinical Biochemistry: Metabolic and Clinical Aspects. New York: Churchill Livingstone, 1995: 765–777. Northway W H, Rosan R C, Porter D Y. Pulmonary disease following respiratory therapy of hyaline-membrane disease. Bronchopulmonary dysplasia. N Engl J Med 1967; 276: 357–368. Campell K. Intensive oxygen therapy as a possible cause of retrolental fibroplasia: a clinical approach. Med J Aust 1950; 2: 48–50. Clyman R I, Saugstad O D, Mauray F. Reactive oxygen metabolites relax lamb ductus arteriosus by stimulating prostaglandin production. Circ Res 1989; 64: 1–8. Lundstom K E, Pryds O, Greisen G. Oxygen at birth and prolonged cerebral vasoconstriction in preterm infants. Arch Dis Child, Fetal Neonatal Ed 1995; 73: 81–86. Saugstad O D, Rootwelt T, Aalen O. Resuscitation of asphyxiated newborn infants with room air or oxygen: an international controlled trial: the Resair 2 study. Pediatrics 1998; 102: 130–137. Crosby E T, Halpern S H. Supplemental maternal oxygen therapy during caesarean section under epidural anaesthesia: a comparison of nasal prongs and facemask. Can J Anaesth 1992; 39: 313–316.
Voting before and after the motion ‘Women having caesarean section under regional anaesthesia should routinely receive supplementary oxygen.’ Voting by Br¨ahler ICS UK Ltd.
5. 6.
7. 8. 9.
285
section under epidural anesthesia. Anesth Analg 1982; 61: 576–581. Marx G F, Mateo C V. Effects of different oxygen concentrations during general anaesthesia for elective Caesarean section. Can Anaesth Soc J 1971; 18: 587–593. Saugstad O D, Rootwelt T, Aslen O. Resuscitation of asphyxiated newborn infants with room air or oxygen: an international controlled trial: the Resair 2 study. Pediatrics 1998; 102: 130–137. Corke R C, Datta G, Ostheimer J, Weiss J B, Alper M H. Spinal anaesthesia for caesarean section. Anaesthesia 1982; 37: 658–662. Kelly M C, Fitzpatrick K T J, Hill D A. Respiratory effects of spinal anaesthesia for Caesarean section. Anaesthesia 1996; 51: 1120–1122. Perreault C, Blaise G A, Meloche R. Maternal inspired oxygen concentration and fetal oxygenation during Caesarean section. Can J Anaesth 1992; 39: 155–157.
doi: ijoa.2002.0991, available online http://www.idealibrary.com on
Opposer: David Hill Ulster Hospital, Belfast, UK It is common practice to give supplementary oxygen to mothers undergoing caesarean section under regional anaesthesia. This intuitive act is based on the perception that the mother and especially the fetus will benefit. The perceived maternal benefits include compensation for the respiratory effects of a high regional block and a reserve of oxygen should an untoward event occur.1 The perceived fetal benefits include the ability to withstand the uterine incision to delivery interval, the loss of blood volume back into the placenta during delivery and the period of suctioning and hypoxia immediately after delivery.2 The principle of supplying the mother an overdose of what the fetus is lacking, however, appears too simple and a close appraisal of the evidence questions this practice. Maternal–fetal gas exchange It is generally agreed that fetal oxygenation takes place by diffusion, although it appears that more shunting occurs in the placenta than in the normal lung.2 Physiological changes during pregnancy ensure that oxygenation of the fetus occurs. Maternal factors 1. Respiratory: maternal hyperventilation and reduction in FRC cause a small rise in maternal PaO2 and a larger fall in maternal PaCO2 . 2. Haematological: the maternal O2 -dissociation curve is shifted to the right increasing the release of oxygen from haemoglobin. This is caused by an increase in 2,3 DPG.
Fetal factors 1. Fetal haemoglobin rises to 16–17 g/100 mL. 2. The fetal O2 -dissociation curve is shifted to the left by a low 2,3 DPG level. This facilitates oxygen binding. 3. Perfusion of fetal organs is high relative to their oxygen demand. 4. Transfer of fetal acid waste products to the mother facilitates fetal oxygen transfer (the double Bohr effect) and likewise the transfer of CO2 from the fetus (the double Haldane effect). It is also worth noting that maternal hyperoxia shifts the CO2 dissociation curve downward and decreases the ability of haemoglobin to transport CO2 (the Haldane effect). As fetal PaO2 is only 25–30% of maternal, increasing maternal PaO2 will raise umbilical PO2 . However, functional shunting on both sides of the placenta, and a high oxygen demand by the placenta, mean that fetal PO2 does not rise pro-rata with maternal PO2 . Maternal hyperoxia It has been shown in many studies that by increasing maternal inspired oxygen (causing maternal hyperoxia), delivery of oxygen to the fetus is improved.3 The relationship between maternal and umbilical PaO2 has been demonstrated during general, epidural and spinal anaesthesia for caesarean section. However, whether maternal hyperoxia is beneficial to the fetus remains uncertain. Studies during labour
David Hill Consultant Anaesthetist, Ulster Hospital, Belfast, UK. E-mail address: [email protected] (D. Hill).
As far back as 1963, Saling,4 using fetal scalp blood samples, found that whilst maternal hyperoxia caused an initial
286
International Journal of Obstetric Anesthesia
rise in fetal scalp PO2 , this was followed by a fall in pH and a simultaneous rise in PCO2 . Saling suggested firstly that maternal hyperoxia caused hypoventilation and CO2 retention and secondly placental vasoconstriction occurred, which impaired feto-maternal gas exchange. Khazin and colleagues,5 also using fetal scalp blood, found that if the fetal PO2 was low (<10 mmHg) maternal hyperoxia increased fetal PO2 and reduced fetal PCO2 . However, if the initial fetal PO2 was normal (>20 mmHg) maternal hyperoxia resulted in little change in fetal scalp gases. Using Doppler ultrasound, Jouppila and collegues6 examined the influence of maternal hyperoxia on the placental circulation in 22 women with fetal impairment secondary to hypertension, diabetes, isoimmunisation or preterm labour. They found a clear decrease in placental blood flow on the maternal side. This was thought to be due to placental vasoconstriction. Studies during caesarean delivery Three studies using general anaesthesia found that fetal PO2 either declined,7 attained a plateau8 or correlated poorly with maternal PO2 .9 Only one general anaesthesia study has claimed fetal benefit. Marx and Mateo8 reported faster times to first respiration and higher Apgar scores with maternal hyperoxia, although their control group did include hypoxic women! Studies of maternal hyperoxia during regional anaesthesia for caesarean section are interesting. Ramanathan and colleagues10 studied 4 groups of 10 women comparing normoxia with 3 levels of hyperoxia. They found a correlation between maternal and umbilical PO2 , but Apgar scores and umbilical pH did not differ between the groups. Based on a small difference of base excess between the normoxic and hyperoxic groups they concluded that maternal hyperoxia improves fetal oxygen stores and acid-base status during caesarean section under epidural anaesthesia. If we examine mean umbilical vein base excess values in their study for normoxic women (−4.5 ± 0.5 mEq/L) we realise that these are perfectly acceptable when normal vaginal delivery reports base excesses between –6 and −10 mEq/L. Furthermore, the authors failed to emphasise the significant increase in umbilical PCO2 that occurred in the hyperoxic groups, which counters the already clinically irrelevant benefit from maternal hyeroxia. More recent studies where spinal anaesthesia was employed questioned any benefit from maternal hyperoxia. Kelly and colleagues1 investigated the effect of spinal anaesthesia for caesarean section on maternal spirometry and the influence of breathing 35% oxygen. Whilst a restrictive ventilatory defect was associated with spinal blockade, maternal PO2 was well maintained even on room air (mean PO2 15.5 kPa). Administration of maternal oxygen (35%) failed to change umbilical blood gases
Table 1. Maternal and fetal blood gases following maternal inhalation of room air (group N) or 35% oxygen (group O). Values are mean (SD)
M1 PaO2 (kPa) M1 PaCO2 (kPa) M2 PaO2 (kPa) M2 PaCO2 (kPa) MBP (mmHg) UvPO2 (kPa) (Uv-Ua)PO2 (kPa) UvpH
Group N
Group O
P
16.6 (3.51) 3.6 (0.22) 15.5 (2.39) 3.4 (0.46) 79 (14.6) 3.59 (0.62) 1.67 (0.62) 7.365 (0.0465)
17.2 (2.80) 3.6 (0.61) 23.6 (4.44) 3.6 (0.41) 81 (11.9) 3.92 (0.83) 1.76 (0.55) 7.336 (0.0857)
0.65 0.95 <0.001 0.2 0.77 0.19 0.62 0.18
M1, maternal values before spinal anaesthesia and M2 after spinal anaesthesia; MBP, mean blood pressure. From Kelly et al.1 with permission.
(Table 1). This has been further substantiated by Cogliano and colleagues.11 They reported that in women undergoing spinal anaesthesia for caesarean section, maternal hyperoxia demonstrated no significant changes in umbilical blood gases (Fig. 1). A third recent study examining the effect of maternal hyperoxia on neonatal outcome during spinal anaesthesia for caesarean section has added to the debate.12 The concern raised in this study is the formation of free radicals with hyperoxia and the potential for harm. Oxygen free radical activity Knaw and colleagues12 investigated the effect of high inspired oxygen fraction (FiO2 0.6) on maternal and fetal oxygenation and oxygen free radical activity in women having caesarean section under spinal anaesthesia. They found that maternal hyperoxia modestly increased umbilical oxygenation but caused a concomitant increase in the activity of oxygen free radicals in both mother and fetus (Fig. 2). Direct detection of free radicals is difficult because of their brief lifespan, therefore the products of attack by free radicals, the lipid hydroperoxides were measured. Interestingly lipid peroxides were much greater in umbilical vein than the umbilical artery blood, suggesting the main site of free radical activity is the placenta. The clinical relevance of this finding is as yet uncertain. We already know that free radicals exacerbate tissue damage in ischaemia reperfusion injury.13 It has been suggested that since free radicals cause depletion of intrinsic antioxidant systems, this could impair the neonate’s ability to withstand any insult. Malondialdehyde, a product of lipid peroxidation, is toxic because it forms disulphide brides across nucleotide or amino acid chains.14 It is already known that hyperoxia mediates tissue injury in bronchopulmonary displasia, retinopathy of prematurity, persistent ductus arteriosus, necrotising enterocolitis and intracranial haemorrhage.15−17 Even the administration of supplemental oxygen in routine neonatal resuscitation is being questioned. Two recent
Controversies
287
Fig. 1 Partial pressure of oxygen in the umbilical artery and vein when mothers inhale room air (air), 40% oxygen (oxygen) or 2 L/min of oxygen via nasal cannulae (NC). From Cogliano et al., with permission.
studies have found worse neonatal outcome associated with hyperoxia and the generation of free radicals.18,19 Other practical issues In clinical practice many mothers complain about the discomfort of oxygen masks, which give them feelings of
claustrophobia and interfere with the bonding experience if left in place following delivery.11,20 Also of practical importance is the potential for error in breathing systems when the fresh gas supply pipe is disconnected to facilitate supplemental oxygen to the mother. Should the need for general anaesthesia arise without remembering to reconnect the fresh gas supply, hypoxia and maternal awareness could ensue.
Summary and conclusion From the available literature we have seen that maternal hyperoxia may disadvantage the fetus by: • Causing maternal hypoventilation and impaired fetal CO2 excretion. • Causing placental vasoconstriction. • Not giving any clear benefit to the fetus during labour. • Not giving any clear benefit to the fetus during caesarean section. • Producing free radical activity particularly from the placenta. • Potentially causing persistent ductus arteriosus.
Fig. 2 Maternal plasma concentrations of malondialdehyde (MDA, a product of lipid peroxidation) at 10-min intervals. Data are mean concentration (95% confidence intervals) for each interval after starting oxygen supplementation. +P < 0.05, *P < 0.01. From Khan et al., with permission.
With all these concerns it is difficult to justify routine supplementary oxygen for caesarean section under regional anaesthesia, particularly when an elective caesarean section is a low risk to both mother and fetus. Even for the compromised fetus the evidence for hyperoxia is not outstanding. However, if the aim is to restore normoxia in a compromised fetus, this is reasonable, but the benefits of hyperoxia have to be questioned.
288
International Journal of Obstetric Anesthesia
Therefore, I oppose the motion that women having caesarean section under regional anaesthesia should routinely receive supplemental oxygen.
11. 12.
REFERENCES 1. Kelly M C, Fitzpatrick K T, Hill D A. Respiratory effects of spinal anaesthesia for Caesarean section. Anaesthesia 1996; 51: 1120–1122. 2. Bassell G M, Marx G F. Optimization of fetal oxygenation. International Journal of Obstetric Anesthesia 1995; 4: 238–243. 3. Bartnicki J, Saling E. The influence of maternal oxygen administration on the fetus. Int Fed Gynecol Obstet 1994; 45: 87–95. 4. Saling E. The effect of maternal oxygenation on the blood gases and the acid-base balance of the fetus. Geburtsh Frauenheilk 1963; 23: 528–532. 5. Khazin A F, Hon E H, Hehre F W. Effects of maternal hyperoxia on the fetus. Am J Obstet Gynecol 1971; 109: 628–637. 6. Jouppila P, Kirkinen P, Koivula, Jouppila R. The influence of maternal oxygen inhalation on human placental and umbilical venous blood flow. Eur J Obstet Gynecol Reprod Biol 1983; 16: 151–156. 7. Rorke M J, Davey D J, Du Toit H J. Fetal oxygenation during caesarean section. Anaesthesia 1968; 23: 585–596. 8. Marx G F, Mateo C V. Effects of different oxygen concentrations during general anaesthesia for elective caesarean section. Can Anaesth Soc J 1971; 18: 587–593. 9. Baraka A. Correlation between maternal and fetal PO2 and PCO2 during caesarean section. Br J Anaesth 1970; 42: 434–438. 10. Ramanathan S, Ghandi S, Arismendi J, Chalon J, Turndof H.
13. 14. 15. 16. 17. 18. 19. 20.
Oxygen transfer from mother to fetus during Cesarean section under epidural anesthesia. Anesth Analg 1982; 61: 576–581. Cogliano M S, Graham A C, Clark V A. Supplementary oxygen administration for elective Caesarean section under spinal anaesthesia. Anaesthesia 2002; 57: 66–69. Khaw K S, Wang C C, Ngan Kee W D, Pang C P, Rogers M S. The effects of high inspired oxygen fraction during elective Caesarean section under spinal anaesthesia on maternal and fetal oxygenation and lipid-peroxidation. Br J Anaesth 2001; 88: 18–23. Wu S, Tamaki N, Nagashima T, Yamaguchi M. Reactive oxygen species in reoxygenation injury of rat brain capillary endothelial cells. Neurosurgery 1998; 43: 577–583. Ward R J, Peters T J. Free radicals. In: Marshall W J, Bangert S K, (eds). Clinical Biochemistry: Metabolic and Clinical Aspects. New York: Churchill Livingstone, 1995: 765–777. Northway W H, Rosan R C, Porter D Y. Pulmonary disease following respiratory therapy of hyaline-membrane disease. Bronchopulmonary dysplasia. N Engl J Med 1967; 276: 357–368. Campell K. Intensive oxygen therapy as a possible cause of retrolental fibroplasia: a clinical approach. Med J Aust 1950; 2: 48–50. Clyman R I, Saugstad O D, Mauray F. Reactive oxygen metabolites relax lamb ductus arteriosus by stimulating prostaglandin production. Circ Res 1989; 64: 1–8. Lundstom K E, Pryds O, Greisen G. Oxygen at birth and prolonged cerebral vasoconstriction in preterm infants. Arch Dis Child, Fetal Neonatal Ed 1995; 73: 81–86. Saugstad O D, Rootwelt T, Aalen O. Resuscitation of asphyxiated newborn infants with room air or oxygen: an international controlled trial: the Resair 2 study. Pediatrics 1998; 102: 130–137. Crosby E T, Halpern S H. Supplemental maternal oxygen therapy during caesarean section under epidural anaesthesia: a comparison of nasal prongs and facemask. Can J Anaesth 1992; 39: 313–316.
Voting before and after the motion ‘Women having caesarean section under regional anaesthesia should routinely receive supplementary oxygen.’ Voting by Br¨ahler ICS UK Ltd.