obstetrical anaesthesia and the foetus

Acta anuesth. Scundinav. 1959, Supplementum 11, 27-34.

OBSTETRICAL ANAESTHESIA A N D T H E F O E T U S

BY

FRANK HOLMES

In operative obstetrics, the anaesthetist has two patients in his care but with present-day anaesthetic management the welfare of the mother should no longer present exceptional difficulties. On the other hand, the proportion of babies who require resuscitation has not been materially reduced and there is no evidence of a substantially increased survival rate in those handicapped by abnormal obstetrical factors or pathological conditions present in the mother.

Furthermore, it is not enough to assess the effects of anaesthesia on the newborn only in terms of survival. While an infant can survive considerable periods of intra-uterine suboxygenation and neonatal apnoea, a relationship between these complications and subsequent clinical signs of neuropathology has been noted. There is some evidence to suggest that neonatal anoxia may have a bear- ing on the development of cerebral palsy. A recent paper on respiratory phenomena in the newborn (I. DONALD, M. M. KERR and I. R. MACDONALD (1958p) ends with these words: “Every cyanotic attack is another nail in the coffin of the child’s intellect.” This will be so until a method is found by which artificial respiration can be applied to the newborn harmlessly and effectively.

Respiratory inadequacy resulting from the administration of depressant agents to the mother may not be immediately apparent. ‘Late’ apnoea after more or less normal respiration at birth has been ascribed to intra-uterine anoxaemia resulting from drug depression (J. S. HALDANE and J. G. PRIESTLEY (1935)e). I t has long been recognised that cerebral anoxia due to depression of the respiratory centre can cause intracranial haemorrhage in the infant without trauma during delivery (W. P. YANT, J. CHORNYAK, H. H. SCHRENK, F. A. PATTY and R. R. SAYERS ( 1934)29), and it is now agreed that intraventricular haemorrhage is associated with cerebral anoxia while subdural haematoma is caused by birth injury.

From the Departmentpf Anaesthetics (Head: JOHN GILLIES), the Royal Infirmary, Edin- burgh, Scotland.

28 FRANK HOLMES

Before respiration has begun, foetal arterial oxygen saturation (A. 0. S.) is normally about 60-65 per cent., and unless ventilation is inadequate it rises rapidly to the adult level of about 95 per cent. According to A. MINKOWSKI'S findings (1955)lS, this adjustment occurs in the normal infant within a few seconds of delivery. MINKOWSKI observed that drug depression causes foetal A.O.S. at birth to be low and E. S. TAYLOR (195lZ3, 195425) noted that the use of general anaesthesia during the terminal phases of labour or operative delivery retards its rise to the adult level, and that the delay is proportional to the duration and depth of anaesthesia. He concludes that if the adult level is not reached in 15 minutes the infant cannot survive. I t seems permissible to infer that lesser delays can cause cerebral damage.

F. F. SNYDER and M. ROSENFELD (1937)22 were able to demonstrate in rabbits that anoxaemia invariably caused, within less than half a minute, a depression of foetal respiratory movements in utero which rapidly progressed to apnoea. The studies of H. C. MILLER and N. W. SMULL (1955)l' suggest that if newly-born babies become anoxic, hyperventilation does not occur to correct this state. On the contrary, these observers found that normal full-term infants, when breathing an atmosphere containing between 10 and 12 per cent. of oxygen, exhibit a rapid and continuous decline of minute and tidal volumes. They postulate that this is due to the chemoreceptor reflexes being more or less inactive for some time after birth. In this respect, they liken the behaviour of the newborn to that of animals subjected to anoxia after their carotid bodies have been denervated. If the chemoreceptor reflexes of the neonate are indeed inactive, it may be for this reason that respiratory stimulants such as nikethamide, which act through this mechanism, are not effective in the treatment of asphyxia neonatorum. The impression that nikethamide is actually harmful could be explained by the same hypothesis. While this drug produces no specific respiratory stimulation, it does cause a general cerebral stimulation which is likely to increase the oxygen requirements of the infant and so widen further the gap between oxygen supply and demand.

In their studies on rabbits, F. F. SNYDER and M. ROSENFELD (1937)22 observed that all narcotic and anaesthetic agents, even in doses which produced no demonstrable effects on the mother, cause profound respiratory depression of the foetus in utero. I t is of interest to note that they found cyclopropane to be the only exception, even when deep surgical anaesthesia was produced.

Anaesthetists are conscious of the possibility of depressing respiratory activ- ity of the newborn when employing general anaesthetics for operative delivery, and S. SJOSTEDT and G. ROOTH ( 1958)21 have recently shown that after Caesar- ean section in uncomplicated cases and before the onset of labour, average foetal A.O.S. was 62.1 per cent. (as after normal spontaneous delivery) when local analgesia was employed, while in similarly selected cases operated on under cyclopropane and oxygen anaesthesia A. 0. S. was only 46.6 per cent. However, the general view is that with careful dosage no serious ill effects to

OBSTETRICAL ANAESTHESIA AND THE FOETUS 29

the baby occur. Although we have no clear-cut criteria to enable us to sub- stantiate such an assertion, it may to some extent hold good when the infant is normal and mature. There is, however, evidence that when the baby is under- developed or distressed such a point of view is more difficult to defend.

Prematurity

In recent reviews of over 1300 cases of Caesarean section, P. C. LUND ( 1955)13 and H. K. WENDL (1955)z' conclude that when the infant is premature, there is a significantly higher infant mortality rate associated with general anaesthesia, even with modern techniques and agents, than with conduction analgesia.

E. S. TAYLOR ( 1954)25 also considers it imperative that general anaesthesia should be withheld when the infant is premature, and observed that in such babies, even when no anaesthesia is employed for delivery, the post-natal rise of A.O.S. to the adult level is always slow (E. S. TAYLOR, W. C. SCOTT and C. D. GOVAN (1951)24). Although R. B. MACKAY (1957)14 found that foetal A. 0. S. tends to decrease somewhat during the last month of pregnancy, this slight advantage with which the premature infant may start life will be more than offset in the immediate postnatal period. A reason for this is indicated by the findings of A. M. MALI and C. E. KIHA ( 1935)l8 and those of E. KLEMOLA (1937)ll who observed that in premature infants the pulmonary vascular bed and elastic tissue are poorly developed. H. J. GOLDBACH ( 1956)4, who examined 142 foetal lungs at various stages of maturity, never found advanced development of the alveolar elastic tissue in babies measuring less than 45 cm in length and often not in those under 60 cm. From a study of the lungs of infants who had died during the first 8 days of life, GOLDBACH also concludes that the post- natal development of pulmonary elastic tissue is markedly slower in premature babies than in those delivered at term. H. K. WENDL (1957)28 finds that the type of neonatal cerebral haemorrhage which is associated with foetal anoxaemia is more commonly seen in premature infants, and I. DONALD, M. M. KERR and I. R. MACDONALD (1958)3 call intraventricular haemorrhage a disease of prematurity, having observed it 12 times more often in premature than in mature babies. Cerebral palsy is more commonly met in children who are born before term.

Since the ability of the newborn to attain full oxygen saturation depends on its pulmonary function, it would seem particularly contra-indicated to burden babies, whose respiratory mechanism is known to be inadequate, with any degree of respiratory depression.

Foetal Distress

This condition is due to impairment of the foetal circulation either in the placenta or the umbilical cord, leading to anoxia which generally cannot be

30 FRANK HOLMES

relieved by administration of oxygen to the mother. I t is obvious that to a distressed infant, born with a low A. 0. S., respiratory depression, by delaying post-natal adjustment of oxygen saturation, will be a serious handicap.

Toxaemia and Diabetes

In these conditions one or both contra-indications to general anaesthesia may exist, namely deterioration of the placental circulation and foetal imma- turity. Placental disease and underdevelopment of the foetus are features of toxaemia of pregnancy, and delivery before term often becomes necessary. R. B. MACKAY (1957)14 found that average A.O.S. at birth after spontaneous vertex deliveries under gas and air analgesia is up to 22 per cent. lower than normal when the mother is pre-eclamptic and that the difference is greatest when gestation is less than 39 weeks.

In the diabetic patient, placental disease is the probable cause of intra- uterine death during the last few weeks of pregnancy and the weight of the foetus is no indication of advanced development. The present-day practice of performing Caesarean section at about 34-36 weeks’ gestation tends to avert intra-uterine death but it involves premature delivery. Not so many years ago diabetes was associated with a foetal mortality of some 50 per cent. More recently, the expectant mother suffering from diabetes has undergone strict ante-natal supervision combined with meticulous control of the diabetic state and operative delivery before foetal oxygenation was impaired. In addition, neonatal care is greatly improved. As a result of these measures foetal loss has been reduced to about 16 per cent.

During the last five years the author has employed spinal analgesia for 41 Caesarean sections on diabetic mothers with a neonatal loss of two babies. I t is felt that the avoidance of general anaesthesia contributed to the survival of some of these infants.

Postmaturity

While it is generally accepted that placental degeneration with its ill effects on foetal circulation is a danger of pregnancies which exceed 40 weeks, one has never heard it suggested that general anaesthesia is contra-indicated in such circumstances. The author has, however, on a number of occasions, observed respiratory depression after operative delivery in postmature infants, even with the most careful anaesthetic technique, and has recently considered whether these babies should be treated by the anaesthetist as potential cases of foetal distress. The work ofJ. WALKER ( 1954)26, who found that foetal A. 0. S. drops sharply after the 40th week of gestation and may reach a critically low level after the 42nd week, lends support to this line of thought. Excluding all cases of foetal distress due to obstetrical causes and selecting only those of whose dates he could be sure, WALKER found A. 0. S. to be low in 50 per cent.


of postmature infants. He also noted that administration of oxygen to the mother had no effect on oxygen saturation which is only to be expected because impairment of foetal circulation results from placental changes. A. MINKOWSKI (1955)18 and R. B. MACKAY (1957)14 observed a similar reduction in foetal A.O.S. after term.

If we agree that general anaesthesia should be avoided in these conditions, we are faced with the question of what form of regional analgesia to select. This is a matter for individual preference except in cases of foetal distress when speed is often of vital importance. In these circumstances, subarachnoid spinal block is the method of choice. Yet much has been said to discourage its use in operative obstetrics. Apart from the frequently reported danger to the mother when spinal analgesia is employed for Caesarean section, which has grown into something of a bogey and which should be avoidable (F. HOLMES (1957)8), the main objection from the point of view of the well-being of the foetus has been the possible effect of a lowered maternal blood pressure and raised uterine tone on placental circulation. With regard to the former, C. B. LULL and R. A. HINCSON (1948)12 found that the blood supply to the foetus is not impaired until the maternal blood pressure falls below 80 mm Hg systolic. With the use of a quick-acting drug such as procaine, proper dosage and avoidance of barbotage, falls of systolic pressure below 100 mm Hg have not been observed.

The fear of impairment of placental circulation due to an increased uterine tone as a result of spinal block has been dispelled by the findings of T. JOHNSON

and C. G. CLAYTON (1955)lO who demonstrated by the use of radioactive sodium a marked improvement of the placental circulation after the induction of extradural spinal block. Their investigation was carried out in cases of prolonged labour in which placental circulation had previously been found to be reduced by up to 50 per cent. I t is of interest that H. RUPPERT (1955)19 was unable to observe any increase of uterine tone following extradural block in an investigation of this problem.

General Anaesthesia

If the foetus is mature and its general condition good, no obvious objections to the use of general anaesthesia for operative delivery appear to exist, but a few points with regard to management and choice of agents invite comment.

Emgtyins of the stomach,-Before general anaesthesia is induced, it has become routine practice to ensure, either by diet or evacuation, that the stomach is empty. For evacuation few anaesthetists will favour the use of apomorphine (J. M. HOLMES (1956)y. The author’s practice is to employ a 6 or 7 gauge polythene tube. Although it will only permit the aspiration of fluids, this prep- aration is considered to be satisfactory since it was found that solids are not readily vomited in the absence of fluid in the stomach. Apart from avoiding

32 FRANK IlOLMES

the obvious danger to the mother, it is important to protect the baby from the anoxia which invariably accompanies vomiting.

Management of respiration.-In recent years many anaesthetists have favoured tracheal intubation and vigorous controlled respiration, aided by relaxants, as a means of reducing the use of depressant drugs to a minimum. Though commendable in its object, this method may deplete the foetal blood of carbon dioxide and cause neonatal apnoea. A clinical investigation which is in progress tends to confirm this. F. F. SNYDER and M. ROSENFELD ( 1937)22 observed that, while maternal carbon dioxide retention had no demonstrable effect on foetal respiration, a carbon dioxide deficit (induced by hyperventilation of the mother) led to a rapidly diminishing respiratory rate and apnoea in the foetus. H. COLLIER (1956)’ recommends cutting out the carbon dioxide absorber some time before ligation of the cord when using controlled respiration, but it is doubtful whether this is a reliable method of restoring carbon dioxide tension.

Choice of Agents

Relaxants.-It has been shown that d-tubocurarine does not cross the placenta (T. C. GRAY (1947)5, J. S. CRAWFORD (1956)2). On the other hand, CRAWFORD has demonstrated after the administration of 80 mg of gallamine readily detectable amounts of this agent in the foetal serum and R. SCHWARZ ( 1958)20 found that the placenta presents no obstacle to the passage of gallamine. This suggests that d-tubocurarine is preferable for obstetrical interventions.

Thiopentone.-For many years the “12-minute rule” (L. M. HELLMAN, L. B. SHETTLES, C. P. MANAHAN and N. J. EASTMAN (1944)’) inhibited the use of this drug in obstetrics but more recent evidence has shown that its build-up and elimination in the foetal blood is parallel with those processes in the mother (F. B. MCKECHNIE and J. G. CONVERSE (1955)15, J. S. CRAWFORD (1956)2); this means the longer the interval between administration of the drug to the mother and delivery, the better it is for the infant, and observation in practice bears this out. While thiopentone is a strong respiratory depressant, the depression is short-lived if a dose of 250 mg is not exceeded. On the other hand, its use facilitates a rapid and quiet induction without respiratory obstruction and its attendant anoxia which is so harmful to the baby.

Cyc1opropane.-It is of interest to recall the observation by F. F. SNYDER and M. ROSENFELD ( 1937)z2 that cyclopropane does not depress foetal respiration, even in high concentrations. At any rate, the anaesthetist finds its flexibility and the fact that it is administered in a mixture with a high proportion of oxygen valuable assets in obstetrical work. I t may, however, be dangerous in cases where pitocin has been administered to the mother, when cardiac arrhyth- mia and arrest are said to occur on occasion.

Chloroform.-Reports of acute yellow atrophy of the liver following chloroform anaesthesia in obstetrics, though rare, make it necessary to restrict the


use of this agent to patients who present a particular indication, namely those in whom relaxation of the uterus is essential for a speedy and successful inter- vention. No other drug is so capable of relaxing uterine muscle in extremely low concentrations and, in these circumstances, avoiding or minimising foetal distress. When given in oxygen the author has met no complications. Fluothane is said to relax uterine muscle and may prove a useful substitute for chloroform in such cases.

Any reduction in perinatal morbidity and mortality achieved in recent years is to a large extent due to the improvements of obstetrical supervision and neonatal care but resuscitation of the newborn and vigilance on the part of the obstetrician have certain limitations. The anaesthetist can by a careful choice of his method of pain relief contribute much towards reducing the number of infants who require resuscitation and improving the chances of those handicapped by obstetrical or pathological complications.

R E F E R E N C E S 1. COLLIER, H.: Caesarean section: A method of anaesthesia. Brit. 3 . Anaesth. 1956,28, 130. 2. CRAWFORD, J. S.: Some aspects of obstetric anaesthesia. Brit. 3. Anaesth. 1956, 28, 146. 3. DONALD, I., M. M. KERR and I. R. MACDONALD: Respiratory phenomena in the new-

4. GOLDBACH, H. J.: Die Entwicklung der elastischen Fasern in der menschlichen Lunge.

5. GRAY, T. C.: d-Tubocurarine in caesarean section. Brit. M. 3 . 1947, i, 444. 6. HALDANE, J. S., and J. G. PRIESTLEY: Respiration. New Haven, Conn. Yale University

Press. 1935, p. 97. 7. HELLMAN, L. M., L. B. SHETTLES, C. P. MANAHAN and N. J. EASTMAN: Sodium pento-

thal anesthesia in obstetrics. Am. 3. Obst. d Gynec. 1944, 48, 851. 8. HOLMES, F.: Spinal analgesia and caesarean section: Maternal mortality. 3. Obst. d

Cynaec. Brit. Emp. 1957, 64, 229. 9. HOLMES, J. M.: The prevention of inhaled vomit during obstetric anaesthesia. 3 . Obst. d Gynaec. Brit. Emp. 1956, 63, 239.

10. JOHNSON, T., and C. G. CLAYTON: Studies in placental action during prolonged and dysfunctional labours using radioactive sodium. 3. Obst. d Cynaec. Brit. Emp. 1955, 62, 513.

1 1 . KLEMOLA, E.: uber den Lungenbau der Friihgeburt und des ausgetragenen Kindes, vor allem mit Riicksicht auf die Entwicklung der elastischen Fasern und der Kapil- laren. Acta Pediat. 1937, 21, 236.

12. LULL, C. B., and R. A. HINGSON: Control ofpain in childbirth. J. B. Lippincott Co., Phila- delphia. 1948, p. 286.

13. LUND, P. C.: Influence of anesthesia on infant mortality rate in cesarean sections. J.A.M.A. 1955, 159, 1586.

14. MACICAY, R. B.: Observations on the oxygenation of the foetus in normal and abnormal pregnancies. 3 . Obst. d Cynaec. Brit. Emp. 1957, 64, 185.

15. MCKECHNIE, F. B., and J. G. CONVERSE: Placental transmission of thiopental. Am. 3 . Obst. B Gynec. 1955, 70, 639.

16. MALI, A. M., and C. E. RAIHA: Vergleich zwischen dem Kapillarnetz des friihgebore- nen und dem des reifen Kindes und iiber die Bedeutung des unentwickelten Kapillar-

born; experiments in their measurement and assistance. Scot. M. 3 . 1958, 3, 151.

Zeitschrft. ges. gericht. Med. 1956, 45, 381.

34 FRANK HOLMES

netzes bei der Entstehung gewisser bei Fruhgeburten vorkommender Eigenschaften . Acta Pediat. 1935, 18, 118.

17. MILLER, H. C., and N. W. SMULL: Further studies on the effects of hypoxia on the respiration of newborn infants. Pediatrics. 1955, 16, 93.

18. MINKOWSKI, A.: Oxygen saturation in the foetal arterial blood at birth. Irish 3 . Med. Sci. 1955, 6, 390.

19. RUPPERT, H.: The influence of extradural spinal anesthesia on the motility of the gravid uterus. Proc. World Cong. Anesth. Burgess Pub. Co., Minneapolis. 1955, p. 161.

20. SCHWARZ, R. : Chemische Untersuchungen zur diaplacentaren Passage von Gallamin. Der Anaesthesist. 1958, 7, 299.

21. SJOSTEDT, S., and G. ROOTH: The influence of anaesthesia on the oxygen saturation of the cord blood during caesarean section. Acta anaesth. Scandinav. 1958, 2, 99.

22. SNYDER, F. F., and M. ROSENFELD: Direct observation of intrauterine respiratory movements of the fetus and the role of carbondioxide and oxygen in their regulation. Am. 3. Physiol. 1937, 119, 153.

23. TAYLOR, E. S., C. D. GOVAN and W. C. Scorn: Oxygen saturation of the blood of the newborn, as affected by maternal anesthetic agents. Am. 3 . Obst. d Gynec., 1951, 61,840.

24. TAYLOR, E. S., W. C. SCOTT and C. D. GOVAN: Studies of blood oxygen saturation and causes of death in premature infants. Am. 3 . Obst. d Gynec. 1951, 62, 764.

25. TAYLOR, E. S.: The role of analgesia and anesthesia in fetal salvage. J.A.M.A. 1954, 156, 1481.

26. WALKER, J.: Foetal anoxia. 3 . Obst. d Gynuec. Brit. Emp. 1954, 61, 162. 27. WENDL, H. K.: Anesthesia for cesarean section. Proc. World Cong. Anesth. Burgess Pub.

28. WENDL, H. K.: Die Asphyxie des Neugeborenen. Der Anaesthesist. 1957, 6, 19. 29. YANT, W. P., J. CHORNYAK, H. H. SCHRENK, F. A. PATTY and R. R. SAYERS: Studies

Co., Minneapolis. 1955, p. 195.

in asphyxia. U. S. Treasury Dept. Pub. Health Bull. 1934, 211.

obstetrical anaesthesia and the foetus

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