1117
Better Perinatal Health FETAL ASPHYXIA IN LABOUR R. W. BEARD
R. P. A. RIVERS
Department of Obstetrics and Gynæcology, and Pædiatric Unit, St Mary’s Hospital Medical School, London W2 ASPHYXIA is generally regarded as the major cause of perinatal death’ and of disability in later life.2 Labour is a time of particular risk to the fetus because intrauterine pressure rises with each contraction, intermittently reducing the transfer of oxygen across the placenta.3 Normally the resultant fall in fetal PO, is slight4 and of no consequence. But when the uteroplacental circulation is already compromised, fetal asphyxia of increasing severity is likely to ensue. CEREBRAL PALSIES
The cerebral palsies are a group of motor disorders which appear before the age of 3 years. They are due to non-progressive lesions which interfere with the development and function of the brain, and are detected in 0.1-0.2% of the child population. There are many causes but perinatal asphyxia is believed to account for about half the cases.5 Until the presence or absence of asphyxia at birth is precisely recorded in all babies, the exact figure will be in doubt, and, in view of the known adverse effects of intrapartum asphyxia on preterm babies,6 we can guess that many cases are wrongly being ascribed to prematurity when the major factor was
asphyxia. Why are cerebral palsies, with their low incidence in the population, so frequently cited as the product of asphyxial brain damage? The reason is that they are among the few recognisable functional disorders that can be attributed to fetal asphyxia. Probably there are many other mental and physical defects which have their origins in severe intrapartum asphyxia but they go unrecognised because they fall within the wide spectrum of acceptable human behaviour. It is therefore difficult to ascribe with certainty causal significance to minor neurological defects which are recognised only some time after birth.’.8 Scott9 followed 23 babies born in very poor condition who survived and there were 6 cases of cerebral palsy; but the others grew up with no evidence of motor or mental defect. Steiner and Nelligan 10 reported similar results. Such a striking difference in outcome is curious and almost unbiological. With all other forms of injury one would expect the outcome to reflect the severity of the initial insult. Perhaps the brain is different from other organs; or perhaps some subtle abnormalities of behaviour will eventually be identified and linked with perinatal asphyxia. DIAGNOSIS OF ASPHYXIA-THEORETICAL ASPECTS
The mature fetus seems able to withstand hypoxia better than the adult because it has greater capacity to metabolise carbohydrate anaerobically and it carries
large stores of glycogen in essential tissues." This anaerobic capacity is the basis of pH measurement to deter-
mine whether the fetus is at risk of tissue damage from hypoxia. Once there is a shift towards anaerobic metabolism, lactate accumulates, causing a metabolic acidosis. Indirect evidence, based on the relation of fetal scalp blood pH to the condition of the baby at birth, 12 suggests that the fetus will come to little harm from hypoxia if the pH remains above 7-25. With progressive decline of pH the condition at birth correspondingly worsens,’3 the Apgar score at birth correlating more closely than the one-minute score with cord pH.14 Is it reasonable to assume that vital organs such as the brain are undamaged by apparently mild asphyxia? The brain might, for instance, become dependent on anaerobic metabolism at an earlier stage of hypoxia than other organs. To obtain more precise information about the effect of asphyxia on the fetus and to develop new diagnostic criteria, we have to turn to the laboratory animal.
Brain Swelling In 1969 Myers and his group15 reported their work on brain damage in the fetal monkey. Until then most investigators had employed a single acute hypoxic episode 16 which chiefly caused thalamic and brainstem necrosis-lesions not commonly seen in the human fetus dying from hypoxia. Myers’ group had found, by chance, that partial fetal asphyxia could be induced by oxytocin-stimulated excessive uterine activity. This lasted several hours and simulated the slowly developing fetal asphyxia found in labour. At delivery, the affected monkey fetuses never showed signs of respiratory activity although their hearts were beating and there was a recordable blood-
Inspection of the brain revealed the classic appearof irreversible brain damage-swelling, with enlargement of the cerebral hemispheres obliterating any space between the surface of the brain and the skull; gyral flattening ; narrowing of the sulci; and herniation of the cerebellum. These findings led to a review of 183 perinatal deaths at 20-40 weeks’ gestational age The brains of these babies had lesions almost identical to those in the monkey fetuses. The severity of the brain swelling was related to gestational age (see figure), intrapartum stillbirth, and growth retardation (see table). pressure. ances
Lactic Acid The relevance of these observations was not clearly understood until lately. The usual assumption was that the primary cause of brain swelling was diminished perfusion of the brain, secondary to failure of the systemic circulation, with a subsequent vicious circle of acidosis, tissue damage, brain swelling, and increasing venous stasis.2 The metabolic studies of Myers18 suggest an alternative explanation. He observed that, in young adult monkeys subjected to hypoxic episodes of identical severity and duration, and with uniformly deranged circulatory function and blood-gas and acid-base values before and after the hypoxia, some died with serious brain damage whilst others recovered without ill effect. The single factor that clearly distinguished the two groups was the appearance of VARIOUS FEATURES OF BRAIN SWELLING FOUND AT NECROPSY IN
31
GROWTH RETARDED
BABIES17
1118
183 perinatal cases studied according to birthweight and gestation.
gyral flattening (0) Gyral flattening (8) in cases with unacceptable menstrual’dates. or no
in
cases
with known and
lactic acid in brain tissue. All the animals with brain swelling had high concentrations of lactate in the cerebral cortex. One might conclude that the higher level of tissue lactate, and the lack of correlation between tissue and blood lactate concentration in the group with brain swelling, were due to diminished perfusion of the brain-were it not for an intriguing observation. Starvation before the experiment seemed to confer protection, whilst administration of glucose before hypoxia invariably resulted in a fetus with brain swelling. Support for this observation is provided by Shelley et al.,19 who showed that in fetal lambs rendered mildly hypoxic, glucose infusion significantly raised the plasma lactate. As plasma lactate rose so the pH fell rapidly and no lamb recovered if the pH was below 7-10. These workers suggested that the tendency for lactate to accumulate when glucose is infused might be due to lack of alternative pathways for pyruvate utilisation, there being a low capacity for oxidative metabolism and gluconeogenesis combined with low pyruvate-dehydrogenase activity.2O Similar observations have been made in human neonates following asphyxia: administration of a glucose load was followed by lacticacidxmia.21
Blood-brain Barrier The blood-brain barrier opens and closes in response to osmolar changes in the intravascular compartment, and this too may be relevant to the pathogenesis of brain swelling; a rapid rise in brain intracellular and interstitial lactate could have similar effects.22 But, in general, the blood-brain barrier seems to be preserved in hypoxia and ischoemia 23 though it may break down when blood flow is restored.24 Fetal
Electrocardiogram
Work in fetal lambs and guineapigs suggests that the fetal electrocardiogram (FECG) may offer a means of distinguishing between hypoxic and non-hypoxic abnormalities in the continuous fetal-heart-rate (FHR) record. 25 Mild hypoxia causes progressive changes in the ST segment; initially the ST segment is raised, with an associated increase in T-wave amplitude. As the severity of hypoxia increases the T-wave becomes
acceptable
menstrual
dates; gyral flattening (.)
or no
gyral flattening
-
smaller. These changes are associated with the generation of lactate by myocardium, and they precede changes in the FHR and systemic blood pH. No relation was found between fetal arterial POz and FECG changes, whereas changes in the FECG were closely related to progressive depletion of myocardial, liver, and brain glycogen. Dawes, Greene, and Rosénz6 judge that it may be possible to distinguish between hypoxic and non-hypoxic fetal bradycardia in man by quantitation of changes in the T-wave relative to the QRS component.
The potential value of these observations is obvious. We badly need a system that will provide reliable early warning of fetal tissue hypoxia, before the fetus is in immediate danger of cerebral damage. If in addition, by means of the FECG, we could distinguish between hypoxic and non-hypoxic abnormalities in the continuous fetal-heart-rate record, this could save many unnecessary interventions during labour to deliver a fetus that is in no danger of hypoxic damage. The FECG may prove to be a sensitive indicator of a shift in energy production from aerobic to anaerobic metabolism during hypoxia. Reliable and continuous records should be easier to secure with this biophysical measurement than with any biochemical one such as lactate production. Administration of glucose in large amounts during labour may be inadvisable-particularly if there is any possibility of fetal hypoxia. Finally, we should be looking at computerised axial tomography27 and ultrasound for the detection of brain swelling, and at noninvasive methods of intracranial pressure monitoring for assessment of new treatments.2g DIAGNOSIS OF ASPHYXIA——CURRENT PRACTICE
The object of intrapartum fetal monitoring is to prothe fetus from the damaging effects of hypoxia. Electronic monitoring of the FHR is widely used as a warning system, and to a variable extent the fetal pH is
tect
1119 to determine the meaning of changes in the FHR. The value of these monitoring systems to clinical care is still widely debated.29 The major point at issue is not whether monitoring is necessary or not but, firstly, whether the new systems are as effective in reducing perinatal mortality and morbidity as claimed, and, secondly, which women need to be monitored intensively. The difficulty in assessing the value of monitoring lies in the end-points that are used to assess "effectiveness". If perinatal death is taken as the end-point then only babies whose death can clearly be attributed to intrapartum asphyxia should be included. Parer30 reviewed ten non-randomised trials of intrapartum fetal monitoring, and showed that, in low-risk women who were not monitored intensively, the mean intrapartum death rate (per 1000 deliveries) was 2-4, whereas in the group of women who were monitored intensively, many of whom were high-risk, the rate was only 0- 5-significantly lower. Four prospective randomised control trials have been reported.31-34 Three of these revealed no obvious benefit in terms of perinatal salvage from electronic monitoring whilst the fourth (from Australia3a) showed considerable benefit. These studies do not provide evidence of the value of monitoring in reducing perinatal mortality. Parer has pointed out that an expected fall in intrapartum stillbirth rate of 1 to 2 per 1000 births requires a population sample considerably larger than that of the four randomised control trials combined. Intrapartum monitoring will not eliminate all the risks which the preterm breech baby faces at delivery. Asphyxia, due to cord compression or delay in delivery of the head, predisposes to intraventricular heemorrage 27 and difficult extractions may cause separation of the occipital bone--occipital osteodiastasis.35 There is still much debate about the advisability of elective cassarean section in preterm labour with a breech presentation; but two recent studies claim that this policy reduces mortality36 and long-term morbidity. 37 All the clinical trials of FHR monitoring without pH measurement, whether prospective or not, have shown a distinct increase in the caesarean-section rate amongst women monitored by the FECG alone.32 This trend is the product of obstetricians’ natural desire to deliver babies before they are damaged by asphyxia, coupled with a monitoring system which has a high incidence of false-positive results. Therefore many hopes are now being placed on fetal pH as the final index of asphyxia. However, a survey of monitoring practice in obstetric units in the U.K .38 suggests that at present the technical problems of instrument maintenance and reliability are such that only 40% of units measure fetal blood pH in conjunction with electronic monitoring. The Roche company has tried to circumvent the limitations of blood pH measurement with its continuous-recording tissue pH electrode; but we can expect to wait some time for an entirely satisfactory system for intrapartum
measured
monitoring. REFERENCES
1. Gruenwald P. Stillbirth and early neonatal death. In: Butler NR, Alberman E, eds. Perinatal problems: second report of the 1958 British Perinatal Mortality Survey. Edinburgh: Livingstone, 1969: chap. 9. 2. Brown JK. Infants damaged during birth. In: Hull D, ed. Recent advances in pædiatrics. Edinburgh: Churchill Livingstone, 1976: chap. 2. 3. Towell ME. The influence of labor on the fetus and the newborn. Pediat Clin N Am 1966; 13: 575-98.
Jansen CAM, Krane EJ, Thomas AL, Beck NFG, Joyce P, Pair M, Nathanielsz PW. Continuous variability of fetal PO, in the chronically catheterised fetal sheep. Am JObstet Gynecol 1979; 134:776-82. 5. Hagberg B, Hagberg G, Olow I. The changing panorama of cerebral palsy in Sweden 1954-70. Acta Paediat Scand 1975; 64: 187-200. 6. Hobel CJ, Hyvarinen MA, OH W. Abnormal fetal heart rate patterns and fetal acid-base balance in low birth weight infants in relation to respiratory distress syndrome. Obstet Gynecol 1972; 39: 83-88. 7. Thomson AJ, Searle M, Russell G. Quality of survival after severe birth asphyxia. Arch Dis Childh 1977; 52: 620-26. 8. de Souza SW, Richards B. Neurological sequelae in newborn babies after perinatal asphyxia. Arch Dis Childh 1978; 53: 564-69. 9. Scott H. Outcome of very severe birth asphyxia. Arch Dis Childh 1976; 51:
4.
712-16. 10. Steiner H, Nelligan H. Perinatal cardiac arrest. Arch Dis Childh 1975; 50: 696-702. 11. Shelley HJ. Glycogen reserves and their changes at birth. Br Med Bull
1961; 17: 137-43. RW, Morris ED, Clayton SG. pH of fetal capillary blood as an indicator of the condition of the fetus. J Obstet Gynæcol Br Commonw 1967;
12. Beard
74: 812-22. 13. Wood EC.
Scalp sampling amnioscopy developing fetal brain, In: Gluck L, Publishers, 1977: chap. 11.
14. Marx
GF, Mahajan S, Miclat
in intrauterine asphyxia and the ed. Chicago: Year Book Medical
MN. Correlation of biochemical data with
Apgar scores at birth and at one minute. Br J Anæsth 1977; 49: 831-33. 15. Myers RE, Beard RW, Adamsons K. Brain swelling in the newborn rhesus monkey following prolonged partial asphyxia. Neurology 1969; 19: 1012-18. 16. Windle WF, Jacobson HN, de Arellano R de R, Combs M. Structural and functional sequelae of asphyxia neonatorum in monkeys (macaca mulatta) Res Publ Assoc Res Nerv Mental Dis 1962; 39; 169- 82. 17. Pryse-Davies J, Beard RW. A necropsy study of brain swelling in the newborn with special reference to cerebellar herniation. J Path 1973; 109: 51-73. 18. Myers RE. Lactic acid accumulation as cause of brain edema and cerebral necrosis resulting from oxygen deprivation, In: Korobkin R, Guilleminault C, eds. Advances in perinatal neurology. New York: Spectrum Publications, 1979: 85-114. 19. Shelley HJ, Bassett JM, Milner RDG. Control of carbohydrate metabolism in the fetus and newborn. Br Med Bull 1975; 31: 37-43. 20. Hommes FA, Kraan GPB, Berger R. The regulation of ATP synthesis in fetal rat liver. Enzyme 1973; 15: 351-60. 21. Tejani N, Lifshitz F, Harper RG. The response to an oral glucose load during convalescence from hypoxia in newborn infants. J Pediat 1979; 94: 792-96. 22. Rapoport SI, Matthews K, Thompson HK, Pettigrew KD. Osmotic opening of the blood-brain barrier in the rhesus monkey without measurable brain oedema. Brain Res 1977; 136:23-29. 23. Bradbury M. The concept of a blood-brain barrier. Bristol: John Wiley,
1979:chap. 12. 24. Lou HC, Lassen NA, Tweed WA, Johnson G, Jones M, Palahniuk RJ. Pressure passive cerebral blood flow and breakdown of the blood-brain barrier in experimental fetal asphyxia. Acta Pædiat Scand 1979; 68: 57-63. 25. Rosén KG, Hökegård KH, Kjellmer I. A study of the relationship between the electrocardiogram and hemodynamics in the fetal lamb during asphyxia. Acta Physiol Scand 1976; 98: 275-84. 26. Dawes GS, Greene KR, Rosén KG. Fetal ECG changes in the lamb and preliminary results in human studies: In: Copeland K, ed. Report of the meeting on foetal and neonatal physiological measurements, Oxford, September 1979. London: Biological Engineering Society, c/o The Royal College of Surgeons, 1979: 1.6. 27. Pape K, Wigglesworth JS. Haemorrhage. In: Copeland K, ed. Ischaemia and the perinatal brain. London: Spastics International Medical Publications, 28.
1979:chap.7. Phillip AGS. Non-invasive monitoring of intracranial pressure.
Clin Perina-
tol 1979; 6:123-137. 29. Hobbins JC, Freeman R, Queenan JT. The fetal monitoring debate. Obstet Gynecol 1979; 54:103-09. 30. Parer JT. Fetal heart rate monitoring. Lancet 1979; ii: 632-33. 31. Haverkamp AD, Thompson HE, McFee JG, Cetrulo C. The evaluation of continuous fetal heart rate monitoring in pregnancy. Am J Obstet Gynecol 1976;125:310-20. 32. Haverkamp AD, Orleans M, Langendoerfer S, McFee J, Murphy J, Thompson HE. A controlled trial of the differential effects of intrapartum fetal monitoring. Am J Obstet Gynecol 1979; 134: 399-412. 33. Kelso IM, Parsons RJ, Lawrence GF, Arora SS, Edmonds KD, Cooke ID. An assessment of continuous fetal heart rate—a randomised trial. Am J Obstet Gynecol 1978; 131:526-32. 34. Renou P, Chang A, Anderson I, Wood EC. A controlled trial of fetal intensive care. Am J Obstet Gynecol 1976; 126: 470-76. 35. Wigglesworth JS, Husemeyer RP. Intracranial birth trauma in vaginal breech delivery: the continued importance of injury to the occipital bone. Br J Obstet Gynæcol 1977; 84: 684-91. 36. Fairweather DVI, Stewart AL. How to deliver the under 1500 g infant. In: Christian D, Zuspan F, eds. Reid’s controversy in obstetrics and gynecology. Philadelphia: WB. Saunders (in press). 37. Ingemarsson I, Westgren M, Svenningsen NW. Long-term follow up of preterm infants in breech presentation delivered by cæsarean section. Lancet 1978; ii: 172-75. 38. Gillmer MDG, Combe D. Intrapartum fetal monitoring practice in the United Kingdom. Br J Obstet Gynæcol 1979; 86:753-58.
Better Perinatal Health FETAL ASPHYXIA IN LABOUR R. W. BEARD
R. P. A. RIVERS
Department of Obstetrics and Gynæcology, and Pædiatric Unit, St Mary’s Hospital Medical School, London W2 ASPHYXIA is generally regarded as the major cause of perinatal death’ and of disability in later life.2 Labour is a time of particular risk to the fetus because intrauterine pressure rises with each contraction, intermittently reducing the transfer of oxygen across the placenta.3 Normally the resultant fall in fetal PO, is slight4 and of no consequence. But when the uteroplacental circulation is already compromised, fetal asphyxia of increasing severity is likely to ensue. CEREBRAL PALSIES
The cerebral palsies are a group of motor disorders which appear before the age of 3 years. They are due to non-progressive lesions which interfere with the development and function of the brain, and are detected in 0.1-0.2% of the child population. There are many causes but perinatal asphyxia is believed to account for about half the cases.5 Until the presence or absence of asphyxia at birth is precisely recorded in all babies, the exact figure will be in doubt, and, in view of the known adverse effects of intrapartum asphyxia on preterm babies,6 we can guess that many cases are wrongly being ascribed to prematurity when the major factor was
asphyxia. Why are cerebral palsies, with their low incidence in the population, so frequently cited as the product of asphyxial brain damage? The reason is that they are among the few recognisable functional disorders that can be attributed to fetal asphyxia. Probably there are many other mental and physical defects which have their origins in severe intrapartum asphyxia but they go unrecognised because they fall within the wide spectrum of acceptable human behaviour. It is therefore difficult to ascribe with certainty causal significance to minor neurological defects which are recognised only some time after birth.’.8 Scott9 followed 23 babies born in very poor condition who survived and there were 6 cases of cerebral palsy; but the others grew up with no evidence of motor or mental defect. Steiner and Nelligan 10 reported similar results. Such a striking difference in outcome is curious and almost unbiological. With all other forms of injury one would expect the outcome to reflect the severity of the initial insult. Perhaps the brain is different from other organs; or perhaps some subtle abnormalities of behaviour will eventually be identified and linked with perinatal asphyxia. DIAGNOSIS OF ASPHYXIA-THEORETICAL ASPECTS
The mature fetus seems able to withstand hypoxia better than the adult because it has greater capacity to metabolise carbohydrate anaerobically and it carries
large stores of glycogen in essential tissues." This anaerobic capacity is the basis of pH measurement to deter-
mine whether the fetus is at risk of tissue damage from hypoxia. Once there is a shift towards anaerobic metabolism, lactate accumulates, causing a metabolic acidosis. Indirect evidence, based on the relation of fetal scalp blood pH to the condition of the baby at birth, 12 suggests that the fetus will come to little harm from hypoxia if the pH remains above 7-25. With progressive decline of pH the condition at birth correspondingly worsens,’3 the Apgar score at birth correlating more closely than the one-minute score with cord pH.14 Is it reasonable to assume that vital organs such as the brain are undamaged by apparently mild asphyxia? The brain might, for instance, become dependent on anaerobic metabolism at an earlier stage of hypoxia than other organs. To obtain more precise information about the effect of asphyxia on the fetus and to develop new diagnostic criteria, we have to turn to the laboratory animal.
Brain Swelling In 1969 Myers and his group15 reported their work on brain damage in the fetal monkey. Until then most investigators had employed a single acute hypoxic episode 16 which chiefly caused thalamic and brainstem necrosis-lesions not commonly seen in the human fetus dying from hypoxia. Myers’ group had found, by chance, that partial fetal asphyxia could be induced by oxytocin-stimulated excessive uterine activity. This lasted several hours and simulated the slowly developing fetal asphyxia found in labour. At delivery, the affected monkey fetuses never showed signs of respiratory activity although their hearts were beating and there was a recordable blood-
Inspection of the brain revealed the classic appearof irreversible brain damage-swelling, with enlargement of the cerebral hemispheres obliterating any space between the surface of the brain and the skull; gyral flattening ; narrowing of the sulci; and herniation of the cerebellum. These findings led to a review of 183 perinatal deaths at 20-40 weeks’ gestational age The brains of these babies had lesions almost identical to those in the monkey fetuses. The severity of the brain swelling was related to gestational age (see figure), intrapartum stillbirth, and growth retardation (see table). pressure. ances
Lactic Acid The relevance of these observations was not clearly understood until lately. The usual assumption was that the primary cause of brain swelling was diminished perfusion of the brain, secondary to failure of the systemic circulation, with a subsequent vicious circle of acidosis, tissue damage, brain swelling, and increasing venous stasis.2 The metabolic studies of Myers18 suggest an alternative explanation. He observed that, in young adult monkeys subjected to hypoxic episodes of identical severity and duration, and with uniformly deranged circulatory function and blood-gas and acid-base values before and after the hypoxia, some died with serious brain damage whilst others recovered without ill effect. The single factor that clearly distinguished the two groups was the appearance of VARIOUS FEATURES OF BRAIN SWELLING FOUND AT NECROPSY IN
31
GROWTH RETARDED
BABIES17
1118
183 perinatal cases studied according to birthweight and gestation.
gyral flattening (0) Gyral flattening (8) in cases with unacceptable menstrual’dates. or no
in
cases
with known and
lactic acid in brain tissue. All the animals with brain swelling had high concentrations of lactate in the cerebral cortex. One might conclude that the higher level of tissue lactate, and the lack of correlation between tissue and blood lactate concentration in the group with brain swelling, were due to diminished perfusion of the brain-were it not for an intriguing observation. Starvation before the experiment seemed to confer protection, whilst administration of glucose before hypoxia invariably resulted in a fetus with brain swelling. Support for this observation is provided by Shelley et al.,19 who showed that in fetal lambs rendered mildly hypoxic, glucose infusion significantly raised the plasma lactate. As plasma lactate rose so the pH fell rapidly and no lamb recovered if the pH was below 7-10. These workers suggested that the tendency for lactate to accumulate when glucose is infused might be due to lack of alternative pathways for pyruvate utilisation, there being a low capacity for oxidative metabolism and gluconeogenesis combined with low pyruvate-dehydrogenase activity.2O Similar observations have been made in human neonates following asphyxia: administration of a glucose load was followed by lacticacidxmia.21
Blood-brain Barrier The blood-brain barrier opens and closes in response to osmolar changes in the intravascular compartment, and this too may be relevant to the pathogenesis of brain swelling; a rapid rise in brain intracellular and interstitial lactate could have similar effects.22 But, in general, the blood-brain barrier seems to be preserved in hypoxia and ischoemia 23 though it may break down when blood flow is restored.24 Fetal
Electrocardiogram
Work in fetal lambs and guineapigs suggests that the fetal electrocardiogram (FECG) may offer a means of distinguishing between hypoxic and non-hypoxic abnormalities in the continuous fetal-heart-rate (FHR) record. 25 Mild hypoxia causes progressive changes in the ST segment; initially the ST segment is raised, with an associated increase in T-wave amplitude. As the severity of hypoxia increases the T-wave becomes
acceptable
menstrual
dates; gyral flattening (.)
or no
gyral flattening
-
smaller. These changes are associated with the generation of lactate by myocardium, and they precede changes in the FHR and systemic blood pH. No relation was found between fetal arterial POz and FECG changes, whereas changes in the FECG were closely related to progressive depletion of myocardial, liver, and brain glycogen. Dawes, Greene, and Rosénz6 judge that it may be possible to distinguish between hypoxic and non-hypoxic fetal bradycardia in man by quantitation of changes in the T-wave relative to the QRS component.
The potential value of these observations is obvious. We badly need a system that will provide reliable early warning of fetal tissue hypoxia, before the fetus is in immediate danger of cerebral damage. If in addition, by means of the FECG, we could distinguish between hypoxic and non-hypoxic abnormalities in the continuous fetal-heart-rate record, this could save many unnecessary interventions during labour to deliver a fetus that is in no danger of hypoxic damage. The FECG may prove to be a sensitive indicator of a shift in energy production from aerobic to anaerobic metabolism during hypoxia. Reliable and continuous records should be easier to secure with this biophysical measurement than with any biochemical one such as lactate production. Administration of glucose in large amounts during labour may be inadvisable-particularly if there is any possibility of fetal hypoxia. Finally, we should be looking at computerised axial tomography27 and ultrasound for the detection of brain swelling, and at noninvasive methods of intracranial pressure monitoring for assessment of new treatments.2g DIAGNOSIS OF ASPHYXIA——CURRENT PRACTICE
The object of intrapartum fetal monitoring is to prothe fetus from the damaging effects of hypoxia. Electronic monitoring of the FHR is widely used as a warning system, and to a variable extent the fetal pH is
tect
1119 to determine the meaning of changes in the FHR. The value of these monitoring systems to clinical care is still widely debated.29 The major point at issue is not whether monitoring is necessary or not but, firstly, whether the new systems are as effective in reducing perinatal mortality and morbidity as claimed, and, secondly, which women need to be monitored intensively. The difficulty in assessing the value of monitoring lies in the end-points that are used to assess "effectiveness". If perinatal death is taken as the end-point then only babies whose death can clearly be attributed to intrapartum asphyxia should be included. Parer30 reviewed ten non-randomised trials of intrapartum fetal monitoring, and showed that, in low-risk women who were not monitored intensively, the mean intrapartum death rate (per 1000 deliveries) was 2-4, whereas in the group of women who were monitored intensively, many of whom were high-risk, the rate was only 0- 5-significantly lower. Four prospective randomised control trials have been reported.31-34 Three of these revealed no obvious benefit in terms of perinatal salvage from electronic monitoring whilst the fourth (from Australia3a) showed considerable benefit. These studies do not provide evidence of the value of monitoring in reducing perinatal mortality. Parer has pointed out that an expected fall in intrapartum stillbirth rate of 1 to 2 per 1000 births requires a population sample considerably larger than that of the four randomised control trials combined. Intrapartum monitoring will not eliminate all the risks which the preterm breech baby faces at delivery. Asphyxia, due to cord compression or delay in delivery of the head, predisposes to intraventricular heemorrage 27 and difficult extractions may cause separation of the occipital bone--occipital osteodiastasis.35 There is still much debate about the advisability of elective cassarean section in preterm labour with a breech presentation; but two recent studies claim that this policy reduces mortality36 and long-term morbidity. 37 All the clinical trials of FHR monitoring without pH measurement, whether prospective or not, have shown a distinct increase in the caesarean-section rate amongst women monitored by the FECG alone.32 This trend is the product of obstetricians’ natural desire to deliver babies before they are damaged by asphyxia, coupled with a monitoring system which has a high incidence of false-positive results. Therefore many hopes are now being placed on fetal pH as the final index of asphyxia. However, a survey of monitoring practice in obstetric units in the U.K .38 suggests that at present the technical problems of instrument maintenance and reliability are such that only 40% of units measure fetal blood pH in conjunction with electronic monitoring. The Roche company has tried to circumvent the limitations of blood pH measurement with its continuous-recording tissue pH electrode; but we can expect to wait some time for an entirely satisfactory system for intrapartum
measured
monitoring. REFERENCES
1. Gruenwald P. Stillbirth and early neonatal death. In: Butler NR, Alberman E, eds. Perinatal problems: second report of the 1958 British Perinatal Mortality Survey. Edinburgh: Livingstone, 1969: chap. 9. 2. Brown JK. Infants damaged during birth. In: Hull D, ed. Recent advances in pædiatrics. Edinburgh: Churchill Livingstone, 1976: chap. 2. 3. Towell ME. The influence of labor on the fetus and the newborn. Pediat Clin N Am 1966; 13: 575-98.
Jansen CAM, Krane EJ, Thomas AL, Beck NFG, Joyce P, Pair M, Nathanielsz PW. Continuous variability of fetal PO, in the chronically catheterised fetal sheep. Am JObstet Gynecol 1979; 134:776-82. 5. Hagberg B, Hagberg G, Olow I. The changing panorama of cerebral palsy in Sweden 1954-70. Acta Paediat Scand 1975; 64: 187-200. 6. Hobel CJ, Hyvarinen MA, OH W. Abnormal fetal heart rate patterns and fetal acid-base balance in low birth weight infants in relation to respiratory distress syndrome. Obstet Gynecol 1972; 39: 83-88. 7. Thomson AJ, Searle M, Russell G. Quality of survival after severe birth asphyxia. Arch Dis Childh 1977; 52: 620-26. 8. de Souza SW, Richards B. Neurological sequelae in newborn babies after perinatal asphyxia. Arch Dis Childh 1978; 53: 564-69. 9. Scott H. Outcome of very severe birth asphyxia. Arch Dis Childh 1976; 51:
4.
712-16. 10. Steiner H, Nelligan H. Perinatal cardiac arrest. Arch Dis Childh 1975; 50: 696-702. 11. Shelley HJ. Glycogen reserves and their changes at birth. Br Med Bull
1961; 17: 137-43. RW, Morris ED, Clayton SG. pH of fetal capillary blood as an indicator of the condition of the fetus. J Obstet Gynæcol Br Commonw 1967;
12. Beard
74: 812-22. 13. Wood EC.
Scalp sampling amnioscopy developing fetal brain, In: Gluck L, Publishers, 1977: chap. 11.
14. Marx
GF, Mahajan S, Miclat
in intrauterine asphyxia and the ed. Chicago: Year Book Medical
MN. Correlation of biochemical data with
Apgar scores at birth and at one minute. Br J Anæsth 1977; 49: 831-33. 15. Myers RE, Beard RW, Adamsons K. Brain swelling in the newborn rhesus monkey following prolonged partial asphyxia. Neurology 1969; 19: 1012-18. 16. Windle WF, Jacobson HN, de Arellano R de R, Combs M. Structural and functional sequelae of asphyxia neonatorum in monkeys (macaca mulatta) Res Publ Assoc Res Nerv Mental Dis 1962; 39; 169- 82. 17. Pryse-Davies J, Beard RW. A necropsy study of brain swelling in the newborn with special reference to cerebellar herniation. J Path 1973; 109: 51-73. 18. Myers RE. Lactic acid accumulation as cause of brain edema and cerebral necrosis resulting from oxygen deprivation, In: Korobkin R, Guilleminault C, eds. Advances in perinatal neurology. New York: Spectrum Publications, 1979: 85-114. 19. Shelley HJ, Bassett JM, Milner RDG. Control of carbohydrate metabolism in the fetus and newborn. Br Med Bull 1975; 31: 37-43. 20. Hommes FA, Kraan GPB, Berger R. The regulation of ATP synthesis in fetal rat liver. Enzyme 1973; 15: 351-60. 21. Tejani N, Lifshitz F, Harper RG. The response to an oral glucose load during convalescence from hypoxia in newborn infants. J Pediat 1979; 94: 792-96. 22. Rapoport SI, Matthews K, Thompson HK, Pettigrew KD. Osmotic opening of the blood-brain barrier in the rhesus monkey without measurable brain oedema. Brain Res 1977; 136:23-29. 23. Bradbury M. The concept of a blood-brain barrier. Bristol: John Wiley,
1979:chap. 12. 24. Lou HC, Lassen NA, Tweed WA, Johnson G, Jones M, Palahniuk RJ. Pressure passive cerebral blood flow and breakdown of the blood-brain barrier in experimental fetal asphyxia. Acta Pædiat Scand 1979; 68: 57-63. 25. Rosén KG, Hökegård KH, Kjellmer I. A study of the relationship between the electrocardiogram and hemodynamics in the fetal lamb during asphyxia. Acta Physiol Scand 1976; 98: 275-84. 26. Dawes GS, Greene KR, Rosén KG. Fetal ECG changes in the lamb and preliminary results in human studies: In: Copeland K, ed. Report of the meeting on foetal and neonatal physiological measurements, Oxford, September 1979. London: Biological Engineering Society, c/o The Royal College of Surgeons, 1979: 1.6. 27. Pape K, Wigglesworth JS. Haemorrhage. In: Copeland K, ed. Ischaemia and the perinatal brain. London: Spastics International Medical Publications, 28.
1979:chap.7. Phillip AGS. Non-invasive monitoring of intracranial pressure.
Clin Perina-
tol 1979; 6:123-137. 29. Hobbins JC, Freeman R, Queenan JT. The fetal monitoring debate. Obstet Gynecol 1979; 54:103-09. 30. Parer JT. Fetal heart rate monitoring. Lancet 1979; ii: 632-33. 31. Haverkamp AD, Thompson HE, McFee JG, Cetrulo C. The evaluation of continuous fetal heart rate monitoring in pregnancy. Am J Obstet Gynecol 1976;125:310-20. 32. Haverkamp AD, Orleans M, Langendoerfer S, McFee J, Murphy J, Thompson HE. A controlled trial of the differential effects of intrapartum fetal monitoring. Am J Obstet Gynecol 1979; 134: 399-412. 33. Kelso IM, Parsons RJ, Lawrence GF, Arora SS, Edmonds KD, Cooke ID. An assessment of continuous fetal heart rate—a randomised trial. Am J Obstet Gynecol 1978; 131:526-32. 34. Renou P, Chang A, Anderson I, Wood EC. A controlled trial of fetal intensive care. Am J Obstet Gynecol 1976; 126: 470-76. 35. Wigglesworth JS, Husemeyer RP. Intracranial birth trauma in vaginal breech delivery: the continued importance of injury to the occipital bone. Br J Obstet Gynæcol 1977; 84: 684-91. 36. Fairweather DVI, Stewart AL. How to deliver the under 1500 g infant. In: Christian D, Zuspan F, eds. Reid’s controversy in obstetrics and gynecology. Philadelphia: WB. Saunders (in press). 37. Ingemarsson I, Westgren M, Svenningsen NW. Long-term follow up of preterm infants in breech presentation delivered by cæsarean section. Lancet 1978; ii: 172-75. 38. Gillmer MDG, Combe D. Intrapartum fetal monitoring practice in the United Kingdom. Br J Obstet Gynæcol 1979; 86:753-58.
