The obstetrician, KENNETH
R.
NISWANDER,
fetal asphyxia, and cerebral palsy M.D
Davis, Calf&G In the current legal climate, the recognition of cerebral palsy or other major brain dysfunction in a child is likely to lead to a malpractice action against the obstetrician who delivered the child. Perinatal asphyxia is usually considered the most likely cause of the brain damage, and the obstetrician is presumed by the lawyer either lo have failed to recognize the fetal asphyxia or to have ignored it. In this essay, the illogic in this reasoning is discussed. While fetal asphyxia clearly can cause fetal brain damage, the infrequency of this relationship is stressed. The dilemma faced by the obstetrician as a result of modern perinatal care is discussed. (AM. J. OBSTET. GYNECOL. 133:358,
1979.)
CURRENTLY, in many parts of the country, the delivery of a child who is found to suffer from cerebral palsy or other major neurologic deficit can be expected to lead to malpractice action against the obstetrician. This is almost a reflex action. The assumption is made that the neurologic damage must be due to obstetric malpractice during the perinatal period and that the action or inaction of the obstetrician was responsible for the damage to the child. Perinatal asphyxia is the “cause” of brain damage currently in vogue with trial lawyers. Unfortunately, many, if not most, of these legal actions result in judgments against the obstetrician. I say “unfortunately” not because I think physicians should not be held liable for a bad result which can be related to malpractice. Rather, I think the scientific basis for relating perinatal asphyxia to subsequent brain damage in an individual patient is tenuous at best. While there seems no doubt that fetal asphyxia cn~z be followed by fetal brain damage, that is not the question at issue. Rather, we need to know if fetal perinatal asphyxia is usually orfrequently followed by clinical brain damage. Conversely, is cerebral palsy usually caused by fetal perinatal asphyxia? We also need to know what duration and what severity of asphyxia will result in brain damage. Crucial to the issue also is the degree of precision with which the diagnosis and severity of asphyxia of the fetus in utero can be made. What, if any, obstetric intervention can be expected to prevent the brain-damaging effects of asphyxia? Since it has been
From the Department of Medicine, University
of Obstetrics
and Gynecology, of Calfornia-Dark.
Reprint requests: Kenneth R. Nixwander,
School
M.D., Profesw and Chairman, Department of Obstetrics and Gynecology, School of Medicine, University qf California-Dauic, Davis, California 95616.
358
clearly established that episodes of in utero asphyxia which occur long before labor can result in fetal brain damage, we need to know whether these episodes can be prospectively recognized. Perinatal events should not be blamed for brain damage when earlier or later insults are at fault. Selective review of the huge literature on the matter can help answer these questions.
Mechanism Brain damage in an asphyxiated fetus may result simply from decreased blood oxygen levels resulting in subcellular organelle damage. Depending on the degree of damage, the brain stem, the midbrain, or the cerebrum may be affected. The brain damage from asphyxia may also occur less directly through cardiovascular changes induced by the asphyxia. Inadequate blood flow through the brain will then reduce the amount of oxygen available to the brain tissue. Myers’ has observed injury primarily in the brain stem with total asphyxia in the pregnant monkey. Total asphyxia of 10 minutes or less resulted in extended survival of the fetus with no recognizable morbidity in the neonate following delivery. Asphyxia of 25 minutes or longer was followed by severe brain damage, but these animals died in the early hours after delivery of progressive and intractable heart failure due to asphyxial injury of the myocardium. If the asphyxia was allowed to continue for more than 10 but less than 25 minutes, increasing damage to brain-stem structures was observed. This brain-stem injury pattern associated with total asphyxia is rarely seen in the human infant. Myers has also described brain damage in the monkey fetus which results from prolonged partial asphyxia. This experimental design is more directly applicable to the human situation since the pathologic consequences of partial asphyxia are various degrees of 000%9378/79/040358+04$00.40/0
0
1979 The C. V. Mosby Co.
Volume Number
133 4
damage to the cerebral hemispheres, a pathologic picture similar to that observed in the human being with cerebral palsy. Under carefully controlled experimental conditions, Myers noted that late fetal heart decelerations developed when the partial fetal asphyxia resulted in fetal arterial blood pH levels of 7.10 to 7.15. At this level of asphyxia no damage to the fetal brain was observed despite an insult duration of several hours. When the asphyxia was made more severe, with a drop in the fetal blood pH level below 7.00 for an extended period of time, damage to the fetal brain occurred with regularity. This brain damage, however, was of little clinical significance since the animals all died in the neonatal period from heart failure due apparently to myocardial damage. With a degree of asphyxia intermediate between these two extremes, an occasional animal survived with evidence of permanent brain injury. Myers noted, however, that the number of surviving animals in this intermediate group was very small compared with those of the other two groups. It is apparently extremely difficult in the experimental animal to secure the exact amount of asphyxia which will cause brain damage but which will not cause death of the animal. These experimental results were confirmed by a number of similar reports.
Clinical application Certain problems result when an attempt is made to apply animal data to the human situation. Difficulty is encountered in the precise diagnosis of asphyxia in the human subject, especially since the endpoint we wish to study is central nervous system damage. Furthermore, the duration of asphyxia necessary to produce damage remains uncertain. The role played by modern perinatal care in allowing survival of a brain-damaged child who might otherwise have died needs to be clarified. Another problem in relating intrauterine asphyxia to central nervous system damage in the clinical situation results from the observation that there are other causes for similar brain damage, some extremely difficult to prove in a clinical setting. Congenital anomalies of the brain, intrauterine infections, notably cytomegalovirus and toxoplasmosis, immaturity of the brain (premature labor or intrauterine growth retardation), and delivery trauma are examples of such causes. Modern newborn resuscitation with a ventilating apparatus has fortunately reduced the risk of brain damage in a child born in poor condition. The role of the anesthetic and analgesic agents on fetal brain tissue already compromised is uncertain at best. Maternal stress may cause the release of catecholamines with resultant de-
The obstetrician, fetal asphyxia, and cerebral palsy
Table I. Frequency cerebral
of obstetric
complications
359
with
palsy* Complication
I
Placenta previa Malpresentations Abruptio placentae Umbilical cord Bony dystocia *After Lilienfeld
Increase in plLsy 6x 5x 3x 2.5 x 1.3 x
and Parkhurst.’
crease in uterine blood flow and fetal hypoxia. maternal stress result in fetal brain damage?
Does
Diagnosis The diagnosis of asphyxia in the human fetus continues to be an elusive goal of the obstetrician and fetologist. While late fetal heart decelerations and lowered scalp blood pH levels are said to correlate with asphyxia, the precision of this relationship leaves much to be desired. Goodlin,* for example, reported that late fetal heart decelerations “over-read” in utero asphyxia since only about 50% of fetuses with late decelerations had a recorded Apgar score below 7. Similarly, many authors report significant numbers of neonates with a scalp blood pH above 7.25 with low Apgar scores and significant numbers of babies with a pH of 7.15 or less with normal Apgar scores. Hon, Khazin, and Paul,3 for example, noted that 79.0% of infants born following a scalp blood pH of 7.20 or less enjoyed a 5 minute Apgar score of 7 or higher. With a pH greater than 7.20, 20.1% of the infants scored 6 or lower on the 1 minute Apgar and 4.8% were similarly scored on the 5 minute Apgar. While Hon thought many of the discrepancies could be accounted for by a prolonged interval between sampling and delivery, the poor correlation in many cases still could not be accounted for. While a method of diagnosing fetal asphyxia with precision is a great need of the clinician, an even more important desideratum is a method of recognizing neurologic dysfunction in the fetus in utero. Sokol, Rosen, and Chik,a in a prospective study, noted good correlation between an abnormal fetal electroencephalogram (FEEG) and subsequent neurologic abnormality in the child at 1 year of age. The possibility exists, however, that these brain abnormalities may have predated labor. The technical difficulty in obtaining the FEEG and the vagaries of interpretation continue to make this tool of uncertain and unproved value. Insistence on definite evidence of fetal asphyxia before performing a cesarean section for this diagnosis may lead to another complication. Goodlin, Lowe, and Parme? reduced the number of “rapid deliveries,” mostly cesarean sections, for fetal distress in their
360
February Am. J. Obstet.
Niswander
Table II. Neurologic asphyxia at birth*
status of children
born with
I Asphyxiated None with persistent convulsions Febrile convulsions Controls Convulsors Recurring convulsions Single episode, unknown etiology Febrile convulsions
No.
236 0 2 233 16 4 4 8
*After Keith and Gage.‘O Table
III.
Four-year
mean I.Q. score*
Babies
Mature birth weight: 334 Low birth weight: 92
-4
99.1 94.0
I
Control
100.2 92.1
*From Niswander. Gordon, and Drage. ‘* obstetric unit by insisting that a low fetal scalp pH confirm the fetal asphyxia suggested by an abnormal fetal heart rate pattern. Of 11 rapid deliveries for fetal distress under these circumstances, however, six of the fetuses (five delivered by section) had anomalies that were incompatible with life. The authors speculate that “an abnormal fetus will more likely have an abnormal fetal heart rate and scalp pH during labor.”
latrogenic cause What effect does modern obstetric care in high-risk obstetric centers have on the risk of neurologic damage? Does vigorous and expert resuscitation of a depressed human newborn infant occasionally prevent death only to allow a brain-damaged child to live? Does modern obstetric care lower the perinatal death risk at the expense of an occasional brain-damaged child? (Certainly no responsible physician would fail to provide the best resuscitation possible even if this were true. Most depressed babies survive intact.) Should the obstetrician perform a cesarean section for fetal indication in a woman in shock from acute placental separation if the fetal heart rate recording suggests severe asphyxia? The answers to these questions simply are not available. A recent experimental finding suggests the possibility of an even more important question. Myers6 has recently reported that fetal asphyxia of a given degree is more likely to result in brain damage in the surviving animal if the maternal and fetal blood glucose is high. Myers theorizes that the lactate released from glucose metabolism leads to changes in membrane physiologic properties which cause brain edema. Is the clinical application of this experimen-
15, 1979 Gynecol.
tal finding justified? Should intravenous glucose avoided in the parturient with a fetus at risk?
be
Human epidemiologic data Lilienfeld and Parkhurst,’ in their classic paper in 1951 on the etiology of cerebral palsy, reported that certain obstetric complications occurred with greater frequency among children with cerebral palsy than among normal control subjects. They listed placenta previa, malpresentations other than breech, premature separation of the placenta, breech presentation, complications of the umbilical cord, and bony dystocia as related to cerebral palsy in decreasing frequency (Table I). Since these obstetric complications are related to prematurity and low birth weight with approximately the same frequency as they are related to cerebral palsy, it is evident that the failure of these authors to control for the factor of low birth weight/ prematurity, a well known precedent of brain damage, has greatly weakened their thesis. It seems certain that their results reflect, at least partially, the effect of low birth weight rather than of the potentially asphyxiating complications they list. The same observation can be made on the well-known report by Eastman and associate@ in 1962, in which the authors compared the obstetric background of 753 children with cerebral palsy with the background of appropriate control children. Again, prematurity probably accounted for at least some of the observed differences. Cushne? in 1961 followed long-term survivors of prolapse of the umbilical cord who had been delivered at the Johns Hopkins Hospital. Of 66 babies followed, only three were frankly abnormal neurologically. Two of these babies had birth weights less than 1,500 grams. The author concluded that, “Permanent brain damage is a less common sequel in fetal survivals of prolapsed cord than was formerly feared.” In a study at the Mayo Clinic reported in 1960, Keith and Gage’” noted nonfebrile convulsive disorders more frequently among nonasphyxiated babies followed into childhood than among those recognized as asphyxiated at birth (Table 11). Neligan, Prudham, and Steiner” studied the effects of neonatal asphyxia on subsequent cerebral palsy. Perinatal asphyxia had no significant effect “upon general intelligence as we have measured it in our normal school population,” they wrote. In 1970 we recorded the results of 1 year neurologic examinations on surviving babies born following placenta previa, abruptio placentae, or prolapse of the umbilical cord. The data were collected before fetal heart rate monitoring was in general use. The perinatal death rate was high in the cohort from which these babies were selected, confirming the frequency with
Volume Number
133 4
The obstetrician, fetal asphyxia, and cerebral palsy
which fetal asphyxia occurred. At 1 year of age, we were unable to show any differences in neurologic status between these babies and the study population from which they were drawn. Birth weight was used as a control, and the low-birth-weight babies, as expected, were more likely to have exhibited neurologic damage than were those of normal birth weight. The presumed asphyxia in the study babies, however, did not add to this hazard. In a subsequent paper in 1974 Niswander, Gordon and Dragen reported examination of the same group of children at the age of 4 years. They noted no impairment of 4 year I.Q. score (Table III), fine motor score, or gross motor score among study children compared to carefully matched control children. When the babies whose mothers had suffered severe maternal shock were subdivided out for analysis, even this group failed to show any effect on I.Q. or motor scores. In an oft-quoted paper from the Collaborative Perinatal Project, Drage, Berendes, and Fisheri reported that children with a 5 minute Apgar score of 0 to 6 enjoyed a mean 4 year I.Q. no different from that of babies whose 5 minute Apgar scores were 8 to 10. While there was a slight increase in the abnormality rates in the fine and gross motor tests at 4 years among the children with low Apgar score, these differences were very small. One per cent of infants of mature birth weight and of normal 5 minute Apgar score were recorded as abnormal on the 4 year gross and fine motor scores. Only 2% of a comparable group of children with low 5 minute Apgar scores were recognized as abnormal on these examinations.
361
Comment Since a precise tool for the diagnosis of fetal asphyxia or fetal neurologic compromise is not available, it seems evident that the obstetrician not infrequently will be faced with the choice between immediate delivery of an infant who is presumably asphyxiated and may suffer brain damage and continued observation of fetal condition with fetal or neonatal death a likely possibility. Myers has reported that it is difficult in the experimental monkey to titrate fetal asphyxia carefully enough to produce a brain-damaged yet surviving neonate. If this is true in the experimental animal, how can obstetricians be expected to predict which asphyxiated human fetus will be born alive with brain damage? No one will argue that perinatal asphyxia is innocuous, that it does not kill, that it does not occasionally maim. Avoidance of perinatal asphyxia continues to be a primary goal of modern perinatal care. To hold an obstetrician responsible for every case of cerebral palsy on the thesis that fetal perinatal asphyxia is commonly followed by brain damage is patently unjust. Perinatal asphyxia of any degree of severity rarely leads to brain damage. Overreaction to perinatal asphyxia may in itself be damaging to the gravida and sometimes to the fetus. The obstetrician must be freed from the unfair judgments made against him as he tries to bring the best obstetric care to his patients.
REFERENCES
1. Myers,
R.: Two patterns of their conditions of occurrence, 112:246, 1972.
perinatal brain damage and AM. J. OBSTET.
GYNECOL.
2. Goodlin, R. C.: Intrapartum fetal heart rate responses in plethysmographic pulse, AM. J. OBSTET. GYNECOL. 110: 210, 1971. 3. Hon, E., Khazin, A., and Paul, R.: Biochemical studies of the fetus. II. Fetal pH and Apgar scores, Obstet. Gynecol. 33:237, 1969.
4. Sokol, R., Rosen, J., and Chik, L.: Fetal electroencephalographic
related to infant outcome, AM. J. 127:329, 1977. 5. Goodlin, R., Lowe, E., and Parmer, J.: Fetal monitoring: Letter to the Editor, Obstet. Gynecol. 43:474, 1974. 6. Myers, R. E.: Personal communication, 1978. 7. Lilienfeld, A., and Parkhurst, E.: A study of the association of factors of pregnancy and parturition with the development of cerebral palsy: A preliminary report, Am. J. Hyg. 53~262, 1951. OBSTET.
monitoring
GYNECOL.
8. Eastman,
N., Kohl, S., Maisel, J., and Kavaler, F.: The obstetrical background of 753 cases of cerebral palsy, Obstet. Gynecol. Surv. 17:459, 1962. 9. Cushner, I.: Prolapse of the umbilical cord, including a late follow-up of fetal survivors, AM. J. OBSTET. GYNECOL. 81:666, 1961. 10. Keith, H., and Gage, G.: Neurologic lesions in relation to asphyxia of the newborn and factors of pregnancy: Long
term follow-up, Pediatrics 26~616, 1960. 11. Neligan, G., Prudham, D., and Steiner, H.: The Formative Years: Birth, Family, and Development in Newcastle Upon Tyne, London, 1974, University Press. 12. Niswander, K., Gordon, M., and Drage, J.: The effect of intrauterine hypoxia on the child surviving to 4 years, AM. J. OBSTET. GYNECOL. 121:892, 1975. 13. Drage, J., Berendes, H., and Fisher, P.: The Apgar scores and four-year psychological examination performance, Pan. Am. Health Org. Sci. Pub. 185~222, 1969.
R.
NISWANDER,
fetal asphyxia, and cerebral palsy M.D
Davis, Calf&G In the current legal climate, the recognition of cerebral palsy or other major brain dysfunction in a child is likely to lead to a malpractice action against the obstetrician who delivered the child. Perinatal asphyxia is usually considered the most likely cause of the brain damage, and the obstetrician is presumed by the lawyer either lo have failed to recognize the fetal asphyxia or to have ignored it. In this essay, the illogic in this reasoning is discussed. While fetal asphyxia clearly can cause fetal brain damage, the infrequency of this relationship is stressed. The dilemma faced by the obstetrician as a result of modern perinatal care is discussed. (AM. J. OBSTET. GYNECOL. 133:358,
1979.)
CURRENTLY, in many parts of the country, the delivery of a child who is found to suffer from cerebral palsy or other major neurologic deficit can be expected to lead to malpractice action against the obstetrician. This is almost a reflex action. The assumption is made that the neurologic damage must be due to obstetric malpractice during the perinatal period and that the action or inaction of the obstetrician was responsible for the damage to the child. Perinatal asphyxia is the “cause” of brain damage currently in vogue with trial lawyers. Unfortunately, many, if not most, of these legal actions result in judgments against the obstetrician. I say “unfortunately” not because I think physicians should not be held liable for a bad result which can be related to malpractice. Rather, I think the scientific basis for relating perinatal asphyxia to subsequent brain damage in an individual patient is tenuous at best. While there seems no doubt that fetal asphyxia cn~z be followed by fetal brain damage, that is not the question at issue. Rather, we need to know if fetal perinatal asphyxia is usually orfrequently followed by clinical brain damage. Conversely, is cerebral palsy usually caused by fetal perinatal asphyxia? We also need to know what duration and what severity of asphyxia will result in brain damage. Crucial to the issue also is the degree of precision with which the diagnosis and severity of asphyxia of the fetus in utero can be made. What, if any, obstetric intervention can be expected to prevent the brain-damaging effects of asphyxia? Since it has been
From the Department of Medicine, University
of Obstetrics
and Gynecology, of Calfornia-Dark.
Reprint requests: Kenneth R. Nixwander,
School
M.D., Profesw and Chairman, Department of Obstetrics and Gynecology, School of Medicine, University qf California-Dauic, Davis, California 95616.
358
clearly established that episodes of in utero asphyxia which occur long before labor can result in fetal brain damage, we need to know whether these episodes can be prospectively recognized. Perinatal events should not be blamed for brain damage when earlier or later insults are at fault. Selective review of the huge literature on the matter can help answer these questions.
Mechanism Brain damage in an asphyxiated fetus may result simply from decreased blood oxygen levels resulting in subcellular organelle damage. Depending on the degree of damage, the brain stem, the midbrain, or the cerebrum may be affected. The brain damage from asphyxia may also occur less directly through cardiovascular changes induced by the asphyxia. Inadequate blood flow through the brain will then reduce the amount of oxygen available to the brain tissue. Myers’ has observed injury primarily in the brain stem with total asphyxia in the pregnant monkey. Total asphyxia of 10 minutes or less resulted in extended survival of the fetus with no recognizable morbidity in the neonate following delivery. Asphyxia of 25 minutes or longer was followed by severe brain damage, but these animals died in the early hours after delivery of progressive and intractable heart failure due to asphyxial injury of the myocardium. If the asphyxia was allowed to continue for more than 10 but less than 25 minutes, increasing damage to brain-stem structures was observed. This brain-stem injury pattern associated with total asphyxia is rarely seen in the human infant. Myers has also described brain damage in the monkey fetus which results from prolonged partial asphyxia. This experimental design is more directly applicable to the human situation since the pathologic consequences of partial asphyxia are various degrees of 000%9378/79/040358+04$00.40/0
0
1979 The C. V. Mosby Co.
Volume Number
133 4
damage to the cerebral hemispheres, a pathologic picture similar to that observed in the human being with cerebral palsy. Under carefully controlled experimental conditions, Myers noted that late fetal heart decelerations developed when the partial fetal asphyxia resulted in fetal arterial blood pH levels of 7.10 to 7.15. At this level of asphyxia no damage to the fetal brain was observed despite an insult duration of several hours. When the asphyxia was made more severe, with a drop in the fetal blood pH level below 7.00 for an extended period of time, damage to the fetal brain occurred with regularity. This brain damage, however, was of little clinical significance since the animals all died in the neonatal period from heart failure due apparently to myocardial damage. With a degree of asphyxia intermediate between these two extremes, an occasional animal survived with evidence of permanent brain injury. Myers noted, however, that the number of surviving animals in this intermediate group was very small compared with those of the other two groups. It is apparently extremely difficult in the experimental animal to secure the exact amount of asphyxia which will cause brain damage but which will not cause death of the animal. These experimental results were confirmed by a number of similar reports.
Clinical application Certain problems result when an attempt is made to apply animal data to the human situation. Difficulty is encountered in the precise diagnosis of asphyxia in the human subject, especially since the endpoint we wish to study is central nervous system damage. Furthermore, the duration of asphyxia necessary to produce damage remains uncertain. The role played by modern perinatal care in allowing survival of a brain-damaged child who might otherwise have died needs to be clarified. Another problem in relating intrauterine asphyxia to central nervous system damage in the clinical situation results from the observation that there are other causes for similar brain damage, some extremely difficult to prove in a clinical setting. Congenital anomalies of the brain, intrauterine infections, notably cytomegalovirus and toxoplasmosis, immaturity of the brain (premature labor or intrauterine growth retardation), and delivery trauma are examples of such causes. Modern newborn resuscitation with a ventilating apparatus has fortunately reduced the risk of brain damage in a child born in poor condition. The role of the anesthetic and analgesic agents on fetal brain tissue already compromised is uncertain at best. Maternal stress may cause the release of catecholamines with resultant de-
The obstetrician, fetal asphyxia, and cerebral palsy
Table I. Frequency cerebral
of obstetric
complications
359
with
palsy* Complication
I
Placenta previa Malpresentations Abruptio placentae Umbilical cord Bony dystocia *After Lilienfeld
Increase in plLsy 6x 5x 3x 2.5 x 1.3 x
and Parkhurst.’
crease in uterine blood flow and fetal hypoxia. maternal stress result in fetal brain damage?
Does
Diagnosis The diagnosis of asphyxia in the human fetus continues to be an elusive goal of the obstetrician and fetologist. While late fetal heart decelerations and lowered scalp blood pH levels are said to correlate with asphyxia, the precision of this relationship leaves much to be desired. Goodlin,* for example, reported that late fetal heart decelerations “over-read” in utero asphyxia since only about 50% of fetuses with late decelerations had a recorded Apgar score below 7. Similarly, many authors report significant numbers of neonates with a scalp blood pH above 7.25 with low Apgar scores and significant numbers of babies with a pH of 7.15 or less with normal Apgar scores. Hon, Khazin, and Paul,3 for example, noted that 79.0% of infants born following a scalp blood pH of 7.20 or less enjoyed a 5 minute Apgar score of 7 or higher. With a pH greater than 7.20, 20.1% of the infants scored 6 or lower on the 1 minute Apgar and 4.8% were similarly scored on the 5 minute Apgar. While Hon thought many of the discrepancies could be accounted for by a prolonged interval between sampling and delivery, the poor correlation in many cases still could not be accounted for. While a method of diagnosing fetal asphyxia with precision is a great need of the clinician, an even more important desideratum is a method of recognizing neurologic dysfunction in the fetus in utero. Sokol, Rosen, and Chik,a in a prospective study, noted good correlation between an abnormal fetal electroencephalogram (FEEG) and subsequent neurologic abnormality in the child at 1 year of age. The possibility exists, however, that these brain abnormalities may have predated labor. The technical difficulty in obtaining the FEEG and the vagaries of interpretation continue to make this tool of uncertain and unproved value. Insistence on definite evidence of fetal asphyxia before performing a cesarean section for this diagnosis may lead to another complication. Goodlin, Lowe, and Parme? reduced the number of “rapid deliveries,” mostly cesarean sections, for fetal distress in their
360
February Am. J. Obstet.
Niswander
Table II. Neurologic asphyxia at birth*
status of children
born with
I Asphyxiated None with persistent convulsions Febrile convulsions Controls Convulsors Recurring convulsions Single episode, unknown etiology Febrile convulsions
No.
236 0 2 233 16 4 4 8
*After Keith and Gage.‘O Table
III.
Four-year
mean I.Q. score*
Babies
Mature birth weight: 334 Low birth weight: 92
-4
99.1 94.0
I
Control
100.2 92.1
*From Niswander. Gordon, and Drage. ‘* obstetric unit by insisting that a low fetal scalp pH confirm the fetal asphyxia suggested by an abnormal fetal heart rate pattern. Of 11 rapid deliveries for fetal distress under these circumstances, however, six of the fetuses (five delivered by section) had anomalies that were incompatible with life. The authors speculate that “an abnormal fetus will more likely have an abnormal fetal heart rate and scalp pH during labor.”
latrogenic cause What effect does modern obstetric care in high-risk obstetric centers have on the risk of neurologic damage? Does vigorous and expert resuscitation of a depressed human newborn infant occasionally prevent death only to allow a brain-damaged child to live? Does modern obstetric care lower the perinatal death risk at the expense of an occasional brain-damaged child? (Certainly no responsible physician would fail to provide the best resuscitation possible even if this were true. Most depressed babies survive intact.) Should the obstetrician perform a cesarean section for fetal indication in a woman in shock from acute placental separation if the fetal heart rate recording suggests severe asphyxia? The answers to these questions simply are not available. A recent experimental finding suggests the possibility of an even more important question. Myers6 has recently reported that fetal asphyxia of a given degree is more likely to result in brain damage in the surviving animal if the maternal and fetal blood glucose is high. Myers theorizes that the lactate released from glucose metabolism leads to changes in membrane physiologic properties which cause brain edema. Is the clinical application of this experimen-
15, 1979 Gynecol.
tal finding justified? Should intravenous glucose avoided in the parturient with a fetus at risk?
be
Human epidemiologic data Lilienfeld and Parkhurst,’ in their classic paper in 1951 on the etiology of cerebral palsy, reported that certain obstetric complications occurred with greater frequency among children with cerebral palsy than among normal control subjects. They listed placenta previa, malpresentations other than breech, premature separation of the placenta, breech presentation, complications of the umbilical cord, and bony dystocia as related to cerebral palsy in decreasing frequency (Table I). Since these obstetric complications are related to prematurity and low birth weight with approximately the same frequency as they are related to cerebral palsy, it is evident that the failure of these authors to control for the factor of low birth weight/ prematurity, a well known precedent of brain damage, has greatly weakened their thesis. It seems certain that their results reflect, at least partially, the effect of low birth weight rather than of the potentially asphyxiating complications they list. The same observation can be made on the well-known report by Eastman and associate@ in 1962, in which the authors compared the obstetric background of 753 children with cerebral palsy with the background of appropriate control children. Again, prematurity probably accounted for at least some of the observed differences. Cushne? in 1961 followed long-term survivors of prolapse of the umbilical cord who had been delivered at the Johns Hopkins Hospital. Of 66 babies followed, only three were frankly abnormal neurologically. Two of these babies had birth weights less than 1,500 grams. The author concluded that, “Permanent brain damage is a less common sequel in fetal survivals of prolapsed cord than was formerly feared.” In a study at the Mayo Clinic reported in 1960, Keith and Gage’” noted nonfebrile convulsive disorders more frequently among nonasphyxiated babies followed into childhood than among those recognized as asphyxiated at birth (Table 11). Neligan, Prudham, and Steiner” studied the effects of neonatal asphyxia on subsequent cerebral palsy. Perinatal asphyxia had no significant effect “upon general intelligence as we have measured it in our normal school population,” they wrote. In 1970 we recorded the results of 1 year neurologic examinations on surviving babies born following placenta previa, abruptio placentae, or prolapse of the umbilical cord. The data were collected before fetal heart rate monitoring was in general use. The perinatal death rate was high in the cohort from which these babies were selected, confirming the frequency with
Volume Number
133 4
The obstetrician, fetal asphyxia, and cerebral palsy
which fetal asphyxia occurred. At 1 year of age, we were unable to show any differences in neurologic status between these babies and the study population from which they were drawn. Birth weight was used as a control, and the low-birth-weight babies, as expected, were more likely to have exhibited neurologic damage than were those of normal birth weight. The presumed asphyxia in the study babies, however, did not add to this hazard. In a subsequent paper in 1974 Niswander, Gordon and Dragen reported examination of the same group of children at the age of 4 years. They noted no impairment of 4 year I.Q. score (Table III), fine motor score, or gross motor score among study children compared to carefully matched control children. When the babies whose mothers had suffered severe maternal shock were subdivided out for analysis, even this group failed to show any effect on I.Q. or motor scores. In an oft-quoted paper from the Collaborative Perinatal Project, Drage, Berendes, and Fisheri reported that children with a 5 minute Apgar score of 0 to 6 enjoyed a mean 4 year I.Q. no different from that of babies whose 5 minute Apgar scores were 8 to 10. While there was a slight increase in the abnormality rates in the fine and gross motor tests at 4 years among the children with low Apgar score, these differences were very small. One per cent of infants of mature birth weight and of normal 5 minute Apgar score were recorded as abnormal on the 4 year gross and fine motor scores. Only 2% of a comparable group of children with low 5 minute Apgar scores were recognized as abnormal on these examinations.
361
Comment Since a precise tool for the diagnosis of fetal asphyxia or fetal neurologic compromise is not available, it seems evident that the obstetrician not infrequently will be faced with the choice between immediate delivery of an infant who is presumably asphyxiated and may suffer brain damage and continued observation of fetal condition with fetal or neonatal death a likely possibility. Myers has reported that it is difficult in the experimental monkey to titrate fetal asphyxia carefully enough to produce a brain-damaged yet surviving neonate. If this is true in the experimental animal, how can obstetricians be expected to predict which asphyxiated human fetus will be born alive with brain damage? No one will argue that perinatal asphyxia is innocuous, that it does not kill, that it does not occasionally maim. Avoidance of perinatal asphyxia continues to be a primary goal of modern perinatal care. To hold an obstetrician responsible for every case of cerebral palsy on the thesis that fetal perinatal asphyxia is commonly followed by brain damage is patently unjust. Perinatal asphyxia of any degree of severity rarely leads to brain damage. Overreaction to perinatal asphyxia may in itself be damaging to the gravida and sometimes to the fetus. The obstetrician must be freed from the unfair judgments made against him as he tries to bring the best obstetric care to his patients.
REFERENCES
1. Myers,
R.: Two patterns of their conditions of occurrence, 112:246, 1972.
perinatal brain damage and AM. J. OBSTET.
GYNECOL.
2. Goodlin, R. C.: Intrapartum fetal heart rate responses in plethysmographic pulse, AM. J. OBSTET. GYNECOL. 110: 210, 1971. 3. Hon, E., Khazin, A., and Paul, R.: Biochemical studies of the fetus. II. Fetal pH and Apgar scores, Obstet. Gynecol. 33:237, 1969.
4. Sokol, R., Rosen, J., and Chik, L.: Fetal electroencephalographic
related to infant outcome, AM. J. 127:329, 1977. 5. Goodlin, R., Lowe, E., and Parmer, J.: Fetal monitoring: Letter to the Editor, Obstet. Gynecol. 43:474, 1974. 6. Myers, R. E.: Personal communication, 1978. 7. Lilienfeld, A., and Parkhurst, E.: A study of the association of factors of pregnancy and parturition with the development of cerebral palsy: A preliminary report, Am. J. Hyg. 53~262, 1951. OBSTET.
monitoring
GYNECOL.
8. Eastman,
N., Kohl, S., Maisel, J., and Kavaler, F.: The obstetrical background of 753 cases of cerebral palsy, Obstet. Gynecol. Surv. 17:459, 1962. 9. Cushner, I.: Prolapse of the umbilical cord, including a late follow-up of fetal survivors, AM. J. OBSTET. GYNECOL. 81:666, 1961. 10. Keith, H., and Gage, G.: Neurologic lesions in relation to asphyxia of the newborn and factors of pregnancy: Long
term follow-up, Pediatrics 26~616, 1960. 11. Neligan, G., Prudham, D., and Steiner, H.: The Formative Years: Birth, Family, and Development in Newcastle Upon Tyne, London, 1974, University Press. 12. Niswander, K., Gordon, M., and Drage, J.: The effect of intrauterine hypoxia on the child surviving to 4 years, AM. J. OBSTET. GYNECOL. 121:892, 1975. 13. Drage, J., Berendes, H., and Fisher, P.: The Apgar scores and four-year psychological examination performance, Pan. Am. Health Org. Sci. Pub. 185~222, 1969.
