When is it fetal distress? ROBERT




M.D. M.D.

Sa~~~~e~t~, Ca~~~r~~ The value of prepartum fetal movement patterns as a signof fetal health wascompared with intrapartum fetal heart rate patterns. Prepartum rather than intrapart~m surveiilance appeared to be the most effective technique to avoid perinatal deaths. furthermore, it is argued that, except for true birth trauma, the occurrence d cerebral palsy is seldom related to intrapartum factors. (Au. J. OBSTET. GYNECOL. 128: 44Ql977.)

LABORATORY, fetal distressis usually defined in terms of specific acid-base abnormalities or cardiovascular dysfunction. The intrapartum human fetus is not available for similar study and therefore the samedegree of diagnostic precision is not possiblein the clinical setting. This lack of precision leadsto inaccurate clinical evaluation and frequently confusesfetal stresswith distress. For example, in the presenceof maternal intrapartum acidemia (as due to ammonium chloride ingestion), blood gas values in an otherwise apparently normal newborn infant at birth may be similar to those noted in the severely asphyxiated neonate.’ Similarly, fetal heart rate patterns which are supposedlydiagnostic of fetal distressare more often associatedwith normal than with abnormal scalpblood pH valuesin the human intrapartum fetus.” In view of these diagnostic difficulties, it seemsappropriate to evaluate someof the simpler surveillance techniquesof fetal health. While the present seriesis small and the groups are not randomized, the results do suggestrelative values of antenatal and intrapartum monitoring which differ from current concepts.

consisted of a group of I,45 1 women having single newborn infants weighing more than 2 kilograms in whom intrapartum fetal monitoring was done in all and antenatal monitoring was done in approximately 1,100. The women were delivered at either the Santa Cfara Valley Medical Center. SanJose(SCVMC), or the Sacramento Medical Center, Sacramento (SMC). In--m monitaring only. This was a group of 531 consecutive deliveries at SCVMC, all of whom had intrapartum fetal monitoring but in whom no special effort wasmade to monitor the prepartum fetus other than to identify the “high-risk” gravid patient. Chart reviews. Prenatal charts (both SCVMC and SMC) of eight women the fetuses of whom died between the thirty-fourth week of pregnancy and delivery were reviewed. These casesoccurred among approximately 2,500 term deliveries. In addition, three casehistories are presented as examples of newborn centra1 nervous system (CNS) problems which might we11have been ascribed to intrapartum factors but which seemto be related to other events. Pqxtrtxsm monitoring. At SCVMC and at SMC, both the patients and the obstetric staff were instructed to consider any change in fetal activit.y during the third trimester asominous. By gaining the attention of the clinic physician and of the gravid patients, it was expected that any change in fetal activity would first of all be reported and secondwould be seriously evaluated, thus allowing immediate further diagnostic studies to appraise fetal health. htrqsrtum monitoring. Electronic heart rate monitoring (Berkeley, Corometrics, or HewlettPackard fetal monitors) was attempted with every parturient patient on our service. When fetal heart rate (FHR) patterns interpreted as abnormal occurred, scaipblood pH determination and fetal systolic time intervals were undertaken.’


Mattwtst and methods Three different groups of patients or data collection systemsformed the basisof our study. Prepartum and intrapartum fetal monitoring. This From the De~urt~~t of Obstetrics and ~~co~~, The University of cal$omiu, Davis, Smrumnto Medicat Cc?ztrr. Presented at the Forty-third Annual Meeting of the Pa@ Coast Obstetrical and Gynecological SocieEy, Kong, Hawaii, November 7-13, 1976. Reprint requests: Dr. Robert C. Goodlin, Univers* of Caljfornia, Davis, Sacramento Medical Center, D~rt~t of Obstet~s and G~eco~~, 2315 Stockton BIvd., S~rarne~tl~, ~al~~~ia 95817.


Volume 128 Number 4

Fetal distress

Table I. Pregnancies terminated for prepartum distress (decreased fetal movements)



Lowest umbilical artery pH

Method Confsmatory




Positive OCT Stained fluid


cs, 2






Ind., 1 cs, 2 Ind. 1 cs, 1

OCT: Oxytocin challenge test; Ind.: induction venous oxytocin; CS: cesarean section.

7.19 with intra-

Flesults Group A: Antenatal and intrapartum monitoring of fetuses weighing greater than 2 kilograms. Prepartum monitoring. Among approximately 1,100 prenatal registered patients, there were 46 gravid patients who specifically complained of decreased fetal movements after the thirty-fourth week of pregnancy. These women were admitted to the labor ward where electronic fetal heart rate monitoring was undertaken (during oxytocin infusion if no spontaneous uterine contractions occurred), amniocentesis was done if amnioscopy failed, and maternal estriol (either urinary or serum) as well as serum human placental lactogen determinations were obtained. Of these 46 patients, after further diagnostic tests seven had the pregnancies terminated immediately (Table I). In retrospect two of the seven also had decreasing estriol levels. Five of the newborn infants required active resuscitation. As noted below, the infants were discharged in good condition. Zntrapartum monitoring. Electronic monitoring during the intrapartum period was done on 1,451 fetuses (of whom approximately 1,100 had been monitored previously in the prepartum period) who weighed more than 2 kilograms at birth. Excluding the terminal labor period, 87 (6 per cent) had FHR patterns that were considered abnormal (both late deceleration and severe variable). Scalp blood pH determinations were done at least once in 51 (57 per cent) of these, and systolic time intervals were measured in 10 (11 per cent). The remaining fetuses had no confirmatory tests of apparent fetal distress and there were no immediate pregnancy terminations. However, in many there were maternal change of position, oxygen, or decreasing oxytocin. All did well. Eight fetuses had either scalp blood pH or systolic time intervals indicating apparent fetal distress. Five of these had multiple scalp blood pH determinations below 7.15 (with normal maternal pH), of whom two also had abnormal systolic time intervals. Three other


Table II. Pregnancies terminated for intrapartum fetal distress (abnormal FHR patterns) Method Confirmatory test


Abnormal systolic interval (alone) Abnormal scalp pH (alone) Abnormal “interval” and “pH”




cs, 3

Normal, 3

cs, 2 MF, 1 cs, 1 MF, 1

Normal, 2 Anomaly, 1 Resuscitation, 1 Anomaly, 1

CS: cesarean section; MF: midforceps.

fetuses had only abnormal systolic time intervals (Table II). Two of the eight newborn infants had anomalies incompatible with life, and of the other six normal neonates only one required resuscitation and two had an umbilical artery pH values below 7.15.. Of these 1,45 1 newborn infants weighing more than 2 kilograms, only the two infants with anomalies died. Of the eight newborn infants whose labors were terminated for apparent fetal distress, only one (with anomalies) was delivered of a mother seen more than once in our prenatal clinic. We have no information on the subsequent development of the 1,449 newborn infants, other than they were discharged from the hospital in good condition. Group B: 531 deliveries with intrapartum but no special prepartum monitoring. There were no intrapartum deaths, but there were four prepartum fetal deaths between the thirty-fourth week of pregnancy and delivery. Late decelerations were diagnosed in 14 fetuses during labor, of whom six had scalp blood pH. Four infants were delivered by immediate cesarean section; three of these required active resuscitation. Low cord blood pH was found in four of six infants tested. The neonates were discharged in apparent good condition. Group Case

C: Chart review. histories.

CASE NO. 1. A 16-year-old girl, O-O-O-O, had an uneventful pregnancy. At 42% weeks she was induced because of fetal macrosomia. During the terminal phases of labor, the fetal heart tone patterns appeared to be abnormal. A difficult midforceps delivery was done of a 4,460 gram child with Apgar scores of 6 and 8 who had a “staring” gaze. The infant was removed from the delivery room in otherwise good condition but did very poorly in the nursery (lack of sucking, high-pitched generalized seizure-like activity). The cry, and neonatologist’s diagnosis was cerebral abnormality secondary to asphyxia and birth trauma. However, a computerized axial tomography (CAT) scan showed a large porencephalic cyst which provided an obvious


Goodlin and Haesslein

prepartum explanation for the infant’s apparent CNS disease. At the age of two weeks the infant was noted to have optic atrophy; at three weeks the infant began to suck and was discharged to a nursing home where he has continued to do poorly. The infant now has a ventricular peritoneal shunt for expanding hydrocephalus, all ascribed incorrectly to birth asphyxia. CASE: puo. 2. A 2,005 gram female infant was delivered of a 27-year-old white woman, para l-0-2-1, at approximately the thirty-fourth week of pregnancy. The mother’s pregnancy had been complicated by severe pre-eclampsia with hemoconcentration, liver dysfunction, and thrombocytopenia (28,000 cells per cubic millimeter). Throughout labor the FHR had been nonreactive with a loss of beat-to-beat variability, which the staff ascribed to the maternal drug therapy (MagSOG, diazepam). However, at birth, the infant was markedly depressed and required active resuscitation. At 12 hours of age, the neonate was given a whoIe blood transfusion. On the fifth day, a CAT scan demonstrated intravent,ricular hemorrhage and developing hydrocephalus. The neonate had a ventricular peritoneal shunt inserted on the fifteenth day of Iife, and when discharged at three weeks of age the parents were told that he would have significant neurological impairment. The initial pediatric impression had been that the fetus had suffered an intraventricular bleed because of the maternal thrombocytopenia and/or hypoxemia, as suggested by the abnormal FHR tracing. However, the cord blood was 20 per cent adult-type hemoglobin, while blood removed from the intraventricular space was 3 1 per cent adult-type hemoglobin. This indicated that the hemorrhage occurred some time after the transfusion with adult-type blood and not during fetal life. Thus, detailed work-up showed that the intraventricular hemorrhage actually occurred well into the newborn period. CASE NO. 3. A 37-year-old white woman, para O-O-O-O had an uneventful pregnancy until the thirty-second week when she experienced a reaction to an injection while in her physician’s office. She was unconscious and apneic for an indefinite ‘(but short) time, and the FHR was described as being very “slow” for a period of approximately one hour after apnea. The patient recovered and noted that the fetus was less active than before the apneic episode. During labor at term, the fetal heart rate pattern showed a loss of beat-to-beat variability and frequent late decelerations. There was a difficult midforceps delivery of a markedly depressed child (Apgar scores 1 and 3), and in the nursery the infant had generalized seizures during its first day of life. The child has failed to thrive and at age two years has evidence of cerebral palsy, which because of the circumstances of the fetal anoxia can be correctly ascribed to the prepartum period.

June 1.5. 1977 Am. J. Obstct. Gynecol.

Chart YPZ&UI. The review of eight charts of women whose fetuses died prior to the onset of labor showed that six had complained specifically to the obstetrician of decreased fetal movements. because the obstetrician heard a “normal” FHR, these six patients were invariably reassured that all was well. Fetal death occurred within one week in all six cases. One woman had noted decreased fetal movements but had not had a prenatal visit prior to the occurrence of fetal death. and the eighth woman was a depressed and probably schizophrenic patient whose history was considered unreliable. Two of t,he stillborn infants were hydropic and one had the caudai regression syndrome, but in none of the eight was there an obvious explanation for the fetal death despite appropriare studies.

Comment Ever since Kennedy4 reported in 1843 that delayed recovery of the FHR was aminous, obstetricians have been attempting to define which FHR pattern is indicative of fetal distress. The same attention has not been directed toward “decreased fetal movements” and “maternal concern.” although they have been c:onsidered ominous in specific fetal disease such as erythroblastosis fetalis.” With few exceptions,fi however, obstetricians have been reluctant to accept such a history as being ominous for all fetuses. There has been a general belief that such histories are very subjective and only absence of fetal movement has clinical signi~cance. The present report embodies many of the pitfalls of the usual clinical study of fetal distress, for example, the lack of control groups, the imprecise definition of fetal distress (other than acidemia), and the absence of follow-up studies. Nevertheless, one interpretation of our data and those reported elsewhere is that the heafthy, term fetus tolerates labor and, aithough prone to certain accidents such as prolapsed umbilical cord, is not living through a particularly dangerous time period with regard to either death or permanent injury. When fetal accidents, such as prolapsed cord or abruptio placentae have occurred on our service, they were diagnosed not by continu~~us FHR monitoring but by the standard technique of intrapartum surveillance and good nursing care. Fetal surveillance should then be directed toward finding the sick fetus prior to the stress of labor. While our data suggest that prepartum monitoring of the fetus is useful (in order to determine which fetus is healthy) the effectiveness of intrapartum electronic fetal monitoring in identifying the fetus ia trouble is being questioned.‘, ’ Not a single intrapartum fetal death has occurred.on our service (of normal fetuses weighing more than 2

Volume Number

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kilograms) in the last six years, with more than 5,000 deliveries since routine prepartum and intrapartum fetal monitoring was initiated. But during this time of intensive fetal monitoring, scores of supposedly ominous FHR recordings have undoubtedly been ignored (and many benign patterns precipitated STAT cesarean section) and hundreds of FHR recordings were either very brief or were technically unsatisfactory. This superb clinical outcome based on poor data collection and interpretation allows several explanations: (1) We have been very fortunate! (2) There must be direct fetal benefits from the increased bedside personnel required for FHR monitoring. (3) We now avoid the common iatrogenic causes of intrapartum fetal distress, that is, maternal supine position, maternal hypotension, excessive oxytocin stimulation, drug toxicity. (4) Our fetuses now are more healthy because of contraception and abortion on demand, better maternal diets, and so forth. Our experience would suggest that with adequate prepartum screening the occurrence of perinatal death among normal term-size fetuses would be virtually eliminated. Prior to beginning intrapartum fetal heart rate monitoring in 1968, we estimated that approximately three intrapartum fetal deaths per 1,000 deliveries of term-size infants could be prevented by electronic monitoring,g but the present experience suggests that the fetus likely to suffer intrapartum fetal death is ill prior to the onset of labor. An inexpensive and a good prenatal screening test of fetal well-being is to accept the mother’s own impression of the health of the fetus. As suggested by the chart review and follow-up of gravid patients with decreased fetal movements, such a complaint can be an ominous symptom. When prenatal screening for symptoms of decreased movement is not done (as in group B), intrapartum monitoring cannot correct the deficiency. Maternal diaries of fetal activity suggest that the majority of near-term fetuses have definite circadian patterns of activity whose significance is unclear. But when preparturn fetuses had obvious decreased activity plus other symptoms of illness (we noted that when promptly delivered), 81 per cent required resuscitation which suggests prior fetal disease. In our 1968 proposal, it was anticipated that intrapartum monitoring would reduce the incidence of infants with mental retardation and various forms of cerebral palsy and, in addition, prevent a certain number of stillbirths. At that time, it was commonly believed that intrapartum asphyxia among previously healthy fetuses could produce a broad spectrum of de-

Fetal distress


velopmental abnormalities, ranging from mental deficiency or cerebral palsy to minimal reading disorders (in addition to causing fetal or neonatal death)-the “continuum of reproductive wastage” described by Lilienfeld and Parkhurst.” Eight years later, the available literature suggests that this attractive concept is not accurate. Little’s” original papers in 1853 and 1863 suggested that parturition was a causative factor in cerebral palsy, but Freud12 in 1897 disagreed, believing that the basic defect was developmental in nature. Approximately a century after Little’s papers, Eastman13 apparently resolved the issue by proposing that parturition was indeed a significant cause of cerebral palsy. In his famous 1954 paper, “Mount Everest in utero,” he stated that “ . . . knowing as we do that intrauterine anoxia actually kills such a large number of infants, would it not be logical to believe that sometimes the degree of anoxia may not be quite sufficient to kill the infant but enough to inflict irreparable injury to the cerebrum?” While this query may well have been an effort to find “an important avenue for advance in obstetrics”“’ since the research problems of maternal deaths had been largely solved, Eastman’s questions has resulted in “medical-legal defensive” obstetrics with all of its associated problems. Continuing experience suggests Eastman’s basic assumption may have been in error. As Eastman was well aware, prior attempts to correlate the term-size neonate’s condition with subsequent development usually failed to show correlation between newborn asphyxia and cerebral palsy. 15-lg Even the experimental production of cerebral palsy in laboratory animals is difficult, as precise timing of the durations of anoxia and resuscitation is required to produce a live newborn infant with brain damage. Otherwise, in the experimental situation, the fetus either recovers or dies.20 This apparent “all or nothing” phenomenon may be operative in cases of intrapartum asphyxia for the human fetus as well. An answer may be found in data from the Collaborative Perinatal Project, in which evaluation of infants born of mothers who had abruptio placentae, placenta previa with bleeding severe enough to produce maternal shock, or prolapse of the umbilical cord were matched with newborn infants of equal birth weight who were born of mothers with no apparent problems. No difference was demonstrated in performance and Niswander and associate? suggested that the “all or nothing” may indeed apply to the human being as well. The premature infant who contributed to 30 per cent of the cases of cerebral palsy in Eastman’s and


Goodlin and Haesslein

June 15, 1977 Am. ,I. Ohstet. (;ynecol.

Lilienfeld and Parkhurst’s experience now enjoys a much better fate because of the increased expertise of the neonatalogist. ** This marked improvement in the neurologic improvement of premature infants indicates that neonatal factors rather than parturition were responsible for past cases of cerebral dysfunction. A related report suggesting that intrauterine stress may even be “beneficial” is the restudy of the Dutch famine data of World War II. The study suggests that fetuses who survived the severe stresses of malnutrition in utero do better as adults than those who were not stressed (and therefore “selected” in utero).‘” All of these data would seem to indicate that there may indeed be an “all-or-nothing” phenomenon which normally controls the fate of the human intrapartum fetus. It either recovers completely from the effects of asphyxia or it dies, unless we obstetricians rescue the dying fetus. Obviously, the sick, the malformed, the dysmature, or chronically stressed fetus is less likely to recover from any in utero stress. Brain lesions associated with cerebral palsy have been demonstrated to occur before the time of parturition.2” As suggested by o ur case histories, events occurring outside the time of labor can indeed cause the cerebral palsy for which parturition may have been held responsible with a less adequate examination or history. Walke?’ of Scotland has observed in his clinic population that only three per cent of the perinatal problems (risk) are related to factors associated with labor. This implies that 97 per cent of perinatal problems would not have been avoided by circumventing labor and that increased abdominal delivery rates might increase perinatal problems because of factors such as respiratory distress. An academic benefit of routine intrapartum FHR monitoring has been the demonstration that many normal fetuses are inadvertently stressed by active interference with labor, such as excessive oxytocin, the maternal supine position, epidural anesthesia with hypotension, and so forth. Presumably these mismanagements can be avoided without FHR monitoring by

strict attention to detail, as can the cases of birth trauma. A practical shortcoming of FHR monitoring may be the rescue of the seriously ill or malformed fetus from intrauterine death. only to have it exist in extrauterine life with cerebral palsy or severe anomalies.2” The fetal heart and brain may or may not have similar tolerance to asphyxia, but, because of ignorance, our resuscitative efforts for the neonate are largely directed toward the newborn cardiovascular system. This in all probability results in a number of iatrogenic causes of cerebral palsy that are produced each year. It seems appropriate to suggest that the thinking of the last generation may have taken the wrong direction. In the meantime, we would like to propose that fetal distress will manifest itself during the antenatal period with decreased fetal movements along with the other signs of poor fetal health. If these signs are missed, fetal death may occur during the prepartum or intrapartum period. We prefer to think that most cases of cerebral palsy are rwt related to factors of parturition, that its etiology is either prepartum (as in the two cases histories) or in early infancy. Excluding fetal accidents, intrapartum fetal distress probably does not occur (in the sense that underlies the use of electronic fetal monitors) if proper prepartum surveillance has been done. Unfortunately, birth trauma still remains a significant cause of cerebral damage,Y7 and its avoidance requires not fetal monitoring but clinical skill. For those that would argue that monitoring for an hour or two of intrauterine life can appreciably affect the incidence of cerebral palsy, let us be allowed to test the different concepts with a truly controlled study, one comparing prepartum versus intrapartum monitoring. Our own experience indicates that in a well-screened and healthy fetal population, electronic intrapartum fetal monitoring adds little (except to increase the cesarean section rate) in improvement of the perinatal mortality rates or the general well-being of newborn infants.


Goodlin, monium human

R. C., and Kaiser,

I. H.: The effect of amchloride induced maternal acidosis on the fetus at term, Am. J. Med. Sci. 23% 662, 1957.

2. Saling, E.: Advantages of combined supervision of the fetus during labor, in Hodare, M. A., editor, Biochemistry of the Fetus, Springfield, Ill., C Thomas, Publisher. 3. Goodlin, R. C., Haesslein, H. C., et al. Fetal val recorder, Obstet. Gynecol. 46: 69, 1975. 4. Kennedy, E.: Observations on Obstetrical New York, 1843, Langley.

Physiological 1972, Charles cardiac



5. Goodlin, R. C.: Impending fetal death in utero due to isoimmunization, Obstet. Gynecol. 10: 299, 1957. 6. Sadovsky, E., and Yaffe, H.: Daily fetal movement recording and fetal prognosis, Obstet. Gynecol. 41: 845, 1973. 7. Haverkamp, A. D., Thompson, H. E., McFee, J. G., and Cetrulo, C.: The evaluation of continuous fetal heart rate monitoring in high-risk pregnancy, AM. J. OBSTET. GYNECOL. 125: 310, 1976. 8. Renov, P.: A controlled trial of fetal monitoring, Aust. N. Z. J. Ohslet. Gynecol. 15: 122, 1975.

Volume Number

Fetal distress

128 4

9. Goodlin, R. C.: Intrapartum fetal heart rate responses and plethysmographic pulse, AM. J. OBSTET. GYNECOL. 110: 210,197l. 10. Lilienfeld, A. M., and Parkhurst, E.: A study of the association of the factors of pregnancy and parturition with the development of cerebral palsy, Am. J. Hyg. 53: 262, 1961. 11. Little, P.: On the influence of abnormal parturition, difficult labor, premature births and asphyxia neonatorum on the physical and mental condition of the child, especially in relation to deformities, Trans Land Obstet. Sot. 3: 293, 1862. (Quoted by Eastman, N. J.: Obstet. Gynecol. Surv. 17: 459, 1962.) S.: Die infantile cerebrallahmung. (Quoted by 12. Freud, Lilienfeld, A. M., and Parkhurst, E.: Am. J. Hyg. 53: 262, 1961.) 13. Eastman, N. J.: Mount Everest in utero. AM. J. OBSTET. GYNECOL. 67: 701, 1954. 14. Eastman, N. J.: Editorial comments, Obstet. Gynecol. Surv. 7: 645, 1952. 15. Usdin, G. L., and Weil, M. L.: Effect of apnea neonatorum on intellectual development, Pediatrics 9: 387, 1952. 16. Keith, H. M., and Gage, R. P.: Neurologic lesions in relation to asphyxia of the newborn and factors of pregnancy: Long-term follow-up, Pediatrics 46: 616, 1960. 17. Drage, J., Berendes, H., and Fisher, P.: The Apgar scores

Discussion DR. KEITH P. RUSSELL, Los Angeles, California. This may well be one of the most significant papers ever presented





of this discussant,




At the


it is probably the



in the

the most imutilization


electronic fetal heart monitoring in our specialty. The authors have long expressed skepticism regarding the usually accepted benefits of universal fetal monitoring in evaluating “fetal distress,” and in the present communication they document a firm basis for this skepticism. Let us summarize the three essential, and to me acceptable, proposition of their thesis: (1) confusion and demonstrable errors in distinguishing fetal stress from fetal distress; (2) fetal heart rate patterns supposedly diagnostic of fetal distress more often associated with normal than with abnormal fetal scalp blood pH values; (3) newborn central nervous system problems (cerebral palsy and mental retardation) inappropriately ascribed to intrapartum problems when actually related to prepartum or other events. The authors proceed to document acceptable bases for support of the above three basic concerns. One of the parameters utilized was evaluation of antepartum fetal activity during the third trimester,, with the concept that decrease in fetal activity during this time should be considered ominous. A further evaluation involved comparison of FHR patterns with scalp blood pH determinations and fetal systolic time interval evaluations. Admittedly the total numbers involved in these studies were small. The third and final evaluation was a demonstration of documented cases in which a neonatal diagnosis of central nervous system abnormal-

18. 19. 20.



23. 24.

25. 26. 27.


and four-year psychological examination performance, Pan. Am. Health Organ. Sci. Pub. 185: 222, 1969. Myers, R. E.: Discussion of Apgar scores, Pan Am. Health Organ. Sci. Pub. 185: 234, 1969. Editorial: Prognosis of foetal asphyxia, Br. Med. J. 1: 23, 1951. Ginsberg, M., and Myers, R. E.: Fetal brain injury after maternal carbon monoxide intoxication, Neurology 26: 15, 1976. Niswander, K. R., Gordon, M., and Drage, J.: The effect of intrauterine hypoxia on the child surviving to four years, AM. J. OBSTET. GYNECOL. 121: 892, 19’75. Lubchenco, L. O., Delivoria-Papadopoulos, M., et al.: Long-term follow-up studies of prematurely born infants, I, J. Pediatr. 80: 501, 1972. Stein, Z., Susser, M., et al.: Nutrition and mental performance, Science 178: 708, 1972. Towban, A.: Central nervous system damage in the human fetus and newborn infant, Am. J. Dis. Child. 119: 529, 1970. Walker, J.: Prognostic value of antenatal screening, AM. J. OBSTET. GYNECOL. 124: 30, 1976. Goodlin, R. C.: Letter to the editor, Obstet. Gynecol. 43: 474, 1974. Amiel-Tison, C.: In Status of the fetus. Report of the Second Ross Conference on Obstetric Research, Columbus, Ohio, November, 197 1, Ross Laboratories.

ity believed to be associated with birth asphyxia or birth trauma was subsequently determined to be due to pre-existing or other cerebral disease not associated with the birth process. Never before in the history of our specialty have so many cesarean sections been performed in this country on the indication of “fetal distress,” with the subsequent delivery of essentially normal infants based on Apgar scoring. The universal increase in the incidence of what may be termed “unnecessary” cesarean sections has been a concern of even the most vocal proponents of universal intrapartum fetal heart electronic monitoring. Their current posture is that there has been widespread misreading and misinterpretation of fetal heart rate patterns (even while there has been extensive exposition of the various forms of variations in the tracings as bonafide indicators of fetal distress). The emphasis now is placed upon the more proper concept that electronic fetal intrapartum monitoring should be simply a “screening procedure” and that multiple other parameters must be utilized to separate true fetal distress from simply a variation in the FHR tracing. This later concept has been slow in coming. The average resident today, trained in our most modern institutions, graduates ill prepared to manage clinically many obstetric conditions and feels literally that he cannot practice without the presence of a fetal monitor at his fingertips.




of an obstetric



become judged not infrequently by the number of fetal monitors it has available, or the complexity of its computerization. Sinc:e we have all, to an extent, become slaves to the technologic environment, this is an understandable development. My own concern with this phenomenon has become


Goodlin and Haesslein

accentuated by the medical-legal implications. I serve as consultant to a number of legal firms and insurance companies involved in this very vexatious problem. What we are seeing is the increased introduction of an abnormal fetal heart rate tracing as prima facie evidence of any resultant fetal abnormality. Yet, we have documented cases to show that a number of the socalled fetal cerebral damages attributable to intraparturn hypoxia, intrapartum asphyxia, birth trauma, and so forth were in fact due to prepartum or intrapartum maternal infections or congenital cerebral anomalies in the infant which could not, with reasonable medical probability, be attributed to circumstances involved in the management of labor. It should no longer be acceptable for the frequent pediatric or neurologic notation to appear in the record of a patient suffering from cerebral palsy or mental retardation to the effect that the condition was associated with “a hard delivery,” “a prolonged labor, ” “difficult forceps,” or “intrauterine as so long as been the common practice. asphyxia,” Besides being frequently a semantic error, usually based purely upon the mother’s statement or history, it provides grist for the plantiffs attorney’s mill. I am in complete agreement with the authors’ thesis that in most cases other factors do indeed cause the cerebral palsy for which parturition has been held responsible because of an inadequate examination and history of the newborn infant. I also firmly believe that for the average fetus periods of stressare not synonymous with distress and that very frequently variations in fetal heart rate tracings are simply an indication of the former and not of the latter. We must continue to give this problem dedicated study and to resist the kneejerk reaction of rushing to cesarean section on the sole basis of a few variations in the electronic fetal heart rate tracings. A broad spectrum of studies is needed to differentiate acceptable fetal stress from damaging fetal distress as indicators of intrapartum cerebral damage. I have one final comment in the form of a question: In their paper the authors did not specifically delineate and define “decreased fetal activity.” In our own concepts, particularly in our continued evaluation of the problems of premature rupture of fetal membranes, we have used decreased fetal activity, together with fetal tachycardia, as indicators of potential fetal threat. The baseline for fetal activity has been 15 movements per hour, as recorded by the mother, as a so-called normal value. We would be interested in the authors’ concepts as regards this particular evaluation. I believe that time will prove the validity of my opening evaluation of this paper. DR.CLIFFORDC. CH~PPEU, Berkeley,California. A number of years ago we had a rather lively debate about what Dr. Goodlin termed the nervous child, diagnosed by the tracing of the child he was monitoring. He claimed then, and I suspect now, that he could cure that with a small dose of Valium, and the child would becomi less nervous. I noted with some dismay

June Am. J. Obstet.

that this was not included ticular topic this morning. ment on it.

15, 1977 Gynecol.

in his discussion of the par1 wonder if he would com-

DR. CoLIN MCCORRISTON,Honolulu, Hawaii. This is just another laboratory test that we are talking about. It is useful, but it is subject to intelligent interpretation. DR. ROBERTK. CREASY,San Francisco, Callifornia. During the six-month period that Dr. Goodlin indicated he was not supervising patient care and fetal assessment, he was spending his time in a laboratory with which I am associated. Throughout those six months it. was indeed a pleasure to have him with us, for we all learned from his provocative thoughts, a good example of which he has put forward this morning. I would like to caution against some of the enthusiasm which has perhaps been generated by Dr. Goodlin today against the use of intrapartum fetal monitoring. At one point during the presentation Dr. Goodlin indicated that intrapartum fetal monitoring is of no value, and I would take issue with him on this statement. At the present time we have very few ways with which we can directly assess the fetus. We cannot measure fetal cardiac output; we cannot measure umbilical blood flow; we cannot even measure fetal blood pressure, although Dr. Goodlin himself has been trying to deal with that particular problem. Anytime a physician uses indirect methods in assessing a patient I feel it is useful to obtain as much information as possible before arriving at a conclusion, and intrapartum fetal heart rate monitoring is but any of the pieces of information that might assist the obstetrician in caring for his two patients. I would suggest that antenatal assessment techniques, of which patient assessment of fetal activity is but one method, will either not always be performed or not always indicate the fetus which is in chronic distress. Intrapartum fetal heart rate monitoring may then be of definite benefit. If used appropriately it will indicate which fetus should have fetal scalp sampling in order to assess biochemically the presence or absence of fetal asphyxia. It will also indicate which fetus should have the benefit of an alteration in maternal position or maternal oxygen administration. The very fact that Dr. Goodlin has not had an intrapartum death may well be due in part to his wide use of intrapartum fetal heart rate monitoring along with the other points he mentioned. The idea that intrapartum asphyxia is not a significant cause of cerebral palsy is consistent with a number of studies. However, this does not mean that intrapartum asphyxia cannot cause cerebral palsy or a host of other neurologic infirmities. There is little do&t in my own mind that intrapartum asphyxia of a prolonged nature could indeed lead to neurologic damage. The degree and duration of intrapartum asphyxia necessary to produce damage will obviously vary depending upon the antecedent course of the ges-

Volume Number

128 4

tation. Although continuous fetal heart rate monitoring is not always a precise tool, it is one of many tools that may assist the obstetrician, and the fetus. DR. GOODLIN (Closing). Fetal monitoring was my first love and as Tennyson said, it is better to have loved and lost than not to have loved at all. I am still in favor of fetal monitoring all the way. As I said, I keep hoping some day it will prove to be of value. What I wanted to convey was that if a fetus seemingly has normal movement then the fetus can withstand the stresses of labor. Those accidents that happen, such as abruptio placentae or prolapsed cord, in my experience are not diagnosed by the fetal monitor but by obstetric care alone. On the other hand, if a patient is unregistered, if we are unaware of how the fetus has been acting throughout pregnancy, or if she is high risk, then I think monitoring is indeed useful. And we do use it all the time.

Fetal distress


As far as what method we have for fetal monitoring, we give each mother a diary and hope she will fill it out. We ask: “Which time is the fetus most active? When is it asleep? Does it respond to sound? This is what I mean by fetal activity. And each time we see the mother we hopefully reinforce this and ask her how her fetus is. In regard to the question on the use of Valium, I know of four cases in which the fetus was hyperactive in utero and became a hyperactive infant. This is not a new observation. I attempted to secure some grant funds for in utero psychotherapy. I was denied this because of the implication that this was meddlesome obstetrics-dangerous and that sort of thing. So I am a bit more cautious than I was before about in utero therapy.

When is it fetal distress?

When is it fetal distress? ROBERT C. GOODLIN, HANNS C. HAESSLEIN, M.D. M.D. Sa~~~~e~t~, Ca~~~r~~ The value of prepartum fetal movement patterns a...
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