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Fetal heart rate patterns during labor: Neurologic and cognitive development at six to nine years of age
Duckman, Suarez, and Sese
gested that the primary treatment of this tumor should be excision, not hysterectomy, unless the pathology report of the excised specimen indicates a malignancy. We thank Dr. Vincent Tricomi, Chairman of the Department of Obstetrics and Gynecology at The Brooklyn Hospital-Caledonian Hospital Medical Center, for his constructive review of this case report.
October l 'JHH Am J Obstct (;, ncml
REFERENCES I. Lippert LJ, Richart RM. Ferenczv A. Giant benign endocervical polvp: Report of a case. A~I J 0BSTET (;y:o;ECoL
1974;118:1140. 2. Saier FL. Hovadhanakal P, Ostapouvicz F. c;iant cen·ical polvp. Obstet Gynecol 1973:41 :94-6.
Fetal heart rate patterns during labor: Neurologic and cognitive development at six to nine years of age Michael J. Painter, MD, Mason Scott, PhD, Robert P. Hirsch, PhD, Patricia O'Donoghue, MN, PHP, and Richard Depp, MD Pittsburt;h, Pennsylvania, and Chicago, Illinois The development of 50 children relative to the fetal heart rate patterns they demonstrated during labor and delivery was prospectively studied. Normal deceleration patterns were recorded for 12 of the children, while 16 were recorded as moderately severe and 22 as severe variable or late deceleration patterns. The parity and socioeconomic status of the mothers and the sexes of the infants were similar among the groups. A statistically significant developmental difference in favor of children with normal fetal heart rate patterns was seen in the first year of life. However, at 6 to 9 years of age the difference in neurologic and cognitive development was no longer evident. These data do not support the hypothesis that brief abnormal fetal heart rate patterns recorded during labor are indicative of irreversible central nervous system injury. (AM J 0BSTET GYNECOL 1988:159:854-8.)
Key words: Fetal heart rate patterns. fetal heart rate decelerations, neurologic development. cognitive development
Fetal heart rate ( FHR) monitoring is a technique that is widely used to assess fetal well-being during labor. 1 This technique is considered to have greater sensitivitv and a lower false-negative rate than fetal blood sampling or auscultation. It also is credited with predicting the absence of asphyxia better than any other method."' There is a close relationship between patterns, acidosis, and neonatal compromise.' Because FHR monitoring has a low specificitv, a significant number of fetuses subsequently found to be normal at birth will demonstrate abnormal FHR patterns. FHR monitoring is more costly than monitoring with a stethoscope, and its detractors claim the technique is unproved and unnecessarily interferes with the birth process."·' However, there are significant limitations to the randomized controlled studies that have been perFrom the Departments of Neurology, Obstetrics. and Pediatrics. Universit~ of Pittsburgh and Magee Women's Hospital, and the Department of Obstetrics and Gynecology, Northwestern Universit\' Medical School. Received for publication October 19, 1987; revised May 12, 1988; accepted May 19. 1988. Reprint requests: Dr. Michael]. Painter, Children's Hospital of Pittsburgh, One Children's Place, 3705 Fifth Ave. at DeSoto St .. Pitt5burgh. PA 15213.
854
Table I. FHR pattern definitions 1. Moderate-severe variable: Deceleration to 70 to 80 beats/min range for >60 seconds with three contractions or to a rate <70 beats/ min for 30 to 60 seconds 2. Severe variable: Deceleration to a rate <70 beats/min ;.6() seconds (prior to pushing) on two or more occasions 3. Late decelerations: A uniform deceleration of the FHR of any magnitude that occurs consistently in the late phase of each uterine contraction From Painter M.J, Depp R. O'Donoghue P. 1978:132:271-7.
A~I
.J
0Bsn:T
GY:\ECOL
formed to assess monitoring effects on perinatal morbidity, 1 and the duration of a defined FHR abnormality and its implications for the fetus are unknown. The best association of abnormal patterns with the neonatal condition exists when immediate morbidity is high and intervention has been delayed. The association of FHR patterns and subsequent neurologic development is of obvious importance to an understanding of the significance of specific FHR patterns and the significance of the duration of the defined abnormalitv.
FHR patterns during labor
Volume 159 !\umber 4
Table II. Racial distribution of children at 6- to 9-year follow-up evaluation FHR pattern group Normal Moderately severe variable decelerations Severe variable or late decelerations X'
=
White
855
Table III. Abnormal neurologic evaluations Ages of children at examination Black
FHR pattern
H
2
10
4
9
12
Normal Moderatelv severe Severe or iate
Birth
p
2112 10/16 16/22 = 0.002
6-
p
0112 1/16 6/22 = 0.174
\'1"
0/10 0/14
p
2/21 =
1.000
Fisher's exact test.
6.43.
/J = 0.04.
Table IV. Intelligence quotients of each FHR pattern group FHR jmttern Normal Mean± SD 95'lr CJ Significance Moderatelv severe Mean± SD 95'7r CI Significance Severe or late ~lean ± SD 9.~'7r Cl
VSIQ
PSIQ
FSIQ
97.9 ± 17.2 87.2-108.6 f! = 1.23
9H.6 ± 13.3 90.4-106.8 p = 0.72
98.1 ± 16.6 87.8-108.4 p = 1.45
105.5 ± 12.9 98.7-112.3 p = 0.31
I 10.6 ± 13.0 103.8-1 I 7.4 p = 0.50
108.6 ± 13.1 101.7-115.5 p = 0.25
98.1 ± 14.3 92.0-104.2
98.1 ± 14.3 92.0-104.2
99.5 ± 12 ..~ 94.2-104.8
Factorial analvsis of variance with interaction. VSIQ = Verbal-scale intelligence quotient. PSIQ = Performance-scale intelligence quotient. FSIQ = Full-scale intelligence quotient. C/ = Confidence intervals.
In 1978 we reported the results of a prospective study relating intrapartum FHR patterns to development in the first vear of life." This report is a follow-up study of these infants and comprises the results of psychologic testing and detailed neurologic evaluations at G to 9 vears of age. Material and methods
This study, as previously described," consisted of 50 infants who were born at term, were of appropriate weight for their gestational age (i.e., within l SD of the mean), had no observed congenital anomaly at birth, and had a technicallv adequate internal FHR tracing that was continued until at least 30 minutes before deliverv. Thirtv-eight consecutive infants who demonstrated continuous tracing with repetitive moderatdy severe variable, severe variable, or late decelerations in the late phase of labor were identified (Table I). Of these 38 consecutive tracings, 16 demonstrated moderately severe variable decelerations, 15 showed severe variable decelerations, and seven indicated late deceleration patterns. Twelve consecutive infants who demonstrated normal intrauterine FHR patterns were identified as controls. Indications for monitoring were predominantly fetal," the most common being oxvtocin use, meconium-stained amniotic fluid, inertial labor. and premature rupture of the membranes. One perinatologist (R. D.) interpreted all FHR patterns and graded the severity; one pediatric neurologist
(M. J. P.) performed all neurologic evaluations. Results of FHR assessments were unknown to M. J. P. and results of the neurologic evaluations were unknown to R. D. Neurologic evaluations were performed neither less than 12 hours nor more than 3 days after delivery, and the examination of Prectl as modified by Koenigsberger" was used. Sequential neurologic examinations were performed at 2, 4, 6, 9, 12. 18, and 24 months of age and vearly thereafter. Psvchologic testing was performed at appropriate ages by one psychologist (M. S.). The Wechsler Intelligence Scale for Children-Revised (or Leiter International Performance Scale), the Wide Range Achievement Test, and the Bender Visual Motor Gestalt Test were used. FHR pattern interpretations and neurologic evaluations were unknown to M. S. Of the 50 children, 45 (90%) were seen at 6 to 9 years of age for neurologic evaluation and 44 were given psychologic tests. Results
At birth there was no significant difference in the clinic statuses of the mothers or in the mean birth weights or sexes of the infants." There was a statistically significant difference in the races of the mothers among the groups (Table II). Two of the 12 infants with normal FHR patterns and 26 of the 38 with ominous FHR patterns had abnormal neonatal neurologic evaluations. The majoritv of these infants demonstrated hypotonia of the lower extrem-
856
Painter et al.
October 1988 Am J Obstet Gvnecol
Table V. Intelligence quotients of black children FHR pattern
I
Normal Mean± SO 95% CI Moderately severe Mean± SO 95% CI Severe or late Mean± SO 95% CI
VSIQ
PSIQ
FSIQ
97.0 ± 13.5 87.6-106.4
97.8 ± 19.0 87.3-110.7
97.2 ± 17.9 84.8-109.6
94.5 ± 15.6 79.2-109.8
107.2 ± 12.1 95.3-119.1
100.5 ± 13.2 87.6-113.4
93.5 ± 11.4 87.0-100.0
97.3 ± 6.8 93.5-101.1
94.6 ± 7.5 90.4-98.8
Factorial analysis of variance with interaction. VSIQ = Verbal-scale intelligence quotient. PSIQ = Performance-scale intelligence quotient. FSIQ = Full-scale intelligence quotient. C/ = Confidence intervals.
Table VI. Intelligence quotients of white children FHR pattern
I
Normal Mean± SO 95% CI Moderately severe Mean ±·so 95% CI Severe or late Mean± SO 95% CI
VSIQ
PSIQ
FSIQ
101.5 ± 9.2 88.7-114.3
102.0 ± 17.0 78.4-125.6
101.5 ± 14.8 81.0-122.0
109.9 ± 10.8 103.2-116.6
111.9 ± 12.5 I 04.2-119.6
111.9±12.2 104.3-119.:)
I 04.25 ± 19.6
108.6 ± 10.5 I 01.7-115.5
105.3 ± 15.3 95.3-115.3
91.4-117.1
Factorial analysis of variance with interaction. VSIQ = Verbal-scale intelligence quotient. PSIQ = Performance-scale intelligence quotient. FSIQ = Full-scale intelligence quotient. C/ = Confidence intervals.
Table VII. Wide Range Achievement Test subtest results FHR groups
Reading
Normal 100.8 ± 8.5 Moderately 109.6 ± 12 severe Severe or late 101.6 ± 16
Mathematics
104.8 ± 10 100.0 ± 10 107.8 ± 11.3 106.8 ± 8.2 103.2 ± 13.3 104.5 ± 13A
Repeated measures analysis of variance.
p = 0.36
ities. The number of abnormal neurologic evaluations decreased during the first year so that none of the 12 infants with normal FHR patterns had abnormal evaluations at l year of age. One pf 16 infants with moderately severe variable decelerations and six of 22 infants with severe variable or late decelerations had abnormal evaluations at 1 year of age (Table Ill). A significantly greater number of infants with normal FHR patterns demonstrated neurologic abnormalities at birth. The difference at 1 year of age was less apparent, and there was no statistically significant difference at 6 to 9 years of age (Table III). Two children with severe variable or late deceleration patterns during labor and delivery had neurologic abnormalities at 6 to 9 years of age. The one child with developmental arrest who dem-
onstrated almost 10 hours of severe variable decelerations has undescended testes. coarse features. widespread and malformed teeth, and prognathism that have become more evident with increasing age. A computerized tomographic scan performed at his most recent evaluation indicated multiple asvmmetric lowdensity regions involving the cerebral hemispheres and cerebellum, a small cerebellum and brain stem. and a markedlv enlarged fourth ventricle. Manv gvri appeared malformed. The evaluation of this child suggests he has an unspecified dysmorphic svndrome. One child who sustained repetitive late decelerations for at least 130 minutes prior to delivery has a significant neurosensory hearing loss but is otherwise neurologically normal. Cognitive testing as determined bv the Wechsler Intelligence Scale for Children-Revised or the Leiter International Performance Scale revealed no significant difference in verbal-scale intelligence quotient (IQ). performance-scale IQ, or full-scale IQ among the groups (Table IV). Because of a statisticallv significant racial imbalance, subscales of the Wechsler Intelligence Scale for Children-Revised were analvzed separatelv for white and black children. There was no significant difference between black and white children with regard to normal, moderatelv severe variable. severe variable, and late deceleration scores (Tables V, VI). The average ievel of achievement within the areas of read-
FHA patterns during labor 857
Volume lc>lJ !'\umber 4
ing, spelling, and mathematics as measured by the Wide Range Achievement Test indicated no difference between the normal, moderately severe, and severe variable or late deceleration groups (Table VII). The means and SDs presented in these data are calculated according to the assessment of 44 children. The child with the dysmorphic syndrome was untestable. Five children were unavailable for follow-up and were not evaluated at 6 to 9 vears of age. Two of these children were assessed by means of Stanford Binet scales at 4 years 6 months and 3 years 9 months and were found to have intelligence quotients of 94 and 100, respectively. Both of these children had normal FHR patterns. One child with 70 minutes of severe variable decelerations is known to have normal school performance at 7 years 10 months. Two children examined at 3 vears 6 months and 3 years were neurologicallv and developmentallv normal at that time. These two children had moderately severe variable decelerations for 39 and 95 minutes, respectively. Durations of fetal heart rate pattern abnormalities ranged from 23 to 375 minutes in the moderately severe variable group and from 17 to 975 minutes in the severe variable or late deceleration groups.'' Abnormal portions of the tracings ranged from 8% to 100%," and the duration of monitoring varied from 28 to 1860 minutes. There was no correlation between the duration of FHR pattern abnormalities, neurologic abnormalities in the first year of life, and subsequent cognitive abnormalities within this sample. However, interpretation of these data is limited because not all infants were monitored for the same time period. Beat-to-beat variabilitv was not svstematicallv evaluated. Comment
These data demonstrate that neurologic abnormalities detected by detailed neurologic examination during the first vear of life are found more often in children with abnormal FHR patterns than in children with normal patterns. Except for the child with hearing loss, the degree of asphyxia as determined by FHR patterns of this duration and severity and associated with this intervention is unrelated to fixed neurologic deficits and long-term cognitive abnormalities at 6 to 9 vears of age. The most severelv impaired child represents a developmental malformation svndrome. Abnormal FHR patterns in this child mav have been caused by brain malformations unrelated to asphyxia.'" Certainly the neruoanatomic substrate for central nervous svstem anomalies that cause abnormal heart rates appears to be present.'' These data conform with the findings that the majoritv of children considered to be at risk for cerebral palsy in earlv infancv are found to be developmentally
normal at 7 years of age.'~ The children in this sample improved in motor function without demonstrating mental retardation, and early school problems were not evident. Because the predictive value of abnormal FHR patterns in this sample is 2.6% (l of 38), assigning intrapartum asphyxia as the cause of later developmental abnormalities on the basis of FHR patterns alone in populations with a prevalence of asphyxia similar to that seen at Magee Women's Hospital does not appear justified. The judgment that intrapartum asphyxia is the cause of developmental abnormalities should be made onlv after the likelihood of an asphyctic cause has been established by careful interpretation of the data used to define asphyxia, the presence of a neonatal course and physical signs compatible with asphyxia, and the exclusion of developmental malformations. If one accepts that abnormal FHR patterns are related to asphyxia and that asphyxia mav be detrimental to the developing central nervous svstem, this study attests to the value of intrauterine FHR monitoring as a means of preventing central nervous svstem injury. The fact that many infants demonstrated neurologic abnormalities that were reversible, perhaps because of intervention, supports the use of FHR monitoring as a means of identifying the need for intervention. Conversely, however, periods of abnormal FHR patterns continuing for up to 375 minutes in the moderately severe deceleration group and up to 975 minutes in the severe and late deceleration groups were associated with normal outcome at 6 to 9 years of age. Children subsequentlv found to have developmental malformation may not benefit from intervention. Although not all infants were monitored for the same period of time and definitive statements cannot be made regarding the duration of asphyctic insult the fetus can tolerate before fixed neurologic deficit occurs, these data do not support the conclusion that brief periods of abnormal FHR patterns associated with asphvxia result in irreversible brain injurv. We thank Dr. Alan Leviton and Dr. Kenneth Niswander for their suggestions in the preparation of this manuscript and Ms. Margaret Cook for her diligence in maintaining contact with the children and parents of this studv during the past decade. We also thank Dr. Richard Latchaw for his review of the computerized tomographic studies. REFERENCES I. Schifrin B. The fetal monitoring polemic. Clin Perinatol
1982:9:399-408. 2. Schifrin B, Dame L. Fetal heart rate patterns: prediction of Apgar score. JAMA 1972;219: 1322-5. 3. Benson RD, Shu beck F, Deutsch berger J, Weiss W, Berendes H. Fetal heart rate as a predictor of fetal distress: a report from the collaborative project. Obstet Gynecol 1968:32:259-66.
Painter et al.
4. Bower ET, Beard RW. Finster M. et al. Reliabilitv of fetal blood sampling: maternal-fetal relationships. A~I J OBSTET Gv:'\ECOL 1970;107:279-87. 5. Mvers RE, Mueller-Heubach E, Adamsons K. Predictabiiity of the state of fetal oxygenation from a quantitative analvsis of the components of late deceleration. A~t.J OBSTET Gv:-.JECOL 1973;115:1083-94. 6. Haverkamp AD. Orleans M, Langendoerfer S. McFee J. .\furphv .J. Thompson H. A controlled trial of the differential effects of intrapartum fetal monitoring. A~1 .J OBSTET Gn;ECOL 1979:134:399-412. 7. Wood C. Renou P. OatsJ. Farrell E. Beischer N, Anderson I. A controlled trial of fetal heart rate monitoring in a low-risk obstetric population. AM .J OBSTET Gv:'\ECOL 1981:141:527-34.
October 1988 Am .J Obstet Gmecol
8. Koenigs berger MR . .Judgment of fetal age. I. Neurological evaluation. Pediatr Clin North Am 1966:13:823-33. 9. Painter M.J, Depp R, O'Donoghue P. Fetal heart rate patterns and development in the first vear of life. A:vt J DBSTET GY:'\ECOL 1978;132:271-7. 10. Biale Y. Oshrouskv YB, Vaclari I. Fetal heart rate tracings in fetuses with congenital malformations . .J Reprod Med 1985:30:43-7 . II. Talmon W. Cardiovascular regulation and lesions of the central nervous svstem. Ann Neurol 1985;18:1-12. 12. Nelson K. Ellenberg .J. Children who "outgrew" cerebral palsv. Pediatrics 1982:69:529-36.
Postnatal respiratory function after chronic drainage of fetal pulmonary cyst Margaret Blott,* Kypros H. Nicolaides, BSc, and Anne Greenough, MD, London, England Respiratory function was assessed serially in the first 16 months of life in an infant who was treated antenatally by thoracoamniotic shunting. Both compliance of the respiratory system and functional residual capacity were within the reference range constructed from healthy controls. (AM J 0BSTET GvNECOL 1988;159:858-9.)
Key words: Prenatal therapy, thoracoamniotic shunting, cvstic adenomatoid malformation, pulmonary function, lung growth
In children who have undergone successful neonatal correction of congenital diaphragmatic hernia, there is a long-term residual defect of respiratorv function. The most likely explanation for this is that chronic intrauterine compression of the developing lungs results in irreversible pulmonarv damage. Pleural effusions and pulmonarv cvsts are also associated with intrauterine pulmonary compression and pulmonary hvpoplasia. These conditions, however, can now be treated ante-
From the Department of Child Health and Harris Birthright Research Centre for Fetal Medicine. King's College School of Medicine and Dentistn. Received for publication February 16, 1988: accepted March 5, 1988. Reprint requests: Dr. A. Greenough, Senior Lecturer in Neonatology/Consultant Paediatrician, Department of Child Health, King's College School of Medicine and Dentistry, Bessemer Road. London SE5 9PJ, England. "Supported by Action Research Jot· the Crippled Child.
858
natallv bv thoracoamniotic shunting, .. ~ which prevents neonatal pulmonarv insuffi.ciencv. The aim of the present study was to determine the long-term respiratorv function of an infant who had undergone prenatal decompression of a pulmonary cyst.
Case report Cystic adenomatoid malformation tvpe 1, a solitary cvst in the left lower thorax, was diagnosed in a fetus at 20 weeks' gestation at a routine ultrasound examination. At 24 weeks the cyst had expanded to occupy the whole of the left thorax, producing mediastinal shift and compression of the contralateral lung. In view of the risk of pulmonary hypoplasia, the cvst was drained into the amniotic cavity through a Rockett/King's double pig-tailed catheter.' Insertion of the shunt resulted in rapid expansion of the lung and return of the heart to its normal position. The pregnancy progressed uneventfully and serial scans showed no evidence of the
gested that the primary treatment of this tumor should be excision, not hysterectomy, unless the pathology report of the excised specimen indicates a malignancy. We thank Dr. Vincent Tricomi, Chairman of the Department of Obstetrics and Gynecology at The Brooklyn Hospital-Caledonian Hospital Medical Center, for his constructive review of this case report.
October l 'JHH Am J Obstct (;, ncml
REFERENCES I. Lippert LJ, Richart RM. Ferenczv A. Giant benign endocervical polvp: Report of a case. A~I J 0BSTET (;y:o;ECoL
1974;118:1140. 2. Saier FL. Hovadhanakal P, Ostapouvicz F. c;iant cen·ical polvp. Obstet Gynecol 1973:41 :94-6.
Fetal heart rate patterns during labor: Neurologic and cognitive development at six to nine years of age Michael J. Painter, MD, Mason Scott, PhD, Robert P. Hirsch, PhD, Patricia O'Donoghue, MN, PHP, and Richard Depp, MD Pittsburt;h, Pennsylvania, and Chicago, Illinois The development of 50 children relative to the fetal heart rate patterns they demonstrated during labor and delivery was prospectively studied. Normal deceleration patterns were recorded for 12 of the children, while 16 were recorded as moderately severe and 22 as severe variable or late deceleration patterns. The parity and socioeconomic status of the mothers and the sexes of the infants were similar among the groups. A statistically significant developmental difference in favor of children with normal fetal heart rate patterns was seen in the first year of life. However, at 6 to 9 years of age the difference in neurologic and cognitive development was no longer evident. These data do not support the hypothesis that brief abnormal fetal heart rate patterns recorded during labor are indicative of irreversible central nervous system injury. (AM J 0BSTET GYNECOL 1988:159:854-8.)
Key words: Fetal heart rate patterns. fetal heart rate decelerations, neurologic development. cognitive development
Fetal heart rate ( FHR) monitoring is a technique that is widely used to assess fetal well-being during labor. 1 This technique is considered to have greater sensitivitv and a lower false-negative rate than fetal blood sampling or auscultation. It also is credited with predicting the absence of asphyxia better than any other method."' There is a close relationship between patterns, acidosis, and neonatal compromise.' Because FHR monitoring has a low specificitv, a significant number of fetuses subsequently found to be normal at birth will demonstrate abnormal FHR patterns. FHR monitoring is more costly than monitoring with a stethoscope, and its detractors claim the technique is unproved and unnecessarily interferes with the birth process."·' However, there are significant limitations to the randomized controlled studies that have been perFrom the Departments of Neurology, Obstetrics. and Pediatrics. Universit~ of Pittsburgh and Magee Women's Hospital, and the Department of Obstetrics and Gynecology, Northwestern Universit\' Medical School. Received for publication October 19, 1987; revised May 12, 1988; accepted May 19. 1988. Reprint requests: Dr. Michael]. Painter, Children's Hospital of Pittsburgh, One Children's Place, 3705 Fifth Ave. at DeSoto St .. Pitt5burgh. PA 15213.
854
Table I. FHR pattern definitions 1. Moderate-severe variable: Deceleration to 70 to 80 beats/min range for >60 seconds with three contractions or to a rate <70 beats/ min for 30 to 60 seconds 2. Severe variable: Deceleration to a rate <70 beats/min ;.6() seconds (prior to pushing) on two or more occasions 3. Late decelerations: A uniform deceleration of the FHR of any magnitude that occurs consistently in the late phase of each uterine contraction From Painter M.J, Depp R. O'Donoghue P. 1978:132:271-7.
A~I
.J
0Bsn:T
GY:\ECOL
formed to assess monitoring effects on perinatal morbidity, 1 and the duration of a defined FHR abnormality and its implications for the fetus are unknown. The best association of abnormal patterns with the neonatal condition exists when immediate morbidity is high and intervention has been delayed. The association of FHR patterns and subsequent neurologic development is of obvious importance to an understanding of the significance of specific FHR patterns and the significance of the duration of the defined abnormalitv.
FHR patterns during labor
Volume 159 !\umber 4
Table II. Racial distribution of children at 6- to 9-year follow-up evaluation FHR pattern group Normal Moderately severe variable decelerations Severe variable or late decelerations X'
=
White
855
Table III. Abnormal neurologic evaluations Ages of children at examination Black
FHR pattern
H
2
10
4
9
12
Normal Moderatelv severe Severe or iate
Birth
p
2112 10/16 16/22 = 0.002
6-
p
0112 1/16 6/22 = 0.174
\'1"
0/10 0/14
p
2/21 =
1.000
Fisher's exact test.
6.43.
/J = 0.04.
Table IV. Intelligence quotients of each FHR pattern group FHR jmttern Normal Mean± SD 95'lr CJ Significance Moderatelv severe Mean± SD 95'7r CI Significance Severe or late ~lean ± SD 9.~'7r Cl
VSIQ
PSIQ
FSIQ
97.9 ± 17.2 87.2-108.6 f! = 1.23
9H.6 ± 13.3 90.4-106.8 p = 0.72
98.1 ± 16.6 87.8-108.4 p = 1.45
105.5 ± 12.9 98.7-112.3 p = 0.31
I 10.6 ± 13.0 103.8-1 I 7.4 p = 0.50
108.6 ± 13.1 101.7-115.5 p = 0.25
98.1 ± 14.3 92.0-104.2
98.1 ± 14.3 92.0-104.2
99.5 ± 12 ..~ 94.2-104.8
Factorial analvsis of variance with interaction. VSIQ = Verbal-scale intelligence quotient. PSIQ = Performance-scale intelligence quotient. FSIQ = Full-scale intelligence quotient. C/ = Confidence intervals.
In 1978 we reported the results of a prospective study relating intrapartum FHR patterns to development in the first vear of life." This report is a follow-up study of these infants and comprises the results of psychologic testing and detailed neurologic evaluations at G to 9 vears of age. Material and methods
This study, as previously described," consisted of 50 infants who were born at term, were of appropriate weight for their gestational age (i.e., within l SD of the mean), had no observed congenital anomaly at birth, and had a technicallv adequate internal FHR tracing that was continued until at least 30 minutes before deliverv. Thirtv-eight consecutive infants who demonstrated continuous tracing with repetitive moderatdy severe variable, severe variable, or late decelerations in the late phase of labor were identified (Table I). Of these 38 consecutive tracings, 16 demonstrated moderately severe variable decelerations, 15 showed severe variable decelerations, and seven indicated late deceleration patterns. Twelve consecutive infants who demonstrated normal intrauterine FHR patterns were identified as controls. Indications for monitoring were predominantly fetal," the most common being oxvtocin use, meconium-stained amniotic fluid, inertial labor. and premature rupture of the membranes. One perinatologist (R. D.) interpreted all FHR patterns and graded the severity; one pediatric neurologist
(M. J. P.) performed all neurologic evaluations. Results of FHR assessments were unknown to M. J. P. and results of the neurologic evaluations were unknown to R. D. Neurologic evaluations were performed neither less than 12 hours nor more than 3 days after delivery, and the examination of Prectl as modified by Koenigsberger" was used. Sequential neurologic examinations were performed at 2, 4, 6, 9, 12. 18, and 24 months of age and vearly thereafter. Psvchologic testing was performed at appropriate ages by one psychologist (M. S.). The Wechsler Intelligence Scale for Children-Revised (or Leiter International Performance Scale), the Wide Range Achievement Test, and the Bender Visual Motor Gestalt Test were used. FHR pattern interpretations and neurologic evaluations were unknown to M. S. Of the 50 children, 45 (90%) were seen at 6 to 9 years of age for neurologic evaluation and 44 were given psychologic tests. Results
At birth there was no significant difference in the clinic statuses of the mothers or in the mean birth weights or sexes of the infants." There was a statistically significant difference in the races of the mothers among the groups (Table II). Two of the 12 infants with normal FHR patterns and 26 of the 38 with ominous FHR patterns had abnormal neonatal neurologic evaluations. The majoritv of these infants demonstrated hypotonia of the lower extrem-
856
Painter et al.
October 1988 Am J Obstet Gvnecol
Table V. Intelligence quotients of black children FHR pattern
I
Normal Mean± SO 95% CI Moderately severe Mean± SO 95% CI Severe or late Mean± SO 95% CI
VSIQ
PSIQ
FSIQ
97.0 ± 13.5 87.6-106.4
97.8 ± 19.0 87.3-110.7
97.2 ± 17.9 84.8-109.6
94.5 ± 15.6 79.2-109.8
107.2 ± 12.1 95.3-119.1
100.5 ± 13.2 87.6-113.4
93.5 ± 11.4 87.0-100.0
97.3 ± 6.8 93.5-101.1
94.6 ± 7.5 90.4-98.8
Factorial analysis of variance with interaction. VSIQ = Verbal-scale intelligence quotient. PSIQ = Performance-scale intelligence quotient. FSIQ = Full-scale intelligence quotient. C/ = Confidence intervals.
Table VI. Intelligence quotients of white children FHR pattern
I
Normal Mean± SO 95% CI Moderately severe Mean ±·so 95% CI Severe or late Mean± SO 95% CI
VSIQ
PSIQ
FSIQ
101.5 ± 9.2 88.7-114.3
102.0 ± 17.0 78.4-125.6
101.5 ± 14.8 81.0-122.0
109.9 ± 10.8 103.2-116.6
111.9 ± 12.5 I 04.2-119.6
111.9±12.2 104.3-119.:)
I 04.25 ± 19.6
108.6 ± 10.5 I 01.7-115.5
105.3 ± 15.3 95.3-115.3
91.4-117.1
Factorial analysis of variance with interaction. VSIQ = Verbal-scale intelligence quotient. PSIQ = Performance-scale intelligence quotient. FSIQ = Full-scale intelligence quotient. C/ = Confidence intervals.
Table VII. Wide Range Achievement Test subtest results FHR groups
Reading
Normal 100.8 ± 8.5 Moderately 109.6 ± 12 severe Severe or late 101.6 ± 16
Mathematics
104.8 ± 10 100.0 ± 10 107.8 ± 11.3 106.8 ± 8.2 103.2 ± 13.3 104.5 ± 13A
Repeated measures analysis of variance.
p = 0.36
ities. The number of abnormal neurologic evaluations decreased during the first year so that none of the 12 infants with normal FHR patterns had abnormal evaluations at l year of age. One pf 16 infants with moderately severe variable decelerations and six of 22 infants with severe variable or late decelerations had abnormal evaluations at 1 year of age (Table Ill). A significantly greater number of infants with normal FHR patterns demonstrated neurologic abnormalities at birth. The difference at 1 year of age was less apparent, and there was no statistically significant difference at 6 to 9 years of age (Table III). Two children with severe variable or late deceleration patterns during labor and delivery had neurologic abnormalities at 6 to 9 years of age. The one child with developmental arrest who dem-
onstrated almost 10 hours of severe variable decelerations has undescended testes. coarse features. widespread and malformed teeth, and prognathism that have become more evident with increasing age. A computerized tomographic scan performed at his most recent evaluation indicated multiple asvmmetric lowdensity regions involving the cerebral hemispheres and cerebellum, a small cerebellum and brain stem. and a markedlv enlarged fourth ventricle. Manv gvri appeared malformed. The evaluation of this child suggests he has an unspecified dysmorphic svndrome. One child who sustained repetitive late decelerations for at least 130 minutes prior to delivery has a significant neurosensory hearing loss but is otherwise neurologically normal. Cognitive testing as determined bv the Wechsler Intelligence Scale for Children-Revised or the Leiter International Performance Scale revealed no significant difference in verbal-scale intelligence quotient (IQ). performance-scale IQ, or full-scale IQ among the groups (Table IV). Because of a statisticallv significant racial imbalance, subscales of the Wechsler Intelligence Scale for Children-Revised were analvzed separatelv for white and black children. There was no significant difference between black and white children with regard to normal, moderatelv severe variable. severe variable, and late deceleration scores (Tables V, VI). The average ievel of achievement within the areas of read-
FHA patterns during labor 857
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ing, spelling, and mathematics as measured by the Wide Range Achievement Test indicated no difference between the normal, moderately severe, and severe variable or late deceleration groups (Table VII). The means and SDs presented in these data are calculated according to the assessment of 44 children. The child with the dysmorphic syndrome was untestable. Five children were unavailable for follow-up and were not evaluated at 6 to 9 vears of age. Two of these children were assessed by means of Stanford Binet scales at 4 years 6 months and 3 years 9 months and were found to have intelligence quotients of 94 and 100, respectively. Both of these children had normal FHR patterns. One child with 70 minutes of severe variable decelerations is known to have normal school performance at 7 years 10 months. Two children examined at 3 vears 6 months and 3 years were neurologicallv and developmentallv normal at that time. These two children had moderately severe variable decelerations for 39 and 95 minutes, respectively. Durations of fetal heart rate pattern abnormalities ranged from 23 to 375 minutes in the moderately severe variable group and from 17 to 975 minutes in the severe variable or late deceleration groups.'' Abnormal portions of the tracings ranged from 8% to 100%," and the duration of monitoring varied from 28 to 1860 minutes. There was no correlation between the duration of FHR pattern abnormalities, neurologic abnormalities in the first year of life, and subsequent cognitive abnormalities within this sample. However, interpretation of these data is limited because not all infants were monitored for the same time period. Beat-to-beat variabilitv was not svstematicallv evaluated. Comment
These data demonstrate that neurologic abnormalities detected by detailed neurologic examination during the first vear of life are found more often in children with abnormal FHR patterns than in children with normal patterns. Except for the child with hearing loss, the degree of asphyxia as determined by FHR patterns of this duration and severity and associated with this intervention is unrelated to fixed neurologic deficits and long-term cognitive abnormalities at 6 to 9 vears of age. The most severelv impaired child represents a developmental malformation svndrome. Abnormal FHR patterns in this child mav have been caused by brain malformations unrelated to asphyxia.'" Certainly the neruoanatomic substrate for central nervous svstem anomalies that cause abnormal heart rates appears to be present.'' These data conform with the findings that the majoritv of children considered to be at risk for cerebral palsy in earlv infancv are found to be developmentally
normal at 7 years of age.'~ The children in this sample improved in motor function without demonstrating mental retardation, and early school problems were not evident. Because the predictive value of abnormal FHR patterns in this sample is 2.6% (l of 38), assigning intrapartum asphyxia as the cause of later developmental abnormalities on the basis of FHR patterns alone in populations with a prevalence of asphyxia similar to that seen at Magee Women's Hospital does not appear justified. The judgment that intrapartum asphyxia is the cause of developmental abnormalities should be made onlv after the likelihood of an asphyctic cause has been established by careful interpretation of the data used to define asphyxia, the presence of a neonatal course and physical signs compatible with asphyxia, and the exclusion of developmental malformations. If one accepts that abnormal FHR patterns are related to asphyxia and that asphyxia mav be detrimental to the developing central nervous svstem, this study attests to the value of intrauterine FHR monitoring as a means of preventing central nervous svstem injury. The fact that many infants demonstrated neurologic abnormalities that were reversible, perhaps because of intervention, supports the use of FHR monitoring as a means of identifying the need for intervention. Conversely, however, periods of abnormal FHR patterns continuing for up to 375 minutes in the moderately severe deceleration group and up to 975 minutes in the severe and late deceleration groups were associated with normal outcome at 6 to 9 years of age. Children subsequentlv found to have developmental malformation may not benefit from intervention. Although not all infants were monitored for the same period of time and definitive statements cannot be made regarding the duration of asphyctic insult the fetus can tolerate before fixed neurologic deficit occurs, these data do not support the conclusion that brief periods of abnormal FHR patterns associated with asphvxia result in irreversible brain injurv. We thank Dr. Alan Leviton and Dr. Kenneth Niswander for their suggestions in the preparation of this manuscript and Ms. Margaret Cook for her diligence in maintaining contact with the children and parents of this studv during the past decade. We also thank Dr. Richard Latchaw for his review of the computerized tomographic studies. REFERENCES I. Schifrin B. The fetal monitoring polemic. Clin Perinatol
1982:9:399-408. 2. Schifrin B, Dame L. Fetal heart rate patterns: prediction of Apgar score. JAMA 1972;219: 1322-5. 3. Benson RD, Shu beck F, Deutsch berger J, Weiss W, Berendes H. Fetal heart rate as a predictor of fetal distress: a report from the collaborative project. Obstet Gynecol 1968:32:259-66.
Painter et al.
4. Bower ET, Beard RW. Finster M. et al. Reliabilitv of fetal blood sampling: maternal-fetal relationships. A~I J OBSTET Gv:'\ECOL 1970;107:279-87. 5. Mvers RE, Mueller-Heubach E, Adamsons K. Predictabiiity of the state of fetal oxygenation from a quantitative analvsis of the components of late deceleration. A~t.J OBSTET Gv:-.JECOL 1973;115:1083-94. 6. Haverkamp AD. Orleans M, Langendoerfer S. McFee J. .\furphv .J. Thompson H. A controlled trial of the differential effects of intrapartum fetal monitoring. A~1 .J OBSTET Gn;ECOL 1979:134:399-412. 7. Wood C. Renou P. OatsJ. Farrell E. Beischer N, Anderson I. A controlled trial of fetal heart rate monitoring in a low-risk obstetric population. AM .J OBSTET Gv:'\ECOL 1981:141:527-34.
October 1988 Am .J Obstet Gmecol
8. Koenigs berger MR . .Judgment of fetal age. I. Neurological evaluation. Pediatr Clin North Am 1966:13:823-33. 9. Painter M.J, Depp R, O'Donoghue P. Fetal heart rate patterns and development in the first vear of life. A:vt J DBSTET GY:'\ECOL 1978;132:271-7. 10. Biale Y. Oshrouskv YB, Vaclari I. Fetal heart rate tracings in fetuses with congenital malformations . .J Reprod Med 1985:30:43-7 . II. Talmon W. Cardiovascular regulation and lesions of the central nervous svstem. Ann Neurol 1985;18:1-12. 12. Nelson K. Ellenberg .J. Children who "outgrew" cerebral palsv. Pediatrics 1982:69:529-36.
Postnatal respiratory function after chronic drainage of fetal pulmonary cyst Margaret Blott,* Kypros H. Nicolaides, BSc, and Anne Greenough, MD, London, England Respiratory function was assessed serially in the first 16 months of life in an infant who was treated antenatally by thoracoamniotic shunting. Both compliance of the respiratory system and functional residual capacity were within the reference range constructed from healthy controls. (AM J 0BSTET GvNECOL 1988;159:858-9.)
Key words: Prenatal therapy, thoracoamniotic shunting, cvstic adenomatoid malformation, pulmonary function, lung growth
In children who have undergone successful neonatal correction of congenital diaphragmatic hernia, there is a long-term residual defect of respiratorv function. The most likely explanation for this is that chronic intrauterine compression of the developing lungs results in irreversible pulmonarv damage. Pleural effusions and pulmonarv cvsts are also associated with intrauterine pulmonary compression and pulmonary hvpoplasia. These conditions, however, can now be treated ante-
From the Department of Child Health and Harris Birthright Research Centre for Fetal Medicine. King's College School of Medicine and Dentistn. Received for publication February 16, 1988: accepted March 5, 1988. Reprint requests: Dr. A. Greenough, Senior Lecturer in Neonatology/Consultant Paediatrician, Department of Child Health, King's College School of Medicine and Dentistry, Bessemer Road. London SE5 9PJ, England. "Supported by Action Research Jot· the Crippled Child.
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natallv bv thoracoamniotic shunting, .. ~ which prevents neonatal pulmonarv insuffi.ciencv. The aim of the present study was to determine the long-term respiratorv function of an infant who had undergone prenatal decompression of a pulmonary cyst.
Case report Cystic adenomatoid malformation tvpe 1, a solitary cvst in the left lower thorax, was diagnosed in a fetus at 20 weeks' gestation at a routine ultrasound examination. At 24 weeks the cyst had expanded to occupy the whole of the left thorax, producing mediastinal shift and compression of the contralateral lung. In view of the risk of pulmonary hypoplasia, the cvst was drained into the amniotic cavity through a Rockett/King's double pig-tailed catheter.' Insertion of the shunt resulted in rapid expansion of the lung and return of the heart to its normal position. The pregnancy progressed uneventfully and serial scans showed no evidence of the