Intrapartum fetal heart rate and sudden infant death syndrome TOKE HOPPENBROUWERS, PH.D. BERNARDINO ZANINI, M.D. JOAN E. HODGMAN, M.D. Los Angeles, California The intrapartum fetal heart rate (FHA) tracings of 20 infants who died of sudden infant death syndrome (SIDS) and 20 matched control infants, both drawn from a population at increased obstetrical risk, were compared. This is a blind retrospective study aimed at quantifying (a) the incidence of FHA patterns, (b) the range of FHA and variability levels, and (c) the episodes of variable and late decelerations occurring in conjunction with abnormal FHA levels. Tracings of SIDS infants were similar to those of control infants. Although the three infants with bradycardic FHA levels were restricted to the SIDS group, infants in this group could not be reliably differentiated from control infants on the basis of intrapartum FHA tracings. (AM. J. 0BSTET. GYNECOL 133:217, 1979.)
IN THE LAST TWO DECADES, fetal heart rate (FHR) monitoring has gained worldwide clinical acceptance as a tool for evaluating fetal well being. The identification of specific periodic FHR patterns in response to uterine contractions provides useful information for diagnosis of physiopathologic mechanisms underlying fetal disI ,.,h;]=
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risk for SIDS, 8 exhibited higher median respiratory rates during the first weeks of life as compared to matched control infants. This increase in rate was accompanied by a decreased incidence of apneic episodes. The data constitute indirect evidence supporting the hypothesis of mild hypoxia, which is possibly pres-
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Specifically, it has been reto indicate fetal reserve. ported that late decelerations occurred in conditions characterized by uteroplacental insufficiency and chronic hypoxemia, 4- 5 whereas variable decelerations were related to cord compression causing acute asphyxia. 6 Recent pathologic studies in infants dying of sudden infant death syndrome (SIDS) suggest that death was preceded by mild chronic hypoxemia. 7 Subsequent siblings of SIDS victims, found to be at fourfold increased
chronic hypoxemia preceding SIDS has its origin in prenatal life, it could become manifest in fetal heart rate levels and patterns under the stress of labor. In a previous short communication we examined ll fetal heart rate tracings of infants born at LAC/USC Medical Center who subsequently died of SIDS. Visual inspection of these tracings revealed reactive FHR patterns but no clear indication of instability or impaired autonomic control of the heart rate. 10 It was the objective of the present study to verify and extend these observations. This is a retrospective, blind study aimed specifically at quantifying the incidence of FHR patterns and baseline and variability levels in 20 tracings, and comparing these with those obtained from matched control infants drawn from the same high-risk population as the SIDS group.
2 3 -
From the Newborn Division of the Los Angeles County-University of Southern California Medical Center, Department of Pediatrics, University of Southern California School of Medicine. Supported in part by the National Institute of Child Health and Human Development Contract No. N01-HD-2-2777. Received for /Jublication l'.Jovember 21, 1977.
Revised April 21, 1978. Accepted April28, 1978. Reprint requests: Toke Hoppenbrouwers, Ph.D., Director, Sudden Infant Death Syndrome (SIDS), Research Project, Room 4L40B, Women's Hospital, LAC/USC Medical Center, 1240 Mission Rd., Los Angeles, California 90033. 0002-9378/79/020217+04$00.40/0
1979 The C. V. Mosby Co.
Material and monitoring procedure. A total of 40 infants participated in this study. The experimental group consisted of 20 infants who died of SIDS as confirmed by autopsy reports. They were selected from a group of 65 SIDS infants who were de!ivPrPrl :lt 217
Hoppenbrouwers, Zanini, and Hodgman
January 15, 1979
Table I. Characteristics of the study groups Apgar score
SIDS Mean S.D. Range Control Mean S.D. Range
Durati1m FHR monitoring (min.)
I 5 min.
21.8 5.8 17-38
2.2 I· 7
1.2 2.0 0-6
3Y.3 2.1 34-42
3.184.2 736.4 1,800.0-4,405.0
7.8 2.6 3-10
Y.O 2.1 3-10
312 257 32-865
42 30 15-116
24.1 8.6 16-41
2.5* l.Y 1-7
39.5 1.6 36-42
3,327.3 696.5 1,750.0-4,200.0
7.0 2.5 3-10
8.4 2.3 7-1 ()
334 242 88-1012
72 53 20-216
I 2nd Stage
*One subject was excluded as significant outlier.
Table II. Abnormal FHR baseline and variability FHR Bradycardia 160 b. p.m. Abnormal FHR baseline variability (25 b.p.m.)
LAC/USC Medical Center between 1973 and 1976: selection was based on the availability of intrapartum fetal heart rate tracings of at least 30 minutes' duration. The matching criteria for the control group included birth weight, gestational ages, and date of delivery (equal to or less than seven days from the date of delivery of SIDS infants). The mean birth weights and gestational ages of the infants in each group are provided in Table I. All subjects were monitored in the Fetal Intensive Care Unit. Internal monitoring of FHR and uterine activity was obtained with Corometrics units. Data analysis. The evaluation of the FHR tracings was carried out without knowledge of the individual's group designation. The incidence of FHR patterns in response to uterine contractions was tabulated hy means of Hon"s classification.'' Variable decelerations were further classified according to the method of Kubli and associates12 into mild. moderate, and severe categories. It should be noted that in this classification any uterine contraction can be accompanied by more than one FHR pattern. The range of baseline FHR levels and variability observed throughout the monitoring period was measured. Variability was divided into three categories: decreased b.p.m.), average (6 to 25 b.p.m.), and increased (